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Textbook of Peripheral Vascular Interventions
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Textbook of Peripheral Vascular Interventions Second Edition Edited by
Richard R Heuser
MD FACC FACP FESC
Director of Cardiology, St. Luke's Medical Center; Clinical Professor of Medicine, University of Arizona College of Medicine Phoenix, AZ USA and
Michel Henry MD Interventional Cardiologist Cabinet de Cardiologie Nancy France and Global Research Institute, Apollo Clinic Hyderabad India
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© 2008 Informa UK Ltd First edition published in the United Kingdom in 2004 Second edition published in the United Kingdom in 2008 by Informa Healthcare, Telephone House, 69-77 Paul Street, London EC2A 4LQ. Informa Healthcare is a trading division of Informa UK Ltd. Registered Office: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales number 1072954. Tel: +44 (0)20 7017 5000 Fax: +44 (0)20 7017 6699 Website: www.informahealthcare.com All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication, the ultimate responsibility rests with the prescribing physician. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. For detailed prescribing information or instructions on the use of any product or procedure discussed herein, please consult the prescribing information or instructional material issued by the manufacturer. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN-10: 1 84184 643 0 ISBN-13: 978 1 84184 643 9 Distributed in North and South America by Taylor & Francis 6000 Broken Sound Parkway, NW, (Suite 300) Boca Raton, FL 33487, USA Within Continental USA Tel: 1 (800) 272 7737; Fax: 1 (800) 374 3401 Outside Continental USA Tel: (561) 994 0555; Fax: (561) 361 6018 Email:
[email protected] Book orders in the rest of the world Paul Abrahams Tel: +44 207 017 4036 Email:
[email protected] Composition by Cepha Imaging Pvt. Ltd., Bangalore, India. Printed and bound in India by Replika Press Pvt. Ltd.
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I would like to dedicate the textbook to my wife, Shari; my daughter, Alexandra; and the research staff at the Phoenix Heart Center and the staff at the Phoenix Heart Center, all of whom have made this possible. RRH I would like to dedicate the textbook to my wife, Annick; my daughters, Brigitte and Dr Isabelle Henry; my grand-children, Eva, Nicolas and Romain; my sister and brother-in-law, Mr and Mrs Jacques Vallet and Hervé. I would also like to thank Mrs Michele Hugel, my assistant, for our fruitful collaboration, and Mr Noureddine Frid for his technical collaboration, as well as Dr Antonios Polydorou, for his valuable support, skills and assistance. MH
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Contents List of Contributors
xiii
Preface
xix
Color plates SECTION I: INTRODUCTION
1
1.
Epidemiology and pathophysiology of peripheral arterial disease (PAD) GI Pandele and C Dima-Cozma
3
2.
The endovascular suite and equipment K Dougherty and Z Krajcer
7
SECTION II: TECHNIQUES
13
3.
Arterial access for endovascular interventions: vascular access JS Jenkins
15
4.
Arterial access for endovascular interventions: radial and brachial arterial access PW McMullan Jr and JS Jenkins
21
5.
Arterial access for endovascular interventions: transradial approach I Henry, M Henry, and M Hugel
26
6.
Arterial access for endovascular interventions: popliteal access to peripheral procedures M Henry, I Henry, and M Hugel
29
7.
Introducer sheaths, catheters, guiding catheters, and guidewires K Dougherty and Z Krajcer
34
8.
Percutaneous transluminal angioplasty T Collins and PW McMullan Jr
39
9.
Cutting balloon angioplasty S Tyagi
45
10.
SilverHawk® atherectomy device RS Gammon and JR Nelson
50
11.
Percutaneous peripheral atherectomy using the Rotablator I Henry, M Henry, and M Hugel
59
12.
A new rotational thrombectomy and atherectomy catheter: the Rotarex system I Henry, M Henry, and M Hugel
69
13.
Orbital atherectomy system: a novel means of peripheral vascular rotational atherectomy DT Cragen and RR Heuser
79
14.
Subintimal angioplasty G Markose and A Bolia
83
15.
Recanalization devices for chronic total occlusions (including optical coherent reflectometry) G Baweja and RR Heuser
92
16.
Catheter-directed intra-arterial thrombolytic therapy NN Khanna and RR Kasliwal
99
17.
Thromboaspiration and thrombectomy in peripheral vessels NN Khanna
111
18.
The future of thrombolysis T McNamara
118
vii
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19.
Endovascular treatment for acute and chronic lower extremity deep vein thrombosis PE Thorpe and FJ Osse
119
20.
Stents RR Heuser, KL Waters, CW Hatler, and LM Kelly
132
21.
Role of covered stents in peripheral arterial diseases M Henry, I Henry, and M Hugel
140
22.
Embolic protection devices M Henry, I Henry, A Polydorou, and M Hugel
156
23.
Vascular closure devices ZG Turi
168
24.
Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis JA Silva and JS Jenkins
179
SECTION III: NEUROVASCULAR
185
25.
Epidemiology and pathophysiology of neurovascular disease C Klonaris, A Papapetrou, and A Katsargyris
187
26.
Neuroradiological anatomy MH Wholey and WS Wu
192
27.
Doppler ultrasound and carotid angioplasty: carotid ultrasonography and transcranial Doppler S Kownator and F Luizy
199
28.
The value of transcranial Doppler ultrasonography before, during, and after surgery for carotid occlusive disease NM Bornstein and AY Gur
207
29.
Carotid plaque characterization using ultrasound AN Nicolaides, M Griffin, S Kakkos, G Geroulakos, E Kyriacou, and N Georgiou
211
30.
Cerebral perfusion imaging W-J Jiang
229
31.
Stent-assisted angioplasty for symptomatic atherosclerotic intracranial stenosis W-J Jiang
238
32.
Intracranial stenting for cerebrovascular pathology EI Levy, AS Boulos, BR Bendok, SH Kim, AI Qureshi, LR Guterman, and LN Hopkins
247
33.
The stroke unit P Lylyk and JF Vila
255
34.
Interventional treatment of acute ischemic stroke: past, present, and future CS Eddleman, ZA Hage, DL Surdell, EI Levy, RM Samuelson, YA Mikhaeil, and BR Bendok
288
35.
Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations M Henry, A Polydorou, I Henry, Ad Polydorou, and M Hugel
300
36.
Complications of internal carotid artery stenting and their management DL Surdell, ZA Hage, CS Eddleman, S Das, E Duckworth, MK Eskandari, IA Awad, HH Batjer, and BR Bendok
336
37.
Which patients should be referred for surgical endarterectomy and not have carotid stenting FJ Criado and C Gallagher
345
38.
Common carotid artery: PTA stenting J Franke, G Robertson, and H Sievert
348
39.
Percutaneous transluminal angioplasty of the subclavian arteries M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
353
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ix
40.
Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis V Polydorou, I Henry, A Polydorou, M Henry, Ad Polydorou, J Stephanides, M Hugel, and S Anagnostopoulou
371
41.
Elective endovascular revascularization of the intracranial cerebral arteries HC Schumacher, PM Meyers, B Bateman, and RT Higashida
382
SECTION IV: UPPER EXTREMITY ARTERIAL DISEASES
399
42.
Upper extremity arterial diseases J Laredo and BB Lee
401
43.
Compression syndromes of the superior thoracic aperture JE Molina
408
SECTION V: THORACIC AORTA
415
44.
Thoracic aorta: epidemiology and pathophysiology EB Diethrich
417
45.
Radiology and anatomy of the thoracic aorta AR Owen, GH Roditi, and AW Reid
422
46.
Thoracic aorta: thoracic aortic aneurysms EB Diethrich
432
47.
Thoracic aortic dissection J May, GH White, and JP Harris
439
SECTION VI: ABDOMINAL AORTA
447
48.
Abdominal aortic aneurysm treatment by endoluminal exclusion: a historical perspective JC Parodi, CJ Schönholz, and RR Heuser
449
49.
Role of Doppler ultrasound in the assessment of peripheral vascular disease K Irshad, M Ali, AW Reid, A Sinha, and DB Reid
456
50.
Abdominal aortic dissections OC Morcos, JC Pereda, and ML Marin
461
51.
Endovascular treatment of abdominal aortic occlusive disease C Klonaris and A Katsargyris
467
SECTION VII: THORACOABDOMINAL ANEURYSMS AND DISSECTIONS
473
52.
475
Thoracoabdominal aneurysms and dissections: current indications and management JF Dowdall, Q Lu, and RK Greenberg
SECTION VIII: ATHEROSCLEROTIC RENAL ARTERY STENOSIS
485
53.
Atherosclerotic renal artery stenosis: epidemiology and pathophysiology KI Paraskevas, DP Mikhailidis, and G Hamilton
487
54.
Radiological assessment of the renal arteries A Al-Kutoubi
494
55.
Endovascular treatment of a renal artery stenosis: techniques, indications, and results M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
502
56.
Renal angioplasty and stenting under protection devices M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
525
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57.
Renal artery stenosis: when to refer to surgery? C Klonaris, A Katsargyris, and A Giannopoulos
539
58.
Non-atherosclerotic renovascular disease JM Garasic and K Rosenfield
544
SECTION IX: CELIAC AND MESENTERIC ARTERIES
551
59.
Etiology, natural history, and pathophysiology of mesenteric ischemia JA Silva
553
60.
Assessment of mesenteric ischemia JA Silva
557
61.
Conventional angiography, CTA, and MRA of the mesenteric arteries Y-W Chi and JA Silva
562
62.
Duplex ultrasound of the mesenteric arteries Y-W Chi and JA Silva
570
63.
Endovascular therapy for mesenteric ischemia JA Silva
574
64.
Mesenteric ischemia: surgical revascularization and indications for surgery JA Silva and DE Allie
581
SECTION X: LOWER EXTREMITY
587
65.
Epidemiology and pathophysiology of peripheral arterial disease of the lower extremities C Klonaris, A Papapetrou, and A Giannopoulos
589
66.
Lower extremity arterial disease assessment KF Murphy, K Irshad, A Sinha, and DB Reid
593
67.
Lower extremity: other techniques ML Brennan and L Cho
601
68.
Iliac occlusive diseases DT Cragen and RR Heuser
606
69.
Procedures for the hypogastric artery J Cynamon and P Prabhaker
614
70.
Femoropopliteal disease E Calabrese and F Camerano
625
71.
When to refer to surgery for femoropopliteal disease N Morrissey
630
72.
Infrapopliteal arterial diseases: angioplasty and stenting E Calabrese
633
73.
Critical limb ischemia DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola
639
74.
Acute limb ischemia DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola
648
75.
Endovascular treatment for infrainguinal failing graft A de Carvalho Lobato and DF Colli Jr
656
76.
Thromboangiitis obliterans (Buerger’s disease) A Pokrovsky and AV Chupin
661
77.
Percutaneous endovascular treatment of peripheral aneurysms M Henry, I Henry, and M Hugel
670
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SECTION XI: OTHER LOCALIZATIONS
681
78.
Embolization in peripheral territory CJ Schönholz, E Mendaro, and K Ehrens
683
79.
Uterine artery embolization for fibroids J Pisco and M Duarte
692
80.
Hemodialysis access intervention E Calabrese and B Yasin
699
81.
Endovascular surgery in treatment of some congenital heart defects BG Alekyan, VP Podzolkov, VA Garibyan, MG Pursanov, KE Kardenas, and E Yu Danilov
703
82.
Endovascular treatment of some congenital diseases: hemangiomas and vascular malformations BB Lee, J Laredo, DH Deaton, and RF Neville
712
SECTION XII: UNUSUAL VASCULAR DISEASES OF THE EXTREMITIES 83.
Endovascular management of Budd-Chiari syndrome – suprahepatic inferior vena cava occlusive disease BB Lee, J Laredo, DH Deaton, and RF Neville
723 725
84.
Unusual vascular conditions of the extremities DH Deaton, RF Neville, J Laredo, and BB Lee
732
85.
Interventions in inflammatory arterial disease S Rajagopal and L Gopalakrishnan
736
86.
Vascular involvement in Behçet’s disease TW Kwon
743
SECTION XIII: MULTIVASCULAR DISEASE 87.
Potential of endovascular surgery in the treatment of patients with ischemic heart disease associated with other arterial pools’ pathology LB Bockeria, BG Alekyan, Yu I Buziashvili, EZ Golukhova, TG Niritina NP Mironov, AV Ter-Akopyan, NV Zakarian, and AV Staferov
749 751
SECTION XIV: TREATMENTS FOR RESTENOSIS
761
88.
Pathophysiology of restenosis E Kedhi, J-F Tanguay, and L Bilodeau
763
89.
Interventional therapy: new approaches E Kedhi and L Bilodeau
770
90.
Update on peripheral vascular brachytherapy R Waksman
776
91.
Gene-based and angiogenesis therapy in cardiovascular diseases R Baffour, S Fuchs, and R Kornowski
782
SECTION XV: PTA/STENTING COMPLICATIONS
789
92.
Complications of peripheral interventions DT Cragen and RR Heuser
791
93.
Contrast-induced nephropathy G Marenzi and AL Bartorelli
799
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SECTION XVI: PHARMACOLOGICAL TREATMENTS AND RISK FACTOR MANAGEMENT
809
94.
Pharmacological treatment in peripheral arterial disease GI Pandele and C Dima-Cozma
811
95.
Risk factors in peripheral arterial disease GI Pandele and C Dima-Cozma
822
SECTION XVII: VENOUS DISEASE
827
96.
The anatomy, epidemiology, and pathophysiology of venous disease JI Greenberg, N Angle, and J Bergan
829
97.
Diagnostic evaluation of venous disease B Abai and N Labropoulos
835
98.
Contrast imaging studies of the lower extremity GE Pineda and D Mukherjee
841
99.
Interventional therapy for pulmonary embolism S Faintuch, FB Collares, and GM Martinez Salazar
849
100.
Superior and inferior vena cava thrombosis J Pisco and M Duarte
858
101.
Varicose veins CK Shortell and J Bergan
864
102.
Endovenous laser therapy for varicose veins NN Khanna
870
103.
Vena caval filters NN Khanna
873
104.
Foam treatment of varicose veins JI Greenberg, N Angle, and J Bergan
879
Index
889
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Contributors B Abai
Department of Surgery, Robert Wood Johnson Medical School, Cooper University Hospital, Camden, NJ, USA.
MD
BG Alekyan M Ali
MD PhD
Department of Radiology, King Edward Medical University, Lahore, Pakistan.
MD
A Al-Kutoubi DE Allie
Interventional Cardiology and Angiology Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Department of Diagnostic Radiology, The American University of Beirut Medical Center, Beirut, Lebanon.
MD FRCR DMRD
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
MD
S Anagnostopoulou
MD PhD
Anatomy Department, University of Athens, Greece.
N Angle
MD FACS
IA Awad
BS MSC MD DABNS FACS FICS
R Baffour
B Bateman HH Batjer G Baweja
J Bergan
Interventional Cardiology, Centro Cardiologico Monzino, IRCCS, Institute of Cardiology of the University of Milan, Milan, Italy.
College of Physicians and Surgeons, Columbia University Medical Center, New York, NY, USA.
MD FACS
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Sarver Heart Center, University of Arizona, Tucson, AZ, USA.
MD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD
Department of Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA.
MD
L Bilodeau
Montreal Heart Institute, Montreal, Quebec, Canada.
MD
LB Bockeria A Bolia
MD
MD
BR Bendok
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
The Cardiovascular Research Institute, Washington Hospital Center, Washington, DC, USA.
PhD
AL Bartorelli
Section of Vascular Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA.
MD PhD
Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
MBChB DMRD FRCR
Department of Radiology, Leicester Royal Infirmary, Leicester, UK.
NM Bornstein
MD
AS Boulos
Section of Endovascular Surgery, The Neuroscience Institute; Division of Neurosurgery, Albany Medical Center, Albany, NY, USA.
MD
ML Brennan
Stroke Unit, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
PhD
Clinical and Diagnostic Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Yu I Buziashvili
MD PhD
E Calabrese
National Center for Limb Salvage Clinical Institute “Città di Pavia,” Pavia, Italy.
MD
F Camerano National Center for Limb Salvage, Clinical Institute “Città di Pavia,” Pavia, Italy. Y-W Chi L Cho
DO RVT RPVI FSVMA
Vascular Lab Cardiology, Heart and Vascular Institute, Metairie, LA, USA.
Women’s Cardiovascular Center, The Cleveland Clinic Foundation, Cleveland, OH, USA.
MD FACC
AV Chupin, AV Vishnevsky Institute of Surgery, Moscow, Russia. FB Collares DF Colli Jr TJ Collins
MD MD
Vascular and Interventional Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Angiography Unit, Hospital Samaritano-SP, São Paulo, Brazil.
MD FACC
DT Cragen
MD
Department of Cardiovascular Diseases, Ochsner Medical Center, New Orleans, LA, USA.
Department of Cardiology, St. Luke's Hospital and Medical Center, Phoenix, AZ, USA.
Frank J Criado
MD FACS FSVM
J Cynamon
Division of Vascular Interventional Radiology, Montefiore Medical Center, Bronx, NY, USA.
MD
Vascular Surgery and Endovascular Intervention, Union Memorial Hospital-MedStar Health, Baltimore, MD, USA.
Department of Psychology and Center for Neuroscience, University of Wisconsin-Madison, Madison, WI, USA.
E Yu Danilov
PhD
S Das
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD PhD
A de Carvalho Lobato DH Deaton
MD FACS
EB Diethrich
MD
PhD
Vascular & Endovascular Surgery Institute, Beneficência Portuguesa de São Paulo Hospital, São Paulo, Brazil.
Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA.
Department of Cardiovascular Surgery, Arizona Heart Institute and Hospital, Phoenix, AZ, USA.
xiii
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Contributors
C Dima-Cozma Department of Internal Medicine, 6th Medical Clinic, Iasi University of Medicine and Pharmacie, “Gr. T. Popa,” Iasi, Romania. K Dougherty JF Dowdall M Duarte
CRTT SICP
Peripheral Vascular Interventional Research, St. Luke’s Episcopal Hospital and the Texas Heart Institute, Houston, TX, USA.
Cleveland Clinic Foundation, Cleveland, OH, USA.
MD
Hospital Pulido Valente, Lisbon, Portugal.
MD
E Duckworth
MD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
CS Eddleman
MD PhD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University Chicago, IL, USA.
K Ehrens Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA. M K Eskandari
MD
S Faintuch
Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
J Franke S Fuchs
MD
Cardiovascular Center Frankfurt, Seckbacher Landstrasse, Frankfurt, Germany.
MD MD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
The Cardiovascular Research Institute, Washington Hospital Center, Washington, DC, USA.
C Gallagher
MD
Union Memorial Hospital-MedStar Health, Baltimore, MD, USA.
RS Gammon
MD
Austin Heart Physician’s Association, Austin, TX, USA.
JM Garasic
Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA.
MD
VA Garibyan N Georgiou
MD
RN
Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Vascular Screening and Diagnostic Centre, Nicosia, Cyprus.
G Geroulakos FRCS DIC PhD Department of Cardiology, Charing Cross and Ealing Hospital; Imperial College of Science Technology and Medicine; Royal Society of Medicine, London, UK. A Giannopoulos EZ Golukhova
MD
MD PhD
L Gopalakrishnan Chennai, India. JI Greenberg
AY Gur
MD
LR Guterman NY, USA.
Non-Invasive Arrhythmology Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. Department of Cardiology, Institute for Cardiac Treatment and Research, Southern Railway Headquarters Hospital, Perambur, Department of Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA.
Department of Endovascular Research, Cleveland Clinic Foundation, Cleveland, OH, USA.
MSc PhD
MD PhD
ZA Hage
MD
MD FRCS
RK Greenberg M. Griffin
Department of Surgery, Athens University Medical School, Athens, Greece.
The Vascular Noninvasive Screening and Diagnostic Centre, London, UK.
Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
PhD MD
Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo State, University of New York, Buffalo,
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University Chicago, IL, USA.
MD
G Hamilton MD FRCS Academic Department of Surgery, Royal Free Hospital and Royal Free University College Medical School, University College London, London, UK. JP Harris, Department of Surgery, University of Sydney, Sydney, New South Wales, Australia. CW Hatler CJ Hebert I Henry
PhD RN
RT-R RCIS
Cabinet de Cardiologie, Nancy, France; Global Research Institute, Apollo Clinic, Hyderabad, India.
MD
RR Heuser
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA
Polyclinique Bois Bernard, Bois Bernard, France.
MD
M Henry
Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
MD FACC FACP FESC
RT Higashida
MD
Department of Cardiology, St. Luke's Medical Center; University of Arizona College of Medicine, Phoenix, AZ, USA.
Department of Radiology, University of California, San Francisco Medical Center, San Francisco, CA, USA.
LN Hopkins
MD
M Hugel
RN
Cabinet de Cardiologie, Nancy, France.
K Irshad
FRCS
JS Jenkins
Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Buffalo, NY, USA.
King Edward Medical University, Lahore, Pakistan.
MD FACC FSCAL
Ochsner Heart & Vascular Institute, New Orleans, LA, USA.
W-J Jiang MD PhD Department of Neuroradiology and Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University (CPU), Beijing, People’s Republic of China. S Kakkos
MD PhD DIC
KE Kardenas
MD PhD
Division of Vascular Surgery, Imperial College, London, UK. Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
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Contributors
xv
RR Kasliwal Indraprastha Apollo Hospitals, New Delhi, India. A Katsargyris E Kedhi
Medisch Centrum Rijnmond Zuid (MCRZ) - Hospital Rotterdam, Rotterdam, The Netherlands.
MD
LM Kelly
1st Department of Surgery, Vascular Division, Athens University Medical School, Athens, Greece.
MD
Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
RN MBA
NN Khanna
MBBS MD DM FICC FEISI
Department of Cardiology, Indraprastha Apollo Hospitals, New Delhi, India.
SH Kim MD Department of Neurosurgery, Toshiba Stroke Research Center, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. C Klonaris
R Kornowski S Kownator Z Krajcer
Athens University Medical School, Athens, Greece.
MD
Baylor College of Medicine, University of Texas Health Science Center, Houston, TX, USA.
Department of Computer Science and Engineering, Frederick University Cyprus, Palouriotisa, Nicosia, Cyprus.
PhD
N Labropoulos
MD PhD
EI Levy
MD
MD
BSc (Med) PhD DIC RVT
MD PhD RVT
BB Lee
Q Lu
Department of Surgery, University of Ulsan College of Medicine and Asan Medical Center, Songpa-gu, Seoul, South Korea.
MD PhD
E Kyriacou
J Laredo
Cabinet de cardiologie, Thionville, France.
MD
MD
TW Kwon
Cardiac Catheterization Unit, Department of Cardiology, Rabin Medical Center, Petah Tikva, Israel.
MD
Department of Surgery, Stony Brook University Medical Center, Stony Brook, NY, USA.
Division of Vascular Surgery, Georgetown University Hospital, Washington, DC, USA.
Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA.
Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Millard Fillmore Gates Circle Hospital, NY, USA.
Cleveland Clinic Health Systems Foundation, Cleveland, OH, USA.
F Luizy
MD
Cabinet de cardiologie, Thionville, France.
P Lylyk
MD
Clinica Medica Belgrano and FLENI, Buenos Aires, Argentina.
G Marenzi ML Marin
MD
Department of Surgery, Mount Sinai School of Medicine, New York, NY, USA.
MD
G Markose
Coronary Care Unit, Centro Cardiologico Monzino, IRCCS, Institute of Cardiology of the University of Milan, Milan, Italy.
BSc (HONS.) MBBS MRCP (UK) FRCR
Department of Radiology, Leicester Royal Infirmary, Infirmary Square, Leicester, UK.
GM Martinez Salazar MD Vascular and Interventional Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. J May
MD MS FRACS FACS
Department of Surgery, University of Sydney, New South Wales, Australia.
PW McMullan Jr
MD
T McNamara
Section of Interventional Radiology, University of California School of Medicine, Los Angeles, CA, USA.
MD
Department of Interventional Cardiology, Ochsner Medical Center, New Orleans, LA, USA.
E Mendaro MD Department of Vascular Interventional Radiology, Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA. PM Meyers MD Neuroendovascular Services, Department of Radiology and Neurosurgery, Columbia and Cornell University Medical Centers, New York, NY, USA. YA Mikhaeil
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD
DP Mikhailidis BSc MSc MD FACB FFPM FRCP FRCPath Department of Clinical Biochemistry (Vascular Disease Prevention Clinic), Royal Free Hospital and Royal Free University College Medical School, University College London, London, UK. NP Mironov
Volynskaya Hospital, Moscow, Russia.
MD
EV Mitran
MD PhD
JE Molina
MD
OC Morcos
Division of Vascular Surgery, University of Illinois at Chicago, Chicago, IL, USA.
MD FACS
D Mukherjee KF Murphy
Cardiothoracic Surgery, Minneapolis, MN, USA.
MD
N Morrissey
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
MD
MRCS
JR Nelson
BS
RF Neville
MD
Division of Vascular Surgery, New York-Presbyterian Hospital, Weill Medical College, Cornell University, New York, NY, USA.
Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA. Vascular & Endovascular Institute, Wishaw Hospital, Scotland.
Austin Heart Physician’s Association, Austin, TX, USA. Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA.
AN Nicolaides MS FRCS FRCSE PhD (HON.) Imperial College, London; University of Cyprus, Vascular Screening and Diagnostic Centre, Nicosia, Cyprus.
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Contributors
TG Niritina
MD PhD
FJ Osse
Endovascular Surgery, Sanmaritano Hospital, São Paulo, Brazil.
MD
AR Owen
Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
BSc MRCP FRCR
GI Pandele
MD PhD
A Papapetrou
Department of Radiology, Glasgow Royal Infirmary, Glasgow, UK.
Department of Internal Medicine, 6th Medical Clinic, Iasi University of Medicine and Pharmacie, “Gr. T. Popa,“ Iasi, Romania. Department of Vascular Surgery, Athens University School of Medicine, Athens, Greece.
MD FEBVS
KI Paraskevas MD FASA Department of Clinical Biochemistry (Vascular Disease Prevention Clinic) and Academic Department of Surgery, Royal Free Hospital and Royal Free University College Medical School, University College London, London, UK. JC Parodi
Department of Vascular Surgery, Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
MD
RR Patlola JC Pereda
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
MD
South Miami Hospital, Miami, FL, USA.
MD
GE Pineda
MD
J Pisco
New University of Lisbon, Lisbon, Portugal.
MD
Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA.
VP Podzolkov A Pokrovsky
MD PhD
Congenital Heart Disease Surgery Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
AV Vishnevsky Institute of Surgery, Moscow, Russia.
MD
A Polydorou General Hospital “Agios Panteleimon,” Nikaea, Piraeus, Greece. Ad Polydorou
MD
General Hospital “Agios Panteleimon,” Nikaea, Piraeus, Greece.
V Polydorou
MD
General Hospital Nikaea Piraeus “Agios Panteleimon,” Greece.
P Prabhaker
MD
Division of Vascular Interventional Radiology, Montefiore Medical Center, Bronx, NY, USA.
MG Pursanov AI Qureshi
MD PhD
Department of Interventional Cardiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Department of Neurology and Neurosciences, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
MD
S Rajagopal MD Department of Cardiology, Institute for Cardiac Treatment and Research, Southern Railway Headquarters Hospital, Perambur, Chennai, India. AW Reid DB Reid
MD FRCR FRCP
Vascular & Endovascular Institute, Wishaw Hospital, Scotland.
MD FRCS
G Robertson GH Roditi
MD
Emory University Heart and Vascular Center, Atlanta, GA, USA.
FRCP FRCR
K Rosenfield
MD
Glasgow Royal Infirmary, Glasgow, Scotland.
Department of Radiology, Glasgow Royal Infirmary, Glasgow, UK.
Division of Vascular Medicine and Intervention, Massachusetts General Hospital, Boston, MA, USA.
RM Samuelson MD Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Millard Fillmore Gates Circle Hospital, Buffalo, NY, USA. CJ Schönholz CK Shortell
MD
MD
Department of Radiology, Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
Division of Vascular Surgery, Duke University Medical Center, Durham, NC, USA.
HC Schumacher MD Doris and Stanley Tanenbaum Stroke Center, Neurological Institute, Interventional Neuroradiology, New York Presbyterian Hospital, Columbia University Medical Center, NY, USA. H Sievert MD FSCAI FESC FACC Cardiovascular Center Frankfurt, Sankt Katharinen, Frankfurt, Germany; Cath Lab for Peripheral Vascular Interventions and Structural Heart Defects, Washington Hospital Center and Cardiovascular Research Institute, Washington, DC, USA. JA Silva
MD FACC FACAI
A Sinha
FRCS
Tchefuncte Cardiovascular Associates and TCA Research, Covington, LA, USA.
Vacular & Endovascular Institute, Wishaw Hospital, Scotland.
AV Staferov MD PhD Department of Interventional Cardiology and Angiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. J Stephanides DL Surdell
MD
MD
J-F Tanguay
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD
Montreal Heart Institute, Montreal, Quebec, Canada.
AV Ter-Akopyan PE Thorpe ZG Turi
Department of Surgery, Veterans Hospital, Athens, Greece.
MD PhD
MA MD FSIR
MD
Hospital Volynskaya, Moscow, Russia.
Endovascular Surgery & Interventional Radiology, Arizona Heart Hospital, Phoenix, AZ, USA.
Robert Wood Johnson Medical School, Camden, NJ, USA.
S Tyagi MD DM FAMS Department of Cardiology, G.B. Pant Hospital & Maulana Azad Medical College, New Delhi, India. R Waksman
MD
Cardiovascular Research Institute, Washington Hospital Center, Washington, DC, USA.
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MD
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Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
KL Waters
FNP-C
Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
GH White
MBBS FRACS
Department of Surgery, University of Sydney, Sydney, New South Wales, Australia.
MH Wholey MD MBA Central Cardiovascular Institute of San Antonio, University of Texas Health Science Center, San Antonio, TX, USA. WS Wu
MD
Central Cardiovascular Institute of San Antonio, University of Texas Health Science Center, San Antonio, TX, USA.
B Yasin
MD
National Center for Limb Salvage, Clinical Institute “Città di Pavia,“ Pavia, Italy.
NV Zakarian MD PhD Department of Interventional Cardiology and Angiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
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Preface This textbook, the second edition of our original Textbook of Peripheral Vascular Intervention, is a collaborative effort with Dr. Henry, myself, and Alan Burgess from Informa Healthcare Publishing. We have incorporated contributions from world opinion leaders in the areas of technical developments of endovascular devices and new treatment strategies. Our goal is to make the second edition the most definitive textbook available. As the nature of medical care becomes more preventive, rather than crisis-driven, the diagnosis of treatments for peripheral vascular disease becomes more relevant to everyday practice. Helping patients deal with lifestyle changes resulting from disease becomes more relevant as our population ages. Approximately two million patients in Europe and the United States suffer from critical limb ischemia. Nearly half of these sufferers will require major amputation within one year after the onset of limb ischemia. In addition, in the United States, prevalence of abdominal aortic aneurysm is quite significant. In 2002, 200 000 abdominal aortic aneurysms were diagnosed, adding to the estimated one and half million patients who currently experience this disease. In fact, 10% of men older than 80 years of age have had a significant abdominal aortic aneurysm. Furthermore, 20% of the patients who undergo coronary intervention have renal artery stenosis, with as many as 50% of those patients having critical stenosis. Embolic protection traditionally used for carotid intervention is now being applied in both femoral and renal applications.
We have also seen an explosion in our ability to screen patients with peripheral vascular disease; a potent predictor of comorbid cardiovascular disease. The Textbook of Peripheral Vascular Interventions, Second Edition will discuss therapies that can make a real difference in the lives of patients. Effective, less invasive approaches to therapies for critical limb ischemia, chronic total occlusions, as well as therapies for some subsets, will be discussed. It is clear that in the future patients will be demanding less invasive procedures. This book stands as a tribute to the pioneering work of Charles Dotter and Andreas Gruentzig. Their initial vision and successful demonstration of early techniques for peripheral intervention have guided the development of these endovascular interventions for the last 43 years. We hope that this textbook will serve as a practical source of information for students, physicians in training, radiologists, cardiologists, and vascular surgeons performing peripheral intervention, and that it will become a comprehensive introduction to endovascular techniques. Dr. Henry and I would like to acknowledge the hard work of Mrs Valérie Davot whose help in coordinating our contributing authors was invaluable. Richard R Heuser MD has donated all his royalties for this textbook to The American Heart Association and the Osler Fund at Johns Hopkins Hospital. Richard R Heuser MD
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SECTION I Introduction
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Epidemiology and pathophysiology of peripheral arterial disease (PAD) GI Pandele and C Dima-Cozma
Epidemiology Peripheral arterial occlusive disease (PAD) of atherosclerotic origin has an incidence and prevalence nearly equal to coronary artery disease.1 The reported prevalence of PAD depends greatly on the demographic factors of the population and on the method of diagnosis. The first step is to measure the ankle–brachial index resting and during exercise, which is normally greater than 0.90. PAD is still underdiagnosed because only 10–30% of all PAD patients have symptoms such as intermittent claudication.2,3 It affects almost 12 million people in the US and 20% of symptomatic patients with PAD have diabetes. PAD is also a risk factor for lower-extremity amputation and for systemic vascular disease in coronary, cerebral, and renal vessels.4 Incidence and prevalence The incidence of PAD in the Framingham Study5 was 3.5/1000 for women and 7.1/1000 for men. In a study of 2327 subjects conducted in the Netherlands6, the incidence for asymptomatic PAD was 7.8/1000 for women and 12.4/1000 for men. The PARTNERS program enrolled 6979 patients and characterized patients with polyvascular determinations. Of the total number of patients enrolled, 16% had PAD and cardiovascular disease, 13% had PAD but no cardiovascular disease, 24% had no PAD but had cardiovascular disease, and 47% had evidence of neither.7,8 Another survey of patients with diabetes9 who were more than 50 years of age showed a prevalence of PAD of 29%. Morbidity and mortality Patients with PAD have a higher risk of contracting coronary, renal, and cerebrovascular disease. In the ARIC study, subjects with PAD had twice the frequency of cardiovascular disease than those without PAD. The ankle–brachial index (ABI) is an independent predictor of mortality. The total mortality relative risk (RR) is 4.5 for all patients with an ABI smaller than 0.40. The total mortality is slightly increased in men.7
Pathophysiology The main cause of PAD is atherosclerosis, responsible for more than half of all deaths in Western industrialized countries. Atherosclerosis, a slowly progressing arterial disease with
an asymmetric and asynchronous evolution, is initiated in intima by the deposition of fibrous and lipid materials that gradually narrow the lumen and diminish the blood supply to various tissues such as the brain, heart, kidney, intestine, and limbs (in particular the lower limbs). The process of atherogenesis is, in order of site frequency, localized at the abdominal aorta, coronary arteries, popliteal, and cerebral arteries.2 Endothelial damage seems to be the primary event and is produced by high mechanical stress caused by hypertension. A direct effect of chlamydial infection may lead to plaque formation, as a consequence of increased lipid uptake in the vessel wall and the adhesion of monocytes and thrombocytes, under the influence of homocysteine.7 After monocytes penetrate into the intima, they transform into macrophages. The macrophage is able to release reactive O2 radicals, the superoxide anion that damages the endothelial cells and inactivates endothelium-formed nitric oxide (NO). The loss of NO action results in adhesion of platelets and monocytes to the endothelium, with proliferation and vasoconstrictive effects in the vascular musculature that favors spasm. The low-density lipoprotein cholesterol (LDL) particles that penetrate into the endothelium are modified by oxidation, and oxidized LDL aggresses the endothelium by enhancing expression of adhesion molecules, which allows the vessel musculature to proliferate. Unrecognized by Apo B 100 receptors, the oxidized LDL particles are gathered by scavenger receptors, which are numerous within macrophages. The macrophages phagocytize LDLs (oxidized lipoprotein particles) and become foam cells. At the same time, chemotactic factors, synthesized and released by monocytes and thrombocytes, determine the migration of smooth muscle cells from the media into the intima, where they are stimulated to proliferate under the influence of PDGF (platelet-derived growth factor) and other growth-promoting factors produced by damaged endothelium and from the muscle cells. They too are transformed into foam cells by the uptake of oxidized LDLs and can also form an extracellular matrix from collagen, elastin, and proteoglycans.11 By plaque deposition, the lumen of the arteries in cerebral, coronary, mesenteric, renal, and peripheral territories is progressively diminished and the consequences are painful ischemia, such as that found in coronary, mesenteric, and peripheral disease, or painless symptoms with critical ischemia in all vascular territories, resulting in cerebral infarction or stroke, mesenteric and renal infarction, and peripheral gangrene. Another consequence is the stiffening of the vessel wall, and bleeding into the plaques and the vessel wall, with 3
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the development of a thrombus which narrows and obstructs the lumen and is the source of emboli in cerebral, coronarian, renal, mesenteric, and peripheral arteries. In addition, the hemorrhage into the plaque-generating hematoma is able to narrow the arterial lumen.11 The atherosclerotic process gives way to the development of aneurysms by weakening the vessel wall. In 90–95% of cases, an aneurysm is caused by atherosclerosis with hypertension. In order of frequency, the location of aneurysms is abdominal and thoracic aorta, cerebral, and peripheral arteries. Besides atherosclerosis, other etiologies of aneurysms include: ● ●
●
congenital; cystic medial necrosis: Marfan’s, Ehlers-Danlos or GsellErdheim syndrome; infection: lues, mycosis in immune-deficient patients.
One of the complications of aneurysms is rupturing, accompanied by hemorrhagic shock if it occurs in a large vessel. Rupture of an intracranial artery will result in a cerebral hematoma and subarachnoid bleeding and a dissecting aneurysm near the heart can lead to acute pericardial tamponade or aortic regurgitation, if the aortic root is involved and thrombosis in the aneurysm occurs with emboli to distal vessels.12,13 Peripheral arterial disease of other etiology than atherosclerosis Acute occlusion of arteries may be the result of a thromboembolism, which usually originates in the heart: from the left atrium in mitral stenosis, atrial fibrillation, left atrial mixoma, the left ventricle in myocardial infarction, dilated cardiomyopathy, or from cardiac valves, which can occur in aortic stenosis, endocarditis, from prosthetic valves, or by paradoxical embolism in intracardiac shunts.14 Pathophysiological characteristics of PAD PAD is generally a bilateral disease and, in the presence of intermittent claudication, the lower extremity blood flow may be normal or slightly diminished in rest with an inability to increase it with exercise.15 In experimental models of ischemic limb, performed in animals by arterial ligation, the intact capacity to produce angiogenic factors is important for maintaining blood flow. The impaired angiogenic response in basic fibroblast growth factor (bFGF) or vascular endothelial growth factor (VEGF) will result in a severe reduction in blood flow, reproducing the clinical situation of patients with critical limb ischemia.16 The extent and intensity of ischemia is more important and sustainable in diabetes, hypercholesterolemia, and hyperhomocysteinemia. Most patients with diabetes demonstrate abnormalities of endothelial function. Hyperglycemia blocks the function of endothelial nitric oxide synthase (eNOS) and free fatty acids may have numerous deleterious effects on normal vascular homeostasis. Diabetes leads to a hypercoagulable state and abnormalities in platelet biology.17 In observational studies, elevated homocysteine levels are associated with PAD. Among other atherothrombotic biomarkers, the total cholesterol/ high density lipoprotein (HDL) cholesterol ratio and C-reactive protein (CRP) were the strongest independent predictors of development of PAD.18,19
Atherothrombosis, an insidious and long-term progressive phenomenon, begins as the result of action of biological, chemical, and mechanical factors that can change the vascular endothelium in different segments of arteries, beginning with the aorta and muscular arteries. Aggression of the endothelium leads to deposition and oxidation of LDL cholesterol, which triggers the subendothelial migration of blood monocytes, which are recognized as scavengers by oxidized LDL and transformed into foam cells. At the site of the injury, foam cells and T-lymphocytes accumulate into the intima and form the fatty streak. The progressive plaque growth is realized by migration of the smooth muscle cells from the media to the intima, where, in response to locally released growth factors, they proliferate. The plaque may be the place of rupture or erosion, followed by exposure of the lipid-rich content to the blood flow allowing platelet adhesion to the damaged endothelium. Platelet activation will determine structural and biochemical modification with the release of adenosine diphosphate, serotonin, thromboxane A2, fibrinogen, and thrombin. By aggregation of the activated platelets, the arterial thrombus will be initiated with partial or total occlusion, producing ischemia in arterial territories of coronary, cerebral, mesenteric, renal, or peripheral vessels. The severity of ischemia depends on the size of the thrombus and also of the possibility of supplying the ischemic territory by collateral circulation. Until now it has remained unclear whether all lesions containing lipids are necessarily precursors of clinically significant atherosclerotic plaques.20 Both age and atherosclerosis are able to determine intimal and total wall thickening besides the lumen diameter modification. Intimal thickening may represent the adaptive response of increased wall stress as has been observed in infants and intrauterine life and was demonstrated experimentally in coronary, carotid, superficial femoral arteries, and the abdominal aorta.21 The direct effect of intimal plaque deposition is the decrease in lumen diameter, which increases the blood flow velocity and wide shear stress, both of which induce dilatation of the lumen to restore the baseline shear stress levels. An increase in intimal plaque volume will determine the increase in outside artery diameter. Another process that maintains an adequate lumen calibrum of the artery is the medio-atrophy that allows the wall to bulge at the level of the atherosclerotic plaque. The selective distribution of plaques is dependent on wall shear stresses that act as a tangential force produced by the blood progression in the artery. The wall shear stress is directly proportional in magnitude to blood flow and blood viscosity and inversely proportional with r3, where r is the radius of the lumen. Acute experimental shear stress enhancement could cause endothelial fracture which starts the process of platelet activation, aggregation, and clot formation.22 The oscillation of shear stress is proportional to the heart rate, which is considered nowadays as an independent risk factor for atherosclerosis. Another important factor in the evolution of atherosclerotic plaque is turbulence of the flow. Turbulence is not an initiating factor of atherogenesis, but may play an important role in plaque disruption and atherothrombosis.23 Hypertension is recognized as an important risk factor for the increase in extent and severity of atherosclerosis. Isolated elevated blood pressure does not reduce atherosclerosis in
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Epidemiology and pathophysiology of peripheral arterial disease (PAD) experimental animal models, but associated with hyperlipemia, hypertension will induce and enhance plaque formation. Even in the presence of hypertension, plaque formation is reduced when cholesterol levels are decreased.24,25 Natural history of atherosclerosis Evolution of atherosclerosis is not always continuous and is characterized by artery stenosis and plaque complications like fracture and thrombosis. After the initiation of the process characterized by biochemical and cellular recruitment into the intima because of the altered endothelial function, smooth muscle cells migrate and proliferate into the subendothelial tissue induced by circulating mitogens. In the evolution of atherosclerosis it is not clear whether inhibiting the recruitment of activated cells will be able to control the evolution of clinical events. For very old people with no clinically manifest atherosclerotic disease in their life, angioscopy of different vascular territories and, finally, the autopsy may reveal advanced atherosclerotic plaques. A very important process operating in atherosclerosis is plaque regression, which may be determined by the resorption of lipids or the extracellular matrix or by cell death and migration. Recently, lipid-lowering diets and treatment with statins have been shown to increase plaque regression. The regression of atherosclerotic lesions has been demonstrated by angiography in the coronary and peripheral arteries.26 The vascular tree susceptibility to plaque formation At the level of the abdominal aorta, the infrarenal segments are particularly susceptible to the development of obstructive
5
atherosclerotic plaques, thrombosis, ulcerations, and aneurysms. The blood flow in the infrarenal aorta is conditioned by muscular activity in lower limbs. Reduced physical activity and sedentarism may result in the reduction of flow velocity in the abdominal aorta. Another factor contributing to atheromatous degeneration of the abdominal aorta is the tendency of the aorta to enlarge with age, and the poor development of intramural vasa vasorum in this segment.27 Superficial femoral artery The arteries of the lower limbs are the elective site of atherosclerotic plaque deposition, because of the differences in hydrostatic pressure and marked variations in flow, depending on the level of physical activity. As shown previously, cigarette smoking and diabetes mellitus are the main risk factors associated with atherosclerosis in femoropopliteal and tibial territories.28 Although the superficial femoral artery is most likely to be affected by multiple stenotic lesions, the profunda femoris tends to be spared. An explanation may be the increased susceptibility to plaque deposition in the superficial femoral artery at the site of stretching by the tendon of adductor magnus. The pathophysiology of intermittent claudication is also explained by metabolic changes present in ischemic skeletal muscle fiber (accumulation of metabolic intermediates, altered control of mitochondrial respiration, increased systemic oxidative stress, and accumulation of somatic mitochondrial DNA mutations) compatible with an “acquired metabolic myopathy” that manifests clinically as muscle weakness, functional impairment, and walking limitation.29
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
11.
Gardner AW, Poehlman ET. Exercise rehabilitation programs for the treatment of claudication pain. A meta-analysis. JAMA 1995; 274: 975–80 Almahameed A. Peripheral arterial disease: recognition and medical management. Cleve Clin J Med 2006; 73 (7): 621–6 McDermott MM, Greenland P, Liu K, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA 2001; 286: 1599–606 Criqui MH. Peripheral arterial disease: epidemiological aspects. Vasc Med 2001; 6 (Suppl. 1): 3–7 Kannel WB, McGee DL. Update on some epidemiologic features of intermittent claudication: The Framingham Study. J Am Geriatr Soc 1985; 33: 13–18 Stoffers HE, Rinkens PE, Kester AD. The prevalence of asymptomatic and unrecognized peripheral arterial occlusive disease. Int J Epidemiol 1996; 25: 282–290. Higgins JP, Higgins JA. Peripheral arterial disease (part I): diagnosis, epidemiology and risk factors. J Okla State Med Assoc 2002; 95 (12): 765–71 Hirsch AT, Hiatt WR, Criqui MH, McDermott MM. PARTNERS: a national survey of peripheral arterial disease symptoms and treatment intensity. J Am Coll Cardiol 2001; 37 (Suppl. A): 126–91 Fowkes FG, Housley E, Cawood EH. Edinburgh Artery Study: prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol 1991; 20: 384–392 Aboyans V, Criqui MH, Denenberg JO, Knoke JD, Ridker PM, Fronek A. Risk factors for progression of peripheral arterial disease in large and small vessels. Circulation 2006; 113 (22): 2623–9 Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 1993; 362: 801–9
12. 13. 14. 15. 16.
17. 18.
19.
20. 21.
Silbernag I, Lang A. Color Atlas of Pathophysiology. Stuttgart: Thieme, 2000: 236–41 Kinlough-Rathbone RL, Mustard JF. Atherosclerosis: current concepts. Am J Surg 1981; 141: 638 Meru AV, Mittra S, Thyagarajan B, Chugh A. Intermittent claudication: an overview. Atherosclerosis 2006; 187 (2): 221–37 Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on the prevalence of peripheral arterial disease. The San Luis Valley Diabetes Study. Circulation 1995; 91: 1472–79 Rajagopalau S, Mohler ER, Raderman RI, et al. A phase II randomized double blind controlled study of adenoviral delivery of VEGF121 in patients with disabling intermittent claudication. Regional angiogenesis with vascular endothelial growth factor (VEGF) in peripheral arterial disease. Circulation 2003; 108: 1933–38 Steinberg HO, Baron AD. Vascular function, insulin resistance and fatty acids. Diabetologia 2002; 45: 623–34 Guallar E, Silbergeld EK, Navas-Acien A, et al. Confounding of the relation between homocysteine and peripheral arterial disease by lead, cadmium and renal function. Am J Epidemiol 2006; 163 (8): 700–8 Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis. A comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein (a) and standard cholesterol screening as predictors of peripheral arterial disease. JAMA 2001; 285 (19): 2481–85 Geng YJ, Libby P. Progression of atheroma: a struggle between death and procreation. Arterioscler Thromb Vasc Biol 2002; 22: 1370–80 Zarins CK, Zatino MA, Giddens DP, et al. Shear stress regulation of artery lumen diameter in experimental atherogenesis. J Vasc Surg 1987; 5: 413
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Textbook of peripheral vascular interventions Fry DL. Acute vascular endothelial changes associated with increased blood velocity gradients. Circ Res 1968; 22: 165 Khalifa AM, Giddens DP. Characterization and evolution of poststenotic flow disturbances. J Biomech 1981; 14: 279 Xu CP, Glagow S, Zatine MA, et al. Hypertension sustains plaque progression despite reduction of hypercholesterolemia. Hypertension 1991; 18 (2): 123 Olin JW. Hypertension and peripheral arterial disease. Vasc Med 2005; 10: 241–6
26. 27. 28. 29.
McDermott MM, Guralnik JM, Greenland P, et al. Statin use and leg functioning in patients with and without lower-extremity peripheral arterial disease. Circulation 2003; 107: 757–61 Cozzi PI, Lyon RT, Davis HR, et al. Aortic wall metabolism in relation to susceptibility and resistance to experimental atherosclerosis. J Vasc Surg 1988; 7: 706 Gordon T, Kannel WB. Predisposition to atherosclerosis in the head, heart and legs: The Framingham Study. JAMA 1972; 221: 661–6 Brass EP, Hiatt WR. Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease. Vasc Med 2000; 5: 55–9
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The endovascular suite and equipment K Dougherty and Z Krajcer
Introduction Endovascular interventions have enjoyed an explosive growth over the last decade. As the number of endovascular procedures being performed each year continues to rise, so does the demand for technologies to improve patient care. Designing the endovascular suite requires careful planning so that all necessary options are taken into consideration. First of all it is important to know who will be using the room. Will it be a vascular surgeon, cardiothoracic surgeon, interventional cardiologist, or interventional radiologist? Consequently, a multidisciplinary team should be created to determine the optimal environment for performing combined surgical and endovascular procedures. The endovascular suite should offer sterile conditions to allow the endovascular specialist a complete gamut of options to treat patients with complex vascular disease. Fully operative sterile conditions will allow immediate conversion from endovascular intervention to a conventional surgical procedure if unexpected complications should occur. The endovascular suite should be large enough to accommodate the equipment and staff needed for emergent surgical conversions, and endoscopic, robotic and hybrid (combined off-pump bypass and coronary angioplasty and stent implantation) surgical procedures.
Design of the procedure room In order to comfortably accommodate the core equipment needed for a state-of-the-art endovascular suite, the size of the suite should be at least 1000 square feet (Figure 2.1),1 with at least two-thirds of the space devoted to procedure area and 350 square feet to the control/observation area (Figure 2.2). The ceiling height should be at least 10 feet2 and the walls should be shielded with 1 mm of lead to provide radiation protection for personnel in surrounding work areas. Observation windows and doors should also be lead treated. The suite should be equipped with emergency power outlets located on the operating table and all four walls of the suite. The endovascular suite should have compressed air, oxygen, and extra suction outlets at both ends of the operating table. The operating table should be non-metallic or radiolucent to minimize radiation exposure and provide exceptional visualization. Communications capabilities should include in-room intercoms, video input and output links to high-bandwidth image routing network, and video/audio recording.
Most of the typical angiography suites and cardiac catheterization suites are primarily designed for catheterbased procedures and do not meet operating room requirements. To offer operating room sterility the endovascular suite should have laminar or negative airflow, and seamless floors, ceilings, and walls that can be washed. An electronic imaging workstation should also be available in the room so that digital computed tomography (CT), magnetic resonance (MR) and ultrasound images can be reviewed during the procedure (Figure 2.2). The suite should be equipped with limited inroom storage using stainless steel cabinets with glass doors. Procedure specific equipment should be stored on carts that can be easily moved in and out of the room (Figure 2.3). In addition, the suite should have certified operating-room shatterproof lighting that allows low, medium, and ultra-bright capabilities. Individual xenon headlamps are also necessary for hybrid procedures. Vascular instrumentation and instrument tables should be readily available in the room. There should also be adequate space for the anesthesiologists, anesthesia equipment, and circulators. The room should have controlled access and outside indicators to specify activation of the fluoroscopic equipment so that inadvertent radiation exposure is prevented.
Requirements for anesthesia The anesthesiologist is consulted for a variety of procedures that are performed in an endovascular suite. The spectrum of anesthesia needed in the endovascular suite ranges from local to general, depending on the needs of the patient and the endovascular team. The organization of the procedural area, therefore, is case-specific, and identifying the location of the high-pressure lines is important to determine where to place the anesthesia equipment. Use of compact anesthesia equipment specifically designed for remote or ambulatory applications allows anesthetic flexibility and improves the efficiency in smaller spaces. Additional portable lead glass shields should be available to protect the anesthesiologist during fluoroscopy and angiography (Figure 2.4).
Fluoroscopy equipment The key component and success of endovascular procedures are dependent on high-quality imaging equipment.1–3 Digital imaging has made large steps since its introduction in the 1980s. 7
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Figure 2.1 A large room is necessary when accommodating endovascular, hybrid, and robotic equipment, and the support staff needed to perform those procedures.
Digital flat-panel detector technology is a film-less environment that has the capability to store images easily in a picture archiving and communications system (PACS) and can be modified at any time.4 Flat-panel detectors not only increase image quality, but also significantly reduce the radiation dose to the patient, staff, and physician, due to improved detective quantum efficiency (DQE).5–7 Additional high-resolution dual LCD video monitors that provide display during live fluoroscopy is of great benefit (Figure 2.5). The video monitors should be able to move from side to side. In addition many systems are also equipped with an integrated optional ultrasound display to improve patient diagnosis and treatment. The operating table should be able to rotate from side to side, tilt for Trendelenburg and Fowlers positions and should be able to rotate on its center axis 180° to allow unobstructed access for antegrade, as well as retrograde, panning. They should be equipped with a table side-controlled system that permits selection of table height, gantry rotation, image magnification,
and storage. In addition, the table should be motor-driven to allow remote high-speed bolus-chase during digital peripheral studies, as well as digital stepping angiography. Digital subtraction angiography has many advantages, including lower contrast amount for diagnostic studies and the ability to perform post-image acquisition to magnify images and improve the image resolution. This digital feature is extremely valuable when using other contrast agents such as CO2 or gadolinium in patients who might be at increased risk for iodinated contrast angiography. CO2 and gadolinium provide lower resolution than iodinated (nephrotoxic) agents and are commonly used for patients with chronic renal insufficiency and for patients with severe allergy to iodinated agents. The fluoroscopy system can be either single or bi-plane. Almost all neuro-endovascular interventions require a biplane system (Figure 2.6); however, for other peripheral endovascular interventions a single plane system will suffice. The fluoroscopy equipment is either fixed or mobile. A fixed
Figure 2.2 A separate control room/observation area protected with lead shielding allows staff members to process and record procedural data without interrupting the intervention. An electronic imaging workstation should also be included so that CT scans, MRAs and ultrasound images can be reviewed during the procedure.
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The endovascular suite and equipment
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Figure 2.3 Procedure-specific equipment carts should be able to move easily in and out of the suite and be stored in a secured central storage.
Figure 2.4 Additional portable lead glass shields should be available to protect the anesthesiologist during long procedures that require general anesthesia.
(a)
(b)
Figure 2.5 (a) Multiple high-resolution screens provide AP and lateral image storage, as well as live fluoroscopy; and (b) additional high-resolution screens should be positioned around the endovascular suite for endoscopic and robotic procedures. (See Color plates.)
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Figure 2.6 The Axiom Artis dBA flat-panel imaging system (Axiom Artis BA, Siemens Medical Solutions, Erlangen, Germany) has a much larger field of view and 3D digital subtraction angiography.
flat-panel detector system uses less radiation and provides approximately 40% more coverage with a larger field of view than older image-intensifier systems. The dynamic range of a flat-panel detector system is 5–10 times greater than the conventional image-intensifier, which allows improved visualization of the vasculature. With improved visualization, contrast agent use can be reduced by approximately 30%.8 This is particularly important when imaging patients with existing renal dysfunction. Advancements in technologies have lead to the implementation of new angiographic applications that provide the interventionalist with information that was previously unavailable in the endovascular suite. Angiographic computed tomography (ACT) offers two-dimensional fluoroscopic images that appear in real time, and superimposes threedimensional reconstructions to provide CT-like 3D images (Dyna CT, Seimens Medical Solutions, Erlangen, Germany) (Figure 2.7a and b). Other system features include orbital and rotational C-arm movements as fast as 60° per second. This feature offers 3D imaging, collimator adjustments, extended dynamic range filtering, and injection triggering during rapid panning. An adjustable source to intensifier distance and
Figure 2.7
processing offers results in immediate image availability. Fixed systems also allow image-review functions to be directly accessible from handheld, in-room remote controls. This option can streamline procedures and minimize delays while archiving angiographic information. Post-processing, and digital image archiving are usually performed at the system console in the control/observation bay area (Figure 2.2). Variable frame rates can also be used to acquire angiographic images, from 0.5 to 30.0 frames per second. Coronary angiography requires 30 frames per second, while most peripheral procedures use 1–5 frames per second. Slower frame rates also reduce radiation exposure, but compromise image clarity.
Imaging techniques Proper positioning of the equipment and good radiographic imaging technique are crucial to the safety and success of endovascular procedures. Angiography using calibrated marker catheters and a graduated marker tape are useful safety measures when deploying stents and stent grafts. The flat-panel
(a) Digitally subtracted and; (b) 3D reconstructed angiography of a carotid pseudoaneurysm.
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The endovascular suite and equipment detector imaging system provides constant resolution over the entire field of view up to ten times greater than the standard 7- or 9-inch image intensifiers that are used in the cardiac catheterization laboratory.8 The square surface configuration of the flat panel eliminates the need for panning or multiple runs. During endovascular thoracic or abdominal aortic aneurysm repair, it is important that the entire field of endograft deployment can be seen on a single view. “Road-mapping” is an imaging technique that allows superimposition of a real-life fluoroscopy on a previously recorded angiographic image. These images are retained as a road map and used to facilitate the positioning of interventional devices. They are also helpful to compare anatomy before and after intervention, and to perform online measurement of the severity of stenosis. This technique is extremely beneficial when negotiating wires and catheters through tortuous vessels and reduces the contrast dose when there is concern of contrast-induced renal dysfunction. High-speed rotation is another useful imaging technique. This is especially helpful when evaluating the degree of stenosis and eccentricity of the vasculature like in the extra-cranial carotid arteries. It can also be used effectively to evaluate the thoracic and abdominal aorta, iliac, and femoral arteries. Like all digital images, however, the drawback of road-mapping and high-speed rotation is that any motion of the vascular structures decreases the quality of the image. Primary sources of movement include cardiac, diaphragmatic, ureteric, and intestinal. Pain is also a frequent cause of movement of the patients. Adequate sedation of patients and the use of lower-osmolality radiographic dyes can help reduce the motion artifact. Because the x-ray beam is shaped like a cone, radial elongation or distortion of the structures occurs at the edges of the field, known as parallax. This type of artifact is also exaggerated by movement and was a problem when using imaging equipment prior to the introduction of flat-panel technology. There is no distortion in the center of the field, but if the position changes from the road map, relative distances change dramatically increasing the parallax artifact. To avoid image artifacts caused by parallax, it is important for the patient and the table to remain stationary during the crucial part of the intervention. Therefore, for precise placement of stents or stent grafts, no movement should occur once the road map has been obtained and no measurements attempted in the outer 20% of the field of view. Parallax is not present when using flat-panel technology. Image storage and reproduction are other important features. Angiographic runs stored on digital memory can be played back for immediate review and can be stored in magnetic or optical discs. Post-processing allows the elimination of artifacts that degrade image quality. Motion artifacts can be eliminated by selecting a new digital mask frame just before the contrast arrives.
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greater need for significant lead shielding to ensure the safety of patients and health-care personnel. Mechanisms to reduce radiation exposure can be divided into those directed at reducing the output of the x-ray unit and those designed to limit the amount radiation in contact with the endovascular team. Staff members should be properly trained in radiation safety principles, equipment, potential complications, and trouble-shooting. Staff members should be able to demonstrate their understanding of the basic concepts of medical imaging and the use of newer imaging systems. The most important method to reduce scatter radiation is to minimize patient dose and the ultimate source of scatter to the operator.9–13 Staff members should monitor judicious use of fluoroscopy and terminate imaging runs as soon as relevant information has been obtained. Other key elements to reduce radiation exposure include collimation, pulsed fluoroscopy, imaging acquisition, frame rates, last image hold, and lower field of magnification. During long procedures the operator and staff members should stand as far back from the unit as possible to take advantage of the fact that radiation exposure decreases exponentially with increased distance from the source. Lead shielding requirements are dictated by stringent radiation safety regulations. Protective lead aprons, thyroid shields, leaded glass screens and leaded eye glasses with side shields are the most effective way to reduce radiation exposure. The suite itself must be lead-lined including the doors, glass, and walls9–13 and all personnel in the room should wear film badges that detect radiation exposure.
Endovascular equipment Supplying an endovascular suite with the necessary tools and equipment can be overwhelming and costly. This task is best solved with a collaborative effort between the endovascular suite, the interventional cardiology suite, and the interventional radiology suite. Much of the same equipment is used for all three specialties and trying to stock a suite with every piece of equipment possible is not practical. The most economical solution is for the departments to work together and have a reimbursement arrangement. However, the endovascular suite should be stocked with the basic necessities such as: ●
●
● ● ●
● ●
puncture needles and guidewires (soft-tip J-wire and peripheral torque wire); various sizes of sheaths (5-French for diagnostics and up to 22-French for stent-grafts); various preformed diagnostic and guiding catheters; non-ionic contrast and power injector (for aortograms); interventional guidewires (0.014–0.018 inches, 180–300 cm in length); balloons (3–40 mm in diameter and 20–60 mm in length); inflation device with gauge; stents and covered stents.
Radiation safety and training
●
With the advent of stents and endoluminal grafts and other endovascular procedures, the use of fluoroscopy is extensive. High-quality, fixed-imaging systems need high heat-capacity tubes to minimize the need for heat-cooling delays that often occur with long imaging times. Furthermore, there is an even
Over time, equipment needs for the endovascular suite will become apparent. Ordering supplies for a special case can be accomplished with careful preplanning on the interventionalist part and collaboration with industry, so that over-expenditure can be avoided.
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Conclusion Endovascular procedures have already changed the way arterial and venous diseases are managed with a greater emphasis on catheter-based interventions. It is likely these techniques will have an even greater influence because of the widespread acceptance of minimally invasive techniques and miniaturization of endovascular devices. Endovascular therapy is the fastest growing area of vascular medicine and requires the fundamental knowledge of modern catheter-based interventions and dedication on the part of practitioners.
Endovascular techniques require specialized skills and training in peripheral vascular diseases, diagnostic angiography, interventional techniques, and therapeutic alternatives. The challenge to the practitioner is intensified by the continual introduction of new products and methods. The establishment of a modern endovascular suite arranged in an ergonomically devised fashion is crucial to remaining on the forefront of developments and will undoubtedly enhance the ability of physicians to provide quality health care to vascular patients with arterial and venous disorders.
REFERENCES 1.
2. 3.
4. 5. 6.
Hodgson KJ, Mattos MA, Summer DS. Angiography in the operating room: Equipment, catheter skills, and safety issues. In: Yao JS, Pearce WH, eds. Techniques in Vascular and Endovascular Surgery. Connecticut: Appleton and Lange, 1998: 25–45 Queral LA. Operating room design for the future. In: Yao JS, Pearce WH, eds. Techniques in Vascular and Endovascular Surgery. Connecticut: Appleton and Lange, 1998: 1–5 Diethrich EB. Endovascular suite design: An integrated approach for optimal interventional performance. In: Criado FJ, ed. Endovascular Intervention: Basic Concepts and Techniques, Armonk. NY: Futura Publishing, 1999: 5–16 Kotter E, Langer M. Digital radiography with large-area flat-panel detector. Eur Radiol 2002; 12: 2562–70 Spahn M, Strotzer M, Völk M, et al. Digital radiography with a largearea, amorphous-silicon, flat-panel x-ray detector system. Invest Radiol 2000; 35: 260–6 Neitzel U, Böhm A, Maack I. Comparison of low contrast detail detectability with five different conventional and digital radiographic imaging systems. In: Krupinski EA, ed. Medical Imaging 2000: Image Perception and Performance. Proc SPIE 2000: 398: 216–23
7. Geijer H, Beckman KW, Andersson T, et al. Image quality vs radiation dose for flat-panel amorphous silicon detector: a phantom study. Eur Radiol 2001; 11: 1704–9 8. Tsapaki V, Kottou S, Kollaros N. Comparison of conventional and a flat-panel digital system in interventional cardiology procedures. Br J Radiol 2004; 77: 562–7 9. ACC/ACR/NEMA Ad Hoc Group. American College of Cardiology, American College of Radiology, and industry develop standards for digital transfer of angiographic images. J Am Coll Cardiol 1995; 25: 800 10. DICOM Media Interchange Standards for Cardiology: Initial interoperability demonstration by Jonathan L. Elion, Brown University 11. Implementation of the principle of as low as reasonable achievable (ALARA) for medical and dental personnel. NCRP Report No. 107. Bethesda, MD: National Council on Radiation Protection and Measurements, 1990 12. Lowe FC, Auster M, Beck TJ, et al. Monitoring radiation exposure to medical personnel during percutaneous nephrolithotomy. Urology 1986; 28: 221–6 13. Bush WH, Jones D, Brannen GE. Radiation dose to personnel during percutaneous renal calculus removal. Am J Radiol 1985; 145: 1261–4
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SECTION II Techniques
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Arterial access for endovascular interventions: vascular access JS Jenkins
Introduction Multiple methods of arterial access have been described since the first documented arterial cannulation in 1733 when Reverend Stephen Hales inserted a brass rod into the surgically exposed artery of a horse and measured pressure via a manometer.1 Since the most common procedural complications involve the initial access to the circulation, this important step deserves full study. The widely used technique of percutaneous retrograde common femoral artery access will not be described here, as it is well described in the literature.2 This chapter will describe the percutaneous techniques of antegrade femoral artery access, contralateral iliofemoral artery access, and popliteal artery access.
Antegrade femoral artery access Anatomy Although the common femoral artery (CFA) is considered by many angiographers to be the safest site for arterial puncture, there is little published data relating the CFA and its bifurcation to the landmarks used to guide arterial puncture. Lechner et al. showed the inguinal skin crease to be distal to the bifurcation of the CFA in 75% of limbs but did not consider other landmarks.3 A thorough understanding of the relationship of the CFA to anatomical landmarks is necessary to ensure safe antegrade CFA puncture. Dotter and Judkins first described the technique of antegrade CFA puncture in 1964.4 The regional anatomy relevant to percutaneous femoral artery puncture is demonstrated in Figure 3.1. The femoral artery and vein are shown coursing underneath the inguinal ligament, which is a band of dense fibrous tissue connecting the anterior superior iliac spine to the pubic tubercle. The inguinal skin crease, which can be highly variable in location, is shown as a dotted line.3 The most important landmark shown in this illustration is the femoral head. In a morphological study of computed tomographic (CT) scans in 50 patients, there was not a single case in which a puncture would have passed cranial to the inguinal ligament or caudal to the femoral artery bifurcation if the common femoral artery were entered at the level of the center of the femoral head.5 Caudal to the femoral head, the CFA is encased in the femoral sheath and bifurcates to the superficial femoral artery medially and the profunda femoral artery laterally. With these anatomical observations in mind, entry of the needle into the CFA at the
center of the femoral head is desirable where osseous support is optimal. Indications and contraindications Endovascular treatment of patients with femoral–popliteal atherosclerotic disease is becoming increasingly more common. Antegrade CFA puncture may be useful or desirable for diagnostic angiography, angioplasty, thrombolytic therapy, or use of atherectomy devices. Anatomical considerations where antegrade CFA puncture may be desirable include an acutely angled common iliac bifurcation and aortoiliac grafts where a contralateral femoral approach may be impossible. Contraindications to antegrade CFA puncture include extreme obesity and atherosclerotic disease involving the CFA. Equipment Equipment necessary to perform antegrade CFA puncture includes a percutaneous needle, a steerable guidewire, and an arterial sheath. A steerable guidewire is desirable to negotiate the CFA bifurcation. A 6-French arterial sheath is the initial size chosen until successful entry is obtained. The sheath size is upgraded if necessary to accommodate larger devices once a treatment plan is formulated. After the arterial sheath is placed in an antegrade fashion, a wire, catheter, or obturator is maintained at all times within the sheath lumen to prevent sheath kinking. Braided sheaths, coiled metal sheaths, or kink resistant sheaths are also useful for antegrade punctures to prevent sheath kinking. Procedure Anatomical landmarks are initially identified by palpation of the anterior superior iliac spine and the pubic tubercle to locate the inguinal ligament, and the femoral head position is confirmed fluoroscopically. Depending on the amount of the subcutaneous fat, a skin incision should be made 1–2 cm cranial to the level of the center of the femoral head. The needle is directed through an oblique downward course while palpating the CFA over the center of the femoral head. Once the CFA has been entered, a steerable guidewire is then advanced under fluoroscopic guidance to select the desired branch. The bifurcation of the CFA is best separated fluoroscopically by a 20° lateral view. Once the sheath has been placed, its lumen is always occupied with a wire or catheter to prevent sheath kinking. 15
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Textbook of peripheral vascular interventions Anterior superior Iliac spine Inguinal skin crease Femoral head
Profunda femoral artery
Inguinal ligament Common femoral artery
Superficial femoral artery
Figure 3.1 The most important landmark is the femoral head. Puncture of the femoral artery at this level almost assures entry caudal to the inguinal ligament and cranial to the femoral artery bifurcation.
Complications Complications of antegrade CFA puncture are most commonly related to either too high or too low arterial entry. When the puncture is too high, a retroperitoneal hemorrhage may occur.6–8 The presence of loose connective tissue in the retroperitoneum can cause large hematomas. The lack of osseous support and the presence of the tense inguinal ligament at the arterial puncture site render manual compression inadequate. Low punctures are complicated by formation of arteriovenous fistulas, false aneurysms and hematomas as well as inadvertent entry into the deep femoral artery or superficial femoral artery, which precludes treatment of ostial disease of either of these vessels.6,7 These complications are avoided by proper identification of bony landmarks and entry into the CFA caudal to the inguinal ligament where the artery can be compressed against the common femoral head. Summary The consistent relationship of the CFA to the femoral head cited in the literature make it the landmark of choice in obtaining antegrade femoral artery access. Reluctance to perform such high skin incision for fear of entering the abdominal cavity has to be avoided to prevent complications of too low a needle entry. Antegrade femoral artery access is a safe technique for performing femoropopliteal angioplasty when reliable landmarks are used.
whether peripheral intervention is a success or failure.6–10 Retrograde common femoral artery access remains by far the most commonly used site and the easiest arterial access method. Peripheral interventionalists should be well familiarized with the contralateral iliofemoral approach as it may be the access of choice for many lesions and a successful technique where other approaches fail. Anatomy Anatomical considerations of the femoral artery and its relationship to the common femoral head have been discussed previously in detail (Figure 3.1). The needle puncture is made in a retrograde fashion through a skin incision 1–2 cm below the midline of the femoral head. The standard retrograde common femoral artery access technique is used and a sheath is placed in the common femoral artery.8 Evaluation of the anatomy of the aortic bifurcation and common iliac arteries is important when considering a crossover technique. The two most common reasons for failure are an acutely angled aortic bifurcation or diffusely diseased and calcified common iliac arteries (Figure 3.2). Initial evaluation begins with an abdominal aortogram performed by placing a pigtail catheter in the terminal aorta. Once suitable anatomy is identified, a flexible guidewire placed in the terminal aorta is directed to the contralateral iliac by means of a 5- or 6-French diagnostic internal mammary artery or Judkins right 4 catheter (Figure 3.3). Once a guidewire is
< 90°
Contralateral iliofemoral artery access Introduction The acquisition and maintenance of vessel access from arterial puncture until sheath removal plays a major role in determining
Figure 3.2 Failure to advance this catheter is caused by the acutely angled aortic bifurcation. Heavily calcified aortic bifurcations also present difficulty in crossing with catheters.
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Guide
Guidewire
6-French IMA diagnostic catheter
Sheath Guidewire
Figure 3.3 A 6-French internal mammary artery (IMA) or Judkins right 4 catheter will direct the guidewire to the contralateral iliac artery.
secured into the contralateral external iliac or common femoral artery, a guiding catheter or long sheath can be advanced to the contralateral side. Indications and contraindications One approach to perform angioplasty of the superficial femoral and profunda femoral artery is via an ipsilateral antegrade common femoral artery puncture.11,12 A contralateral approach is desirable when antegrade access my be difficult to obtain as in obese patients with large panniculus or if lesions are located within the common femoral artery or involve the ostium of the superficial femoral or profunda femoral artery. The proximity of these lesions to the arterial puncture site preclude their treatment if an antegrade ipsilateral approached is used (Figure 3.4). Bifurcation anatomy of the common femoral artery into the superficial femoral and profunda femoral arteries may also render an ipsilateral approach technically impossible and require either a contralateral or popliteal approach.13,14 A contralateral approach also allows treatment of bilateral disease with a single arterial puncture. Other anatomical considerations where a contralateral approach may be desirable include angioplasty of internal iliacs or renal transplant artery stenosis (Figure 3.5). Contraindications to the contralateral approach are generally related to the anatomy of the terminal aortic bifurcation and the anatomy of the lesions to be treated. Acute bends at the bifurcation of the terminal aorta make it difficult to manipulate catheters around the iliac bifurcation and maintain enough pushability in tortuous arteries to cross heavily calcified or obstructive lesions. There is a tendency for guidewires and even guide catheters to prolapse or buckle into the aorta at the bifurcation if the angle is too acute. Aortobifemoral grafts can be negotiated unless the bifurcation angle is too acute. If bulky devices such as peripheral atherocaths or nonsegmented Palmaz stents longer than 30 mm are to be used then
Figure 3.4 The proximity of these lesions to the common femoral artery puncture site precludes antegrade femoral artery access.
a contralateral approach is contraindicated.15 The currently manufactured flexible, premounted balloon expandable stents and self-expanding stents negotiate the aortoiliac bifurcation angle with ease. Equipment and procedure Equipment used to gain contralateral iliofemoral access includes a percutaneous needle, guidewire and arterial sheath to obtain standard retrograde CFA access. Once arterial access is obtained, a guidewire is advanced into the abdominal aorta and a catheter is chosen to access the contralateral common iliac artery. Diagnostic catheters useful in crossing the aortic bifurcations include 5- or 6-French diagnostic Judkins right 4, internal mammary artery, pigtail, and Simmons catheters (Figure 3.3). These catheters placed at the level of the aortic bifurcation will direct a wire into the
Crossover guide Guidewire
Sheath
Figure 3.5 Internal iliac stenoses are best treated from a contralateral approach. An ipsilateral approach necessitates negotiating an acute angle, which is rarely successful.
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contralateral common iliac artery. After positioning a catheter in this manner, either a steerable floppy guidewire such as a 0.035-inch Wholey or an angled Glidewire with its superior lubricity is advanced far into the contralateral femoral artery. The catheter is then advanced over the guidewire into the iliac artery. There are a number of guiding systems that may be used for contralateral iliofemoral angioplasty. They all add the ability to inject contrast during lesion dilations and provide more back-up support when crossing stubborn lesions. Guide catheters which may be used, include a Mullins transseptal sheath, a 40-cm-long Arrow Flex sheath (Arrow International, Inc., Reading PA 19605, USA), a 55-cm-long multipurpose coronary or renal guiding catheter, or a kinkresistant crossover guide currently available from a number of manufactures. Any long sheath chosen should be a braided one as non-braided sheaths have a tendency to kink. The guide is advanced over the aortic bifurcation using the stiff wire. If the guide is a long sheath it is inserted with a dilator. If a guiding catheter is used then a diagnostic multipurpose catheter approximately one French size smaller is inserted through the lumen to extend approximately 1 cm distal to the end of the guide and is secured in place with a Tuohey–Borst Y connector. This minimizes the chance of dissection of the terminal aorta during advancement of the guide contralaterally. Once a guiding system is in place, selective injection of contrast allows visualization of the target lesion. The angioplasty catheter and wire can be positioned under direct visualization with contrast, thus avoiding the need for multiple catheter exchanges over the terminal aortic bifurcation. Complications Complications of contralateral iliofemoral access are most commonly related to the retrograde common femoral artery puncture. They include pseudoaneurysms, arteriovenous fistulas, thromboembolism, infection, retroperitoneal hematomas, and bleeding complications.16–18 The most common bleeding complication is hematoma formation at the arterial access site.19–23 If care is not taken to protect large-bore guides when advancing them over the iliac bifurcation, terminal aortic and common iliac dissections may occur. This complication can be best avoided by protecting the tip of the guide with a diagnostic catheter placed within its lumen to provide a smooth transition from the guidewire to the guiding catheter (Figure 3.6). Crossover sheaths with dilators that create a smooth transition minimize this complication. Summary Historically the ipsilateral approach has been used for superficial femoral artery angioplasty but is limited when treating common femoral artery and proximal superficial artery lesions.12,13,15 With the development of peripheral guiding catheter systems, the contralateral approach extends our ability to perform percutaneous transluminal angioplasty of bilateral disease with a single arterial puncture and treatment of proximal superficial femoral, proximal profunda, and
Guide Guide
6-French catheter
Guidewire (a)
(b)
Figure 3.6 (a) Without protection, the large-bore guide can cause complications; (b) a 6-French diagnostic catheter through the guide lumen will protect against these complications.
common femoral artery lesions, which would be impossible with an ipsilateral approach. Many devices can be used and most stents implanted through this access if the anatomy of the terminal aortic bifurcation is not excessively acute and allows passage of a guiding system. Bulky devices such as the directional atherectomy catheter and long rigid stents are difficult if not impossible to deliver using a contralateral approach. This technique can be performed safely as described and broadens the indications for endovascular treatment of peripheral vascular disease in the lower extremities.
Percutaneous popliteal access Introduction Endovascular treatment of atherosclerotic peripheral vascular disease is most commonly approached via the common femoral artery. Lesion location and anatomy in some scenarios dictate the use of an alternative approach from the brachial artery or popliteal artery which may be successful when standard approaches fail. This section will describe the popliteal anatomy, the technique of popliteal access and its indications. Anatomy It is critical to understand the anatomy of the popliteal fossa when performing percutaneous popliteal artery access to prevent the creation of an arteriovenous fistula. Anatomy textbooks describe the popliteal artery as being anterior and medial to the popliteal vein.24 This anatomical relationship between the artery and vein predisposes percutaneous posterior access to puncture of the popliteal vein (see Figure 3.7). The popliteal artery, vein, and sciatic nerve are encased in a common sheath, which courses upwards along the diagonal of the popliteal fossa as shown. These structures usually remain superficial in location well above the level of the joint space. The semitendinous muscle is seen anterior to the artery.
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Sciatic nerve
Popliteal artery Popliteal vein Tibial nerve Common peroneal nerve
Figure 3.7 The popliteal artery courses medial to the popliteal vein and overlaps 60% of the time at a level of 6.5 cm above the joint space.
Anatomic variations were described by Jean Paul Trigaux et al. by the use of cadaveric specimens, CT scans and plain radiographs of the knee in 67 patients.25 Five levels were studied on a CT scan ranging from the joint space to 6.5 cm cranially. In 92% of all levels studied on CT, the artery was anterior to the vein and in 87% of the levels, more than 25% of the artery overlapped the vein. However, when the most cranial level was considered (6.5 cm cranial to the joint space), overlap occurred in only 60% and the artery was medial to the vein in 25% resulting in the most desirable location for arterial puncture. The plain radiographs of the knee demonstrated the popliteal skin crease to be above the femorotibial joint space in 97% of the cases. This study would indicate the most reliable bony landmark to be the femorotibial joint space and the most favorable puncture site to be 6.5 cm cranial to this space with the puncture needle directed from a medial to lateral course. Puncture of the popliteal artery at this level will also avoid arterial entry below an anomalous high popliteal bifurcation, which occurs in 4.7% of cases.26 Indications and contraindications The popliteal approach is utilized for lesions that have failed the antegrade approach, flush occlusions of the superficial femoral artery or superficial femoral arteries that end in
19
large collaterals which have a tendency to divert angioplasty wires into them. An antegrade approach to superficial femoral artery occlusions generally fails due to the inability to maintain an angioplasty wire within the true lumen of the vessel. Ostial superficial femoral artery and common femoral artery lesions may also be approached via the popliteal access in patients with acute-angled terminal aortic bifurcations. Obese patients with large panniculus and acute-angled terminal aortic bifurcations can be approached with the popliteal access to treat superficial femoral artery disease. Strict contraindications to popliteal artery puncture include aneurysms of the popliteal artery and pathology of the popliteal fossa such as Baker’s cyst. Procedure The patient is first placed in a supine position and retrograde ipsilateral common femoral artery sheath or a contralateral retrograde access is placed for direct visualization of the popliteal artery with contrast medium. This access is secured in place and connected to a high-frequency pressure monitoring line for contrast injections. Visualization of the site to be treated may be afforded with this access. The patient is then turned and placed in a prone position on the angiography table and the popliteal fossa is prepared and draped. The femorotibial joint is the most reliable landmark determined fluoroscopically. An area 3–4 cm above this space is then infiltrated with local anesthetic and a skin incision is made medial to the popliteal artery. Contrast is then injected into the previously placed common femoral artery access for direct fluoroscopic visualization of the popliteal artery during puncture. The puncture needle is directed obliquely from medial to lateral so that the artery is entered 6–7 cm above the level of joint space. A 0.035-inch floppy guidewire is then advanced into the popliteal artery over which a 6-French arterial sheath is placed. In addition to direct contrast visualization, ultrasound guidance can be employed to gain retrograde popliteal artery access. This technique avoids ipsilateral or contralateral CFA access. Complications As with any arterial puncture, hematomas occur at rates of 2–4% when popliteal artery access is used.15,27,28 The anatomical relationship of the popliteal artery to popliteal vein increases the risk of arteriovenous fistula due to transvenous arterial puncture. The risk can be minimized with attention to the anatomical considerations previously discussed and higher punctures directed from medial to lateral. Summary Popliteal access is a useful technique which allows endovascular treatment of peripheral arterial disease not approachable by other techniques. Still, it is probably the least-used access by the peripheral interventionalist. With close attention to the anatomical considerations and technique, it is a safe and reliable approach to many lesions using percutaneous methods.
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REFERENCES 1. 2. 3.
4. 5. 6.
7. 8. 9. 10. 11. 12.
13.
Hales S, Hales S. Statical essays, 3rd edition with amendments. London: Printed for W. Innys and R. Manby, T. Woodward and J. Peele; 1738 Seldinger SI. Catheter replacement of the needle in percutaneous arteriography; a new technique. Acta Radiol 1953; 39(5): 368–76 Lechner G, Jantsch H, Waneck R, et al. The relationship between the common femoral artery, the inguinal crease, and the inguinal ligament: a guide to accurate angiographic puncture. Cardiovasc Intervent Radiol 1988; 11(3): 165–9 Dotter CT, Judkins MP. Transluminal treatment of arteriosclerotic obstruction. Description of a new technic and a preliminary report of its application. Circulation 1964; 30: 654–70 Spijkerboer AM, Scholten FG, Mali WP, et al. Antegrade puncture of the femoral artery: morphologic study. Radiology 1990; 176(1): 57–60 Altin RS, Flicker S, Naidech HJ. Pseudoaneurysm and arteriovenous fistula after femoral artery catheterization: association with low femoral punctures. AJR Am J Roentgenol 1989; 152(3): 629–31 Rapoport S, Sniderman KW, Morse SS, et al. Pseudoaneurysm: a complication of faulty technique in femoral arterial puncture. Radiology 1985; 154(2): 529–30 Greenfield AJ. Femoral, popliteal, and tibial arteries: percutaneous transluminal angioplasty. AJR Am J Roentgenol 1980; 135(5): 927–35 Grossman M. How to miss the profunda femoris. Radiology 1974; 111(2): 482 Keller FS. Percutaneous angioplasty of the femoral, popliteal and tibial arteries. In: Jang GD, ed. Angioplasty. New York: McGrawHill, 1986: 61–82 Bachman DM, Casarella WJ, Sos TA. Percutaneous iliofemoral angioplasty via the contralateral femoral artery. Radiology 1979; 130(3): 617–21 Schwarten DE. Aortic, iliac and peripheral artery angioplasty. In: Castaäneda-Zuäniga WR, Tadavarthy SM, eds. Golden’s Diagnostic Radiology. Baltimore: Williams & Wilkins, 1988: 268–97 Kaufman SL. Angioplasty from the contralateral approach: use of a guiding catheter and coaxial angioplasty balloons. Radiology 1990; 177(2): 577–8
14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.
28.
White CJ, Nguyen M, Ramee SR. Use of a guiding catheter for contralateral femoral artery angioplasty. Cathet Cardiovasc Diagn 1990; 21(1): 15–7 Henry M, Armor M. Stenting of femoral and popliteal arteries. In: Sigward U, ed. Endoluminal Stenting. London: WB Saunders, 1996: 476–86 Cleveland KO, Gelfand MS. Invasive staphylococcal infections complicating percutaneous transluminal coronary angioplasty: three cases and review. Clin Infect Dis 1995; 21(1): 93–6 Ricci MA, Trevisani GT, Pilcher DB. Vascular complications of cardiac catheterization. Am J Surg 1994; 167(4): 375–8 Trerotola SO, Kuhlman JE, Fishman EK. Bleeding complications of femoral catheterization: CT evaluation. Radiology 1990; 174(1): 37–40 Fraedrich G, Beck A, Bonzel T, et al. Acute surgical intervention for complications of percutaneous transluminal angioplasty. Eur J Vasc Surg 1987; 1(3): 197–203 Garti I, Salinger H. Complications in brachial countercurrent arteriography and in retrograde femoral arteriography. Isr J Med Sci. 1969; 5(6): 1192–7 Lang EK. A survey of the complications of percutaneous retrograde arteriography: Seldinger technic. Radiology 1963; 81: 257–63 Redman HC, Reuter SR. Percutaneous transarterial angiography: complications and their avoidance. Angiology 1970; 21(9): 575–9 Sigstedt B, Lunderquist A. Complications of angiographic examinations. AJR Am J Roentgenol 1978; 130(3): 455–60 Paturet G. Traité d’anatomie humaine. Paris: Masson, 1951 Trigaux JP, Van Beers B, De Wispelaere JF. Anatomic relationship between the popliteal artery and vein: a guide to accurate angiographic puncture. AJR Am J Roentgenol 1991; 157(6): 1259–62 Kim D, Orron DE, Skillman JJ. Surgical significance of popliteal arterial variants. A unified angiographic classification. Ann Surg 1989; 210(6): 776–81 Tonnesen KH, Sager P, Karle A, et al. Percutaneous transluminal angioplasty of the superficial femoral artery by retrograde catheterization via the popliteal artery. Cardiovasc Intervent Radiol 1988; 11(3): 127–31 Zaitoun R, Iyer SS, Lewin RF, et al. Percutaneous popliteal approach for angioplasty of superficial femoral artery occlusions. Cathet Cardiovasc Diagn 1990; 21(3): 154–8
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Arterial access for endovascular interventions: radial and brachial arterial access PW McMullan Jr and JS Jenkins
Introduction Transradial arterial access is a valuable skill for the coronary or peripheral interventionist. In the early days of endovascular intervention, sheath and catheter sizes precluded the use of the radial artery.1 However, since 1989 when Campeau first described the technique of successful transradial coronary angiography with 6-French catheters,2 equipment has become progressively more miniaturized and streamlined. Annually, transradial cases account for less than 10% of coronary procedures in the US,3 but this number is expected to rise with increasing operator familiarity and growing patient expectations for procedural comfort and rapid ambulation.
The routine use of heparin during sheath dwell time significantly reduces the probability of occlusion,15 and operator experience correlates directly with procedural success and reduced complication rates.16,17 In one prospective series of 300 radial cases, nine complications occurred in the first 100 patients and only two in the last 100.18 There is evidence that repeated access does not affect procedural success or complication rates.19 Also, the risk of radial artery occlusion is only slightly increased in repeat cases demonstrated by a 117 patient series with 2.6% occlusion in repeated access versus 0% in initial access.12 Obese patients20 and those requiring anticoagulation derive a particular safely benefit from the radial approach.21
Advantages of transradial access
Procedural success
Unlike the common femoral and brachial arteries, the radial artery is not an end vessel; the radial and ulnar arteries come together to form the deep and superficial palmar arches. Therefore, if the arch anatomy is intact, occlusion of one or the other does not compromise the vascular supply of the hand.4 No major nerves or veins lie in the immediate vicinity of the radial artery where it passes just proximal to the styloid process, therefore arteriovenous malformation or nerve damage is infrequent (Figure 4.1).5 Furthermore, a randomized study of transradial versus transfemoral cardiac catheterization demonstrated that patients strongly preferred the radial approach and that it improved measures of bodily pain, back pain, and walking ability both on the day of and over the week following the procedure. Hospital cost and length of stay were also significantly reduced.6
Procedural success via the transradial approach has been clearly demonstrated in coronary angiography and intervention. In a landmark study in 1997 by Kiemeneij and colleagues, 900 patients were randomized to transradial, transbrachial, and transfemoral coronary angioplasty with 6F guiding catheters.9 Successful coronary cannulation was achieved in 279 (93.0%), 287 (95.7%) and 299 (99.7%) patients, respectively (p < 0.001). Inability to access the artery caused most failures. Major entry site complications were encountered in seven patients (2.3%) in the transbrachial group, six patients (2.0%) in the transfemoral group and no patients in the transradial group (p = 0.035). Angioplasty success was achieved in 91.7, 90.7 and 90.7% (p = NS), indicating that the main obstacle to successful intervention was initial access to the radial artery. In more recent years, reported rates of radial access failure range from 1 to 5%.22 In the last decade, numerous studies have validated the concept of the radial approach for elective and emergent coronary intervention9,14,23,24 including primary angioplasty for acute myocardial infarction,11,13,25,26 routine successful access of coronary artery bypass grafts,27 and rotational atherectomy.28 There are also numerous reports of successful peripheral and cerebral angiography29 and endovascular intervention via this approach, including stent placement in the vertebral arteries,30 carotid arteries,31,32 renal arteries,33–35 and the common iliac arteries.36,37 Neuroendovascular interventionists who routinely use lytic therapy along with potent platelet
Safety Safety of radial access has been well established by numerous investigators. Entry site complications and radial artery occlusion occur at a low rate. A meta-analysis of 1,472 radial procedures reported an access site complication rate of only 0.3%.7 The incidence of radial artery occlusion in a series of 563 patients following coronary angioplasty via 6-French radial sheaths was 5.3% at discharge and dropped to 2.8% at followup.8 Other large series report occlusion rates of 0–5%.3,6,9–14
21
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Ulnar artery
Radial artery
Needle entry
2 cm
1 cm
Ulnar nerve Median nerve
Radial styloid process
Deep palmar arch Superficial palmar arch
Figure 4.1
Anatomy of the palmar arch and bony landmarks.
inhibitors are able promptly to remove the radial sheath without reversal of anticoagulation or concerns about major bleeding complications.38
Anatomy and Allen’s testing Approach to the patient’s vascular supply should by begin with palpating for an adequate radial pulse and ensuring that there are no orthopedic deformities that would render the patient unable to extend the wrist or straighten the arm. One should measure blood pressure in both upper extremities to screen for significant narrowing in the proximal arterial supply. Evaluation for adequate collateral supply from the ulnar artery has traditionally been performed by the modified Allen’s test39 (termed “modified” because the original test described in 1929 by Edgar V. Allen demonstrated arterial occlusion, not collateral flow).40 It is accomplished by compressing simultaneously the radial and ulnar arteries while the patient squeezes a fist to express blood from the hand. The hand is then reopened and held in a relaxed position without hyperextension of the fingers while the ulnar artery is released and the radial artery remains compressed.41 A blush indicates adequate blood return, the exact normal timing of which varies from 5 to 10 seconds according to various sources. Reported results from the Allen’s test vary widely. In a study of 1,000 consecutive patients, test responses were divided into categories by the number of seconds to maximal blush. Fortynine percent filled in less than 5 seconds, 24% filled in 5–10 seconds, and 27% filled in greater than 10 seconds;
leading the investigators to conclude that over one-quarter of screened patients would be unsuitable candidates for radial access.42 Another method described by Barbeau and colleagues involves the use of pulse oximetry and plethysmography.43 Barbeau studied both wrists of 1,010 patients who underwent evaluation with the modified Allen’s test followed by placement of a pulse oximeter on the thumb. After release of the clenched fist with continued ulnar compression, plethysmography was recorded for up to 2 minutes. Waveforms were recorded as normal, damped or absent. Results showed that the traditional modified Allen’s test was normal in 93.7% of patients with a mean time to maximal blushing of 4.7 seconds. Plethysmography found 98.5% of patients to have at least a damped wave form at the end of a 2-minute period on one hand or the other, indicating some degree of collateral circulation. Therefore, only 6.3% by standard modified Allen’s testing and 1.5% by plethysmographic testing would be ineligible for radial artery access in one wrist or the other. As it turns out, cadaveric studies indicate that a complete superficial palmar arch is present in 85–96%44,45 and a complete deep palmar arch in 90%46 of the general population, and most hands typically have at least one major vessel connecting the radial and ulnar arteries. This has led some highvolume operators to abandon entirely the use of the Allen’s test prior to radial cannulation,47,48 citing large numbers of unscreened patients who have undergone transradial coronary intervention with no resultant hand or forearm ischemia.49 Nevertheless, the authors recommend vigilant confirmation and documentation of adequate collateral circulation prior to radial artery instrumentation.
Right versus left Choice of access in the right versus the left wrist depends on operator proficiency, patient needs and goals of the case. Access from the right wrist with the arm adducted permits use of a standard lab configuration and does not require the operator to reach across the patient. However, when coronary cannulation is the goal, the acutely angulated path through the right subclavian and innominate arteries down to the aortic root frequently requires special catheters. The Kimny catheter (brand name derived from the catheter’s inventor, Dr. Ferdinand Kiemeneij) is a double-curve catheter designed to fit the left main coronary from the right radial approach. Standard Judkins and other catheters can often be used as well. A good rule of thumb is to choose a catheter one half-size smaller than the equivalent catheter from the standard femoral approach. For example, if the catheter of choice from the femoral approach is a Judkins left 4.0, use a Judkins left 3.5 instead. Benefits of access in the left wrist are ease of approach to the left internal mammary artery and normal functionality of standard catheters for coronary work from that side. There is also evidence that catheter manipulation time is greater from the right than from the left, translating to longer fluoroscopy and total procedure times.50
Procedural technique and equipment The technique of radial artery puncture should be carried out by or under the supervision of an experienced operator.
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Arterial access for endovascular interventions: radial and brachial arterial access Most authors recommend positioning the patient in the supine position on the catheterization table with the access arm abducted at a 45–70° angle and the wrist hyperextended.3,9,24 Prior to sterile prep, one can maintain wrist extension and immobility during access by placing a strip of silk tape across the palm and around the supporting arm-board. The ideal site of puncture is 1–2 cm proximal to the radial styloid process over the pulse’s point of maximal impulse in a direction consistent with the course of the more proximal radial artery. The operator’s index finger should palpate for the pulse and then withdraw to the edge of the artery so that the fingertip abuts the edge of the pulsation. Apply lidocaine sparingly and superficially to avoid eliciting arterial spasm or causing distortion of the anatomy. With a 21-gauge, 4-cm micropuncture needle at a 30–45° angle and the bevel facing up, entry is made without a prior skin nick. Pulsatile flow may not be evident as quickly as in femoral entry, due to the smaller bore needle. Filling the needle with saline allows the operator to see flow immediately upon entry into the artery. The operator should then advance a 0.018-inch floppy-tipped wire with great care to avoid dissection. If smooth wire passage is not immediate, the needle should be withdrawn slightly with one hand while the other hand makes gentle serial attempts at wire advancement. This method allows withdrawal of the needle from the back wall of the vessel without losing access entirely. If initial access attempts are unsuccessful, radial artery spasm may ensue, which makes the pulse weak or absent and the artery much more difficult to cannulate. Adequate sedation lessens the propensity for spasm, and one study demonstrated spasm resolution with subcutaneous injection of 400 µg of nitroglycerin over the radial artery.51 With the wire in place, the operator should advance the plastic tip of the sheath dilator into the vessel until the sheath tip comes within 1–2 mm of the skin. At this point, the operator makes a 1–2 mm longitudinal incision in the skin over the plastic dilator, which facilitates passage of the sheath. Keeping the sheath wet with moist gauze and using a corkscrew insertion motion will ease passage into the artery. A minimum of 2,000 units of heparin should then be administered. Dilution in 10 cm3 of saline lessens discomfort in the hand. Most operators also use a vasodilatory cocktail to flush the sheath throughout the procedure. This mixture contains nitroglycerin and verapamil; some operators also add heparin, lidocaine, or bicarbonate.4 Others advocate the use of hydrophilic sheaths in lengths up to 25 cm to maximize ease of insertion and extraction, which also minimizes the potential for spasm.52 Once access is established, one may adduct the arm and proceed with the catheterization in a standard laboratory setup in which the operator stands along the right side of the patient. The other option is to keep the arm in an abducted position and use a separate table to support the injection manifold. The latter method requires movement of monitors to the head of the patient, and limited upper body shielding increases significantly the operator’s radiation dose compared with the femoral approach.53
Sheath removal Radial artery sheath removal should be performed immediately following the procedure to minimize the risk of thrombosis
23
and occlusion. One should take care to remove the sheath slowly and to be alert to complaints of forearm pain from the patient. This can indicate spasm around the sheath, and there are rare reports of traumatic endarterectomy with sheath removal.3,54,55 Manual compression over the radius with application of a dressing is an adequate method for obtaining hemostasis. There are also several available wrist-strap compression devices that are time-saving and particularly useful when anticoagulation is a factor. Some of these include a thrombin-impregnated pad that overlies the puncture site and promotes surface coagulation. In the immediate period following sheath removal, careful watch for hematoma formation is crucial. Although a rare complication, since a radial artery hematoma has little soft tissue space in which to expand, compartment syndrome requiring fasciotomy can develop if left unattended.14,56
Brachial artery access In addition to percutaneous transradial access, three other methods of upper extremity arterial access remain. These are the percutaneous axillary approach, the percutaneous brachial approach, and the brachial cutdown approach. The axillary approach is used with extreme rarity and will not be covered in this context. The Sones brachial arteriotomy57 requires surgical expertise and has been supplanted largely by the percutaneous method of entry, initially described in 1981 in conjunction with left heart catheterization.58 Indications and success Indications for the brachial approach include peripheral arterial disease precluding femoral access and inadequate collateral hand circulation excluding the radial approach. Occasionally, brachial is preferable to radial access due to inadequate equipment length for work in the lower extremities or needs for sheath diameters 7 French and higher to accommodate larger catheters and equipment. As previously stated, when transbrachial and transfemoral routes were compared in randomized fashion for coronary intervention, coronary cannulation was achieved in 95.7% of the brachial group and in 99.7% of the femoral group.9 Procedural success rates in the modern era for coronary and peripheral angiography and intervention are reported in the range 84–99%, technical failure being more likely in operators who use the technique infrequently.59–62 Complications The most serious complication of percutaneous brachial artery access is thrombotic occlusion of the artery with resultant compromise of the entire vascular supply of the forearm and hand. This event mandates immediate surgical or percutaneous thrombectomy and repair to avoid permanent nerve injury or limb loss.63 Reported rates of brachial artery occlusion from series published over the mid-1980s to the late-1990s vary from 1 to 6%,64 and more recent series employing 4- and 5-French sheaths and catheters report rates below 1%.61,64 The likelihood of thrombosis is greater in
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females (1.24 vs. 0.28% in males in a series of 1,326 procedures by a single experienced operator), probably due to smaller vessel caliber,64 and Duplex ultrasound has demonstrated efficacy in preprocedural screening for unusually small brachial arteries.65 When thrombosis is promptly diagnosed, treatment is generally effective and leaves the patient without long-term sequelae.66 Other complications include arterial dissection, pseudoaneurysm formation, and hematoma. Hematoma enlargement in the antecubital fossa must be diligently monitored due to the potential for median nerve compression, which can lead to long-term disability,67 and large hematomas may rarely require surgical exploration. Randomized data indicate that brachial access site complication rates for experienced operators are roughly equivalent to transfemoral rates,9 but operators who use brachial access only occasionally (ten or fewer cases per year) are more prone to major and minor complications of the technique. Technique Percutaneous entry of the brachial artery is performed with the patient’s upper extremity in the abducted, supinated position with the support of an arm-board. The medial and lateral humeral epicondyles serve as the bony landmarks of the antecubital fossa. Palpation for the brachial pulse should be performed 1 cm proximal to the antecubital skin fold, just medial to the biceps tendon (Figure 4.2). Following sterile skin preparation, draping, and infiltration of the skin with lidocaine, an 18- or 21-gauge needle is inserted at a 30–45° angle to the skin in a direction consistent with the path of the brachial artery. An arterial sheath is then inserted over a wire. Following the
Brachial artery Lateral humeral epicondyte Biceps tendon
Medial Humeral epicondyte 1 cm
Radial artery
Figure 4.2
Needle entry
Ulnar artery
Anatomy of the antecubital fossa.
procedure, sheath removal should be immediate with manual compression applied to the area for a minimum of 15 minutes. Some authors also advocate the use of a moderate-tightness tourniquet for an additional hour59 or transparent pneumatic compression which is released slowly over time.68
REFERENCES 1. 2. 3. 4. 5. 6.
7.
8. 9.
Gruntzig AR, Senning A, Siegenthaler WE. Nonoperative dilatation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty. N Engl J Med. Jul 12 1979; 301(2): 61–8 Campeau L. Percutaneous radial artery approach for coronary angiography. Cathet Cardiovasc Diagn. Jan 1989; 16(1): 3–7 Baim DS, Grossman W. Grossman’s cardiac catheterization, angiography, and intervention. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2006 Archbold RA, Robinson NM, Schilling RJ. Radial artery access for coronary angiography and percutaneous coronary intervention. Bmj. Aug 21 2004; 329(7463): 443–46 Rihal CS, Holmes DR, Jr. Transradial cardiac catheterization: is femoral access obsolete? Am Heart J. Sep 1999; 138(3 Pt 1): 392–93 Cooper CJ, El–Shiekh RA, Cohen DJ et al. Effect of transradial access on quality of life and cost of cardiac catheterization: A randomized comparison. Am Heart J. Sep 1999; 138(3 Pt 1): 430–36 Agostoni P, Biondi–Zoccai GG, de Benedictis ML et al. Radial versus femoral approach for percutaneous coronary diagnostic and interventional procedures; Systematic overview and meta–analysis of randomized trials. J Am Coll Cardiol. Jul 21 2004; 44(2): 349–56 Stella PR, Kiemeneij F, Laarman GJ et al. Incidence and outcome of radial artery occlusion following transradial artery coronary angioplasty. Cathet Cardiovasc Diagn. Feb 1997; 40(2): 156–58 Kiemeneij F, Laarman GJ, Odekerken D et al. A randomized comparison of percutaneous transluminal coronary angioplasty by the radial, brachial and femoral approaches: the access study. J Am Coll Cardiol. May 1997; 29(6): 1269–75
10.
11.
12. 13.
14. 15. 16.
17. 18.
Aptecar E, Pernes JM, Chabane-Chaouch M et al. Transulnar versus transradial artery approach for coronary angioplasty: the PCVI-CUBA study. Catheter Cardiovasc Interv. May 2006; 67(5): 711–20 Valsecchi O, Musumeci G, Vassileva A et al. Safety, feasibility and efficacy of transradial primary angioplasty in patients with acute myocardial infarction. Ital Heart J. May 2003; 4(5): 329–34 Yoo BS, Lee SH, Ko JY et al. Procedural outcomes of repeated transradial coronary procedure. Catheter Cardiovasc Interv. Mar 2003; 58(3): 301–04 Kim MH, Cha KS, Kim HJ et al. Primary stenting for acute myocardial infarction via the transradial approach: a safe and useful alternative to the transfemoral approach. J Invasive Cardiol. Jun 2000; 12(6): 292–96 Lotan C, Hasin Y, Salmoirago E et al. The Radial Artery: An Applicable Approach to Complex Coronary Angioplasty. J Invasive Cardiol. Oct 1997; 9(8): 518–22 Spaulding C, Lefevre T, Funck F et al. Left radial approach for coronary angiography: results of a prospective study. Cathet Cardiovasc Diagn. Dec 1996; 39(4): 365–70 Hildick-Smith DJ, Walsh JT, Lowe MD et al. Transradial coronary angiography in patients with contraindications to the femoral approach: an analysis of 500 cases. Catheter Cardiovasc Interv. Jan 2004; 61(1): 60–6 Heuser RR. At arms’ length: should we teach radial and brachial access techniques? Catheter Cardiovasc Interv. Jan 2000; 49(1): 38. Schneider JE, Mann T, Cubeddu MG et al. Transradial Coronary Stenting: A United States Experience. J Invasive Cardiol. Nov 1997; 9(9): 569–74
9781841846439-Ch04
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Arterial access for endovascular interventions: radial and brachial arterial access 19. 20.
21. 22. 23.
24. 25.
26. 27.
28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43.
Caputo RP, Simons A, Giambartolomei A et al. Safety and efficacy of repeat transradial access for cardiac catheterization procedures. Catheter Cardiovasc Interv. Oct 2001; 54(2): 188–90 Cox N, Resnic FS, Popma JJ et al. Comparison of the risk of vascular complications associated with femoral and radial access coronary catheterization procedures in obese versus nonobese patients. Am J Cardiol. Nov 1 2004; 94(9): 1174–77 Hildick-Smith DJ, Walsh JT, Lowe MD et al. Coronary angiography in the fully anticoagulated patient: the transradial route is successful and safe. Catheter Cardiovasc Interv. Jan 2003; 58(1): 8–10 Valsecchi O, Vassileva A, Musumeci G et al. Failure of transradial approach during coronary interventions: anatomic considerations. Catheter Cardiovasc Interv. Jun 2006; 67(6): 870–78 Bertrand OF, De Larochelliere R, Rodes-Cabau J et al. A randomized study comparing same-day home discharge and abciximab bolus only to overnight hospitalization and abciximab bolus and infusion after transradial coronary stent implantation. Circulation. Dec 12 2006; 114(24): 2636–43 Kiemeneij F, Laarman GJ, de Melker E. Transradial artery coronary angioplasty. Am Heart J. Jan 1995; 129(1): 1–7 Saito S, Tanaka S, Hiroe Y et al. Comparative study on transradial approach vs. transfemoral approach in primary stent implantation for patients with acute myocardial infarction: results of the test for myocardial infarction by prospective unicenter randomization for access sites (TEMPURA) trial. Catheter Cardiovasc Interv. May 2003; 59(1): 26–33 Louvard Y, Ludwig J, Lefevre T et al. Transradial approach for coronary angioplasty in the setting of acute myocardial infarction: a dualcenter registry. Catheter Cardiovasc Interv. Feb 2002; 55(2): 206–211 Sanmartin M, Cuevas D, Moxica J et al. Transradial cardiac catheterization in patients with coronary bypass grafts: feasibility analysis and comparison with transfemoral approach. Catheter Cardiovasc Interv. Apr 2006; 67(4): 580–84 Gioia G, Comito C, Moreyra AE. Coronary rotational atherectomy via transradial approach: a study using radial artery intravascular ultrasound. Catheter Cardiovasc Interv. Oct 2000; 51(2): 234–38 Levy EI, Boulos AS, Fessler RD et al. Transradial cerebral angiography: an alternative route. Neurosurgery. Aug 2002; 51(2): 335–340; discussion 340–42 Fessler RD, Wakhloo AK, Lanzino G et al. Transradial approach for vertebral artery stenting: technical case report. Neurosurgery. Jun 2000; 46(6): 1524–1527; discussion 1527–28 Folmar J, Sachar R, Mann T. Transradial approach for carotid artery stenting: A feasibility study. Catheter Cardiovasc Interv. 2007; 69(3): 355–61 Levy EI, Kim SH, Bendok BR et al. Transradial stenting of the cervical internal carotid artery: technical case report. Neurosurgery. Aug 2003; 53(2): 448–451; discussion 451–52 Kessel DO, Robertson I, Taylor EJ et al. Renal stenting from the radial artery: a novel approach. Cardiovasc Intervent Radiol. MarApr 2003; 26(2): 146–49 Scheinert D, Braunlich S, Nonnast-Daniel B et al. Transradial approach for renal artery stenting. Catheter Cardiovasc Interv. Dec 2001; 54(4): 442–47 Shuck J, Khan A, Cavros N et al. Transradial renal angioplasty: initial experience. Catheter Cardiovasc Interv. Nov 2001; 54(3): 346–49 Staniloae CS, Kurian DC, Coppola JT. Transradial bilateral iliac stenting. J Invasive Cardiol. Oct 2006; 18(10): E256–57 Flachskampf FA, Wolf T, Daniel WG et al. Transradial stenting of the iliac artery: a case report. Catheter Cardiovasc Interv. Jun 2005; 65(2): 193–95 Layton KF, Kallmes DF, Cloft HJ. The radial artery access site for interventional neuroradiology procedures. AJNR Am J Neuroradiol. May 2006; 27(5): 1151–54 Wright IS. Vascular diseases in clinical practice. 2d ed. Chicago,: Year Book Publishers; 1952 Allen EV. Thromboangiitis obliterans: methods of diagnosing chronic occlusive arterial lesions distal to the wrist with illustrative cases. American Journal of Medical Science. 1929; 178: 237–44 Greenhow DE. Incorrect performance of Allen’s test—ulnar-artery folow erroneously presumed inadeguate. Anesthesiology. Sep 1972; 37(3): 356–57 Benit E, Vranckx P, Jaspers L et al. Frequency of a positive modified Allen’s test in 1,000 consecutive patients undergoing cardiac catheterization. Cathet Cardiovasc Diagn. Aug 1996; 38(4): 352–54 Barbeau GR, Arsenault F, Dugas L et al. Evaluation of the ulnopalmar arterial arches with pulse oximetry and plethysmography: comparison with the Allen’s test in 1010 patients. Am Heart J. Mar 2004; 147(3): 489–93
44. 45. 46. 47. 48. 49. 50. 51. 52.
53.
54. 55. 56. 57. 58. 59.
60.
61. 62. 63. 64. 65.
66. 67.
68.
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Gellman H, Botte MJ, Shankwiler J et al. Arterial patterns of the deep and superficial palmar arches. Clin Orthop Relat Res. Feb 2001; 383: 41–6 Ikeda A, Ugawa A, Kazihara Y et al. Arterial patterns in the hand based on a three-dimensional analysis of 220 cadaver hands. J Hand Surg [Am]. Jul 1988; 13(4): 501–9 Ruengsakulrach P, Eizenberg N, Fahrer C et al. Surgical implications of variations in hand collateral circulation: anatomy revisited. J Thorac Cardiovasc Surg. Oct 2001; 122(4): 682–86 Gilchrist IC. Is the Allen’s test accurate for patients considered for transradial coronary angiography? J Am Coll Cardiol. Sep 19 2006; 48(6): 1287; author reply 1288 Hildick-Smith D. Use of the Allen’s test and transradial catheterization. J Am Coll Cardiol. Sep 19 2006; 48(6): 1287; author reply 1288 Ghuran A DG, de Belder A, Holmberg S, Hildick-Smith D. Transradial coronary intervention without pre-screening for a dual palmar blood supply (abstr). Heart. 2005; 91(Supplement): A5-i122 Kawashima O, Endoh N, Terashima M et al. Effectiveness of right or left radial approach for coronary angiography. Catheter Cardiovasc Interv. Mar 2004; 61(3): 333–37 Pancholy SB, Coppola J, Patel T. Subcutaneous administration of nitroglycerin to facilitate radial artery cannulation. Catheter Cardiovasc Interv. Sep 2006; 68(3): 389–91 Kiemeneij F, Fraser D, Slagboom T et al. Hydrophilic coating aids radial sheath withdrawal and reduces patient discomfort following transradial coronary intervention: a randomized double-blind comparison of coated and uncoated sheaths. Catheter Cardiovasc Interv. Jun 2003; 59(2): 161–64 Lange HW, von Boetticher H. Randomized comparison of operator radiation exposure during coronary angiography and intervention by radial or femoral approach. Catheter Cardiovasc Interv. Jan 2006; 67(1): 12–16 Dieter RS, Akef A, Wolff M. Eversion endarterectomy complicating radial artery access for left heart catheterization. Catheter Cardiovasc Interv. Apr 2003; 58(4): 478–80 Abu-Ful A, Benharroch D, Henkin Y. Extraction of the radial artery during transradial coronary angiography: an unusual complication. J Invasive Cardiol. Jun 2003; 15(6): 351–52 Lin YJ, Chu CC, Tsai CW. Acute compartment syndrome after transradial coronary angioplasty. Int J Cardiol. Nov 2004; 97(2): 311 Sones FM, Jr., Shirey EK. Cine coronary arteriography. Mod Concepts Cardiovasc Dis. Jul 1962; 31: 735–38 Fergusson DJ, Kamada RO. Percutaneous entry of the brachial artery for left heart catheterization using a sheath. Cathet Cardiovasc Diagn. 1981; 7(1): 111–14 Hildick-Smith DJ, Khan ZI, Shapiro LM et al. Occasional-operator percutaneous brachial coronary angiography: first, do no arm. Catheter Cardiovasc Interv. Oct 2002; 57(2): 161–165; discussion 166 Nolan J, Batin P, Welsh C et al. Feasibility and applicability of coronary stent implantation with the direct brachial approach: results of a single-center study. Am Heart J. Nov 1997; 134(5 Pt 1): 939–44 Basche S, Eger C, Aschenbach R. Transbrachial angiography: an effective and safe approach. Vasa. Nov 2004; 33(4): 231–34 Kaukanen ET, Manninen HI, Matsi PJ et al. Brachial artery access for percutaneous renal artery interventions. Cardiovasc Intervent Radiol. Sep-Oct 1997; 20(5): 353–58 Mills JL, Wiedeman JE, Robison JG et al. Minimizing mortality and morbidity from iatrogenic arterial injuries: the need for early recognition and prompt repair. J Vasc Surg. Jul 1986; 4(1): 22–27 Armstrong PJ, Han DC, Baxter JA et al. Complication rates of percutaneous brachial artery access in peripheral vascular angiography. Ann Vasc Surg. Jan 2003; 17(1): 107–10 Rath J, Ganschow US, Kelm M et al. [Duplex ultrasound risk stratification of percutaneous puncture of the brachial artery for diagnostic and interventional coronary angiography]. Z Kardiol. Apr 1998; 87(4): 249–57 Khoury M, Batra S, Berg R et al. Influence of arterial access sites and interventional procedures on vascular complications after cardiac catheterizations. Am J Surg. Sep 1992; 164(3): 205–09 Kennedy AM, Grocott M, Schwartz MS et al. Median nerve injury: an underrecognised complication of brachial artery cardiac catheterisation? J Neurol Neurosurg Psychiatry. Oct 1997; 63(4): 542–46 Cardenas JA, Yellayi S, Schatz RA et al. A new method for brachial artery hemostasis following percutaneous coronary angiography. J Invasive Cardiol. Nov-Dec 1994; 6(9): 285–88
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Arterial access for endovascular interventions: transradial approach I Henry, M Henry, and M Hugel
Femoral access is the most often-used approach way for peripheral arterial procedures. However, the management of sheath removal and the prevention of vascular access complications still remain a practical day-to-day problem, including personnel involved to compress, cost of the mechanical compression device or percutaneous closure device, and nursing time and in-hospital stay time, particularly after interventional procedures which require an aggressive anticoagulation therapy. Furthermore, the femoral approach is sometimes impossible for anatomical reasons; for example, iliac stenosis or occlusion, tortuosities, or aneurysm. The transradial approach was first described for coronary procedures and is currently largely used with a very low rate of vascular complication,1,2 allowing an early discharge of the patient. The approach should be well known and should be used more frequently for some good indications.
Technique Patient selection The major inclusion criteria are a good pulsating right or left radial artery, associated with a good cubital artery pulse and the absence of digital ischemia by Allen’s test. This test is considered as normal if, after compression of both ulnar and radial arteries, hand color returns to normal within 10 seconds after releasing the ulnar artery. Exclusion criteria are the following: ● ● ●
● ● ●
absence of radial or ulnar pulse; digital ischemia by Allen’s test (15% of patients); lesions, which can necessitate techniques requiring large guiding catheters. A 7-French guiding catheter is possible in 70% of the patients, an 8-French in 60%; upper extremity vascular disease; Burger’s disease; severe Raynaud’s.
Which radial artery? A right transradial approach is easier to perform for a righthanded operator. The left radial approach may be used with equal success. The choice of the radial artery should also depend on the location of the angioplasty. For example, the 26
right radial artery is preferred to treat a left carotid lesion and the left for the right carotid artery. Patient position The patient’s arm may be extended a few inches from the body for the puncture, but the arm may rest along the body. The patient’s hand may be hyperextended in a supine position, or in a relaxed supine position without hyperextension. Artery puncture Depending on the procedure a neuroleptanalgesia may be performed in addition to local anesthesia with a superficial injection of 1–2 ml 2% lidocaine followed by a light massage. The puncture of the radial artery may be done with an 18–22 gauge bare needle (needle diameter selected in relation to the guidewire) at a 30–45° angle approximately 1 cm from the styloid process. Puncture with a venous catheter is possible and allows injections of antispastic medications before sheath insertion. Several kits (Arrow kit, Cordis kit) are now on the market and can facilitate the technique. Failure of radial artery puncture is rare (6% for Wiper et al.).5 Insertion of sheath The operator may use a long (23 cm), standard (13 cm), or short (7 cm) sheath. A long sheath may serve to mechanically prevent spasm and facilitate movement of a guiding catheter, although it is harder to withdraw. Following puncture using a bare needle, a straight Teflon 0.025-inch wire, 1.50 m in length is used to catheterize the ascending aorta and permits identification of antebrachial or brachial loops. The extremity of the wire is slightly bent manually in order to facilitate insertion in the artery and crossing of tortuous segments. The needle is then withdrawn and the introducer advanced into the artery over the wire (a cut in the skin may be made cautiously). Following puncture with a venous catheter or a kit, the guide is inserted through the small catheter already in place. This wire may be short as it is only used to insert the introducer. Inadequate guiding catheter support with transcranial approach is rare (0.5% for Wiper et al.5 A recent study with 1125 patients undergoing transradial PCI demonstrated similar figures.7
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Arterial access for endovascular interventions: transradial approach Medication cocktail Medication is administered for prevention of spasm and radial thrombosis. We combine fast-acting nitrates (isosorbide dinitrate, molsidomine) and prolonged action verapamil (3–5 mg) injected simultaneously in the radial artery through the side lumen of the introducer. Subsequently, 5000 IU heparin are injected to prevent radial thrombosis, but higher doses can be given to have an actual clotting time (ACT) > 250 seconds for some angioplasty-like carotid angioplasty stenting. Catheterization of the aorta and other arteries This procedure is performed by the combined action of the guidewire and angiographic or angioplasty catheter. In the presence of severe loops (antibrachial, brachial) or tortuous subclavian arteries, hydrophilic wires may be used. Any catheters, guiding catheters, or guidewires can be used in this approach, allowing the catheterization of not only coronary arteries but also renal, mesenteric, vertebral, carotid, and subclavian arteries. Catheterization of the iliac and femoropopliteal arteries is limited by the length of the devices. Introducer sheath removal and hemostasis The arterial sheath is removed immediately after the withdrawal of the guiding catheter at the end of the procedure. The artery is manually compressed only for the time necessary to place a tourniquet set over the puncture site. Local compression is held in place for 30–45 minutes and then pressure is gradually released until hemostasis is obtained. A compressive bandage is applied for 6 hours. The patient may be allowed to stand up for 1 hour after the end of the procedure and the radial pulse is checked by clinical examination. Different devices are currently available on the market to compress the arterial puncture site such as the Radistop radial compression system, Terumo TR Band. Assisted compression devices have also been proposed as topical hemostasis pads and patches.
Advantages There are several advantages of the transradial approach. The sheaths are removed immediately after the procedure and no personnel are needed to compress the radial artery. The patient is able to ambulate 2 hours after the procedure and, if after an observation period of 6 hours no access site-related complications occur, an early discharge in carefully selected patients is possible. Peripheral procedures on an outpatient basis can now be performed, which reduces cost and patient discomfort.
Complications Vascular access complications (hematomas, bleeding, pseudoaneurysms) are reduced compared with femoral access and may occur in 1–2% of the cases, mainly forearm or arm hematomas. Asymptomatic radial artery occlusion has been reported in 6–10%, although 40% appear to spontaneously recanalize after 1 month.10,11 Consistent variables that influence the frequency of these occlusions include artery size at baseline, sheath-to-artery size ratio, duration of sheath placement, prior procedures, and the presence of diabetes mellitus.11–13 A palpable radial artery can be re-punctured and the transradial approach repeated with no increased technical challenge.6 Some concerns about the radial approach must be reported: ●
●
Indications for radial approach Femoral artery access may be difficult in obese patients, patients with extensive post-operative scarring, and in cases of severe peripheral disease; and is impossible in the case of aortic or iliac occlusion, or relatively contraindicated (coagulopathy). For these patients the radial approach may be useful to catheterize supra-aortic, mesenteric, renal, or iliac arteries.8 Angiography and interventional procedures may be performed in this way and most of the stents can be implanted through 6–8-French introducers. This method should be more often used to treat supraaortic and renal arteries, not only when the femoral approach is contraindicated but also in some specific indications like carotid angioplasty stenting in the case of bovine arch or type-3 aortic arch. The transradial approach is safe when used in fully anticoagulated patients with a low risk for subsequent bleeding complications.9
27
The possibility of neurological embolic complications. Some aortic plaques may be detached by catheters or guidewires and can emboli to the brain. The risk is higher in elderly patients with atheromatous aortic arch and/or ulcerated plaques. This radial approach therefore has to be discussed in such patients when the femoral approach is feasible. We always try to perform our peripheral angioplasty by the femoral route to avoid these neurological complications and we reserve the radial or brachial approach for specific indications. The effects of catheterization-induced changes on future clinical uses of the vessel are not nearly as trivial. The radial artery can be used as an additional arterial conduit for aorto-coronary bypass surgery and as the preferred initial artery used in the creation of an arteriovenous fistula for hemodialysis access. Some reports exist in the literature suggesting that prior instrumentation of a radial artery destined for service as a bypass graft may result in a significantly higher likelihood of graft closure,14,15 and although less well studied, pre-existing radial intimal hyperplasia is closely associated with failure of radiocephalic arteriovenous fistulas in hemodialysis patients.16, 17
Conclusion Radial access is a new approach for peripheral procedures and indications should widen as a result of the new generation of
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miniaturized equipment, fewer access site complications, and the development of the procedures on an outpatient basis. However, some concerns may be kept in mind, particularly in multivascular elderly patients where there is a risk of brain embolism (which could be avoided by the use of the femoral approach) and the possibility of a higher graft closure rate after cardiac surgery. So it is perhaps better to reserve the radial approach for patients at low-risk for endothelial
dysfunction and intimal hyperplasia and for those with a low likelihood of requiring future surgical use of the radial artery.17 Also in patients with renal insufficiency the femoral approach could be preferred to preserve the radial artery in the event of a subsequent need for a hemodialysis shunt. Nevertheless, this technique should be known by all interventionists involved not only in coronary procedures but also in peripheral procedures.
REFERENCES 1. 2.
3. 4. 5. 6. 7. 8. 9.
Campaud L. Percutaneous radial artery approach for coronary angiography. Cathet Cardiovasc Diagn 1989; 16: 3–7 Kiemeneij F, Laarman GH, Oderkerken D et al. A randomized comparison of percutaneous transluminal coronary angioplasty by the radial, brachial and femoral approaches. The Access Study. J Am Coll Cardiol 1997; 29: 1269–75 Mann T, Cubeddu G, Bowen J et al. Stenting in acute coronary syndrome. A comparison of radial versus femoral access sites. J Am Coll Cardiol 1998; 32: 572–6 Slagboom T, Kiemeneij F, Laarman GJ et al. Outpatient coronary angioplasty: feasible and safe. Catheter Cardiovasc Interv 2005; 64: 421–7 Wiper A, Kumar S, Mac Donald J et al. Day case transradial coronary angioplasty: a four year single center experience. Cath and Cardiovasc Interventions 2006; 68: 549–53 Eccleshall SC, Banks M, Carroll R et al. Implementation of a diagnostic and interventional transradial programme: resource and organisational implications. Heart 2003; 89: 561–2 Valsecchi O, Musumeci G, Vassileva A et al. Safety and feasibility of transradial coronary angioplasty in elderly patients. Ital Heart J 2004; 5: 926–31 Galli M, Tarantino F, Mameli S et al. Transradial approach for renal percutaneous transluminal angioplasty and stenting: a feasibility pilot study. J Invasive Cardiol 2002; 14: 386–90 Hildick-Smith DJ, Walsh JT, Lowe MD et al. Coronary angiography in the fully anticoagulated patient: the transradial route is successful and safe. Catheter Cardiovasc Interv 2003; 58: 8–10
10. 11.
12. 13.
14. 15. 16.
17.
Marco J, Fajadet J, Cassagneau B et al. Transradial coronary stenting: a passing fad or widespread use in the future. J Invasive Cardiol 1996; 8(suppl E): 16E–21E Stella PR, Kiemeneij F, Laarman GH et al. Incidence and outcome of radial artery occlusion following transradial artery coronary angioplasty. Cathet Cardiovasc Diagn 1997; 40: 156–8 Nagai S, Abe S, Sato T et al. Ultrasonic assessment of vascular complications in coronary angiography and angioplasty after transradial approach. Am J Cardiol 1999; 83: 180–6 Saito S, Ikei H, Hosokawa G et al. Influence of the ratio between radial artery inner diameter and sheath outer diameter on radial artery flow after transradial coronary intervention. Catheter Cardiovasc Interv 1999; 46: 173–8 Kamiya H, Ushijima T, Kanamori T et al. Use of the radial artery graft after transradial catheterization: is it suitable as a bypass conduit? Ann Thorac Surg 2003; 76: 1505–9 Deligonul U. Transradial cardiac catheterization and the use of the radial artery as bypass graft. J Invasive Cardiol 2001; 13: 576–7 Kim YO, Song HC, Yoon SA et al. Preexisting intimal hyperplasia of radial artery is associated with early failure of radiocephalic arteriovenous fistula in haemodialysis patients. Am J Kidney Dis 2003; 41: 422–8 Barman N, Chiuj H, Ellis SG. Transradial catheterization: the Rood Less Travelled. J Invasive Cardiol 2004; 16: 639–40
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Arterial access for endovascular interventions: popliteal access to peripheral procedures M Henry, I Henry, and M Hugel
Introduction In endovascular treatment of peripheral arterial disease, the antegrade or retrograde femoral approach is the most often used access. Lesions at the femoral bifurcation prevent guidewires and introducers from being placed. This leads to the use of other approaches such as the brachial, radial, contralateral, or popliteal accesses. Described herein are the antegrade and retrograde popliteal approaches, as well as the present authors’ experiences, so defining the current technique and its indications.1–9
Techniques Retrograde percutaneous popliteal approach The popliteal artery, together with the sciatic nerve and the popliteal vein, goes upward along the diagonal of the popliteal triangle. The superficial location of the popliteal artery allows retrograde puncture, which is usually performed just above the joint. The patient is preferably in the ventral decubitus position but may alternatively be in the lateral decubitus position. The procedure is usually performed under local anesthesia and complemented by intravenous sedation. General anesthesia, which may still be performed, is rarely required. Before choosing the popliteal approach, one should check that the artery is free from any atheromatous lesion or significant stenosis. Angiography may be sufficient. However, echography provides more information regarding the state of the artery, particularly the presence of an aneurysm, which is a strict contraindication to puncture. Due to overlying lesions, the artery may not be pulsatile. It should then first be located, for which several techniques may be used: ●
●
Angiography: A 4- or 5-French catheter is placed in the abdominal aorta, generally through contralateral access. Contrast media is injected to visualize the course of the popliteal runoff. “Road mapping” renders the puncture easy. Doppler echocardiography (echo-Doppler): Angiography and/or echo-Doppler assists in locating the popliteal artery and the puncture site.
●
“Smart Needle”: A Doppler probe is connected to the needle. The sound of the Doppler helps in locating the popliteal artery.
Once the artery is punctured, an introducer, generally 6- or 7French, is placed in the artery. Larger introducers (8- or 9French) may be used in cases where larger devices are needed, such as burrs or covered endoprostheses, as long as the artery is at least 6 mm in diameter. Although contrast media injections are performed through a contralateral access, the femoral bifurcation and the origin of the deep femoral artery are usually well opacified. The introducer is withdrawn at the end of the procedure. Hemostasis is obtained with manual compression of the puncture site for 10–20 minutes, and then a bandage is applied for 24 hours. Arterial puncture-site-closure devices may also be used at this level.10 Antegrade percutaneous popliteal approach The popliteal artery may be accessed through an antegrade approach in the case of femoral artery obstruction, by using short introducers 6–8 cm in length. This allows access to lesions on the leg, which may be helpful for limb salvage. Applicable endovascular techniques Almost all angioplasty techniques may be performed through this approach, including balloon angioplasty, atherectomy, such as rotational atherectomy (Rotablator),11 or recanalization devices, such as the laser fiber. All stents that may be implanted in the femoral artery may be introduced through this access. This also allows placement of covered stents,13 as compared to the contralateral access, which is limited due to the rigidity of the introduction of some materials. Intravascular ultrasound examinations may also be performed through this access and all mechanical thrombectomy devices may be used, for example, Hydrolyser, AngioJet,14 Rotarex, etc. In situ fibrinolysis may be attempted for limb salvage.4–6 However, it should be performed carefully due to risks of compression hematomas at this level. Small-diameter introducers should be used with preference. 29
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Drugs (pharmacological milieu) The pharmacological environment for an angioplasty performed through the popliteal approach is the same as for any angioplasty performed from another approach. The day before the procedure, patients are given aspirin, ticlopidine, or clopidogrel if a stent is envisaged. During the procedure, a bolus injection of 5000 units of heparin is given intravenously after the introducer is placed. Following the procedure, they are given aspirin indefinitely and ticlopidine or clopidogrel if stents are implanted.
Indications to popliteal approach Retrograde femoral approach There are two major classes of indications. Popliteal approach as first choice There are three types of indications. 1. The femoral approach is contraindicated or may not be performed due to severe atheromatous lesions at the puncture site or due to heavy calcifications. An arterial echo-Doppler examination at the puncture site should be performed prior to the procedure to reveal lesions that were previously undetected, thus contraindicating the femoral approach. 2. The other contralateral or brachial approach may not be used or are contraindicated. The contralateral approach may be difficult due to tortuous, stenosed, very atheromatous arteries, or an aortobifemoral bypass at a very acute aortic angle. They may also prevent the introduction of some devices. Certain atherectomy devices may not be used or long covered stents may not be placed though contralateral access due to the rigidity of the materials that may not cross the bifurcation. In addition, risks through the brachial access are even higher (thrombosis at the puncture site, cerebral embolization risks, etc.).
(a)
(b)
3. The popliteal approach may be chosen as first choice due to the localization of the lesions: a. ostial lesions of the superficial femoral artery i. lesions in the proximal part of the artery ii. diffuse lesions (proximal and mid-third) b. lesions of the common femoral artery i. associated lesions (common femoral, proximal part of the superficial femoral artery) ii. stenosis of a superior anastomosis of a bypass graft c. total occlusion of the superficial femoral, which now often requires placement of long covered stents. Indeed, these lesions are often difficult to treat when the catheterization is done through puncture of the ipsilateral common femoral artery since the puncture site is not far enough away from the lesion. Popliteal approach as second choice After failure of the angioplasty procedure through an antegrade femoral access, particularly in the case of femoral desobstruction, it seemed logical to us that the popliteal approach should be proposed, thus increasing the chances of success of interventional techniques. The contralateral (or crossover) access did not seem to present more benefits in those cases. This approach may also be proposed after failure of the brachial or contralateral access chosen as first choice to treat proximal femoral lesions. Antegrade popliteal puncture In cases where femoral obstructions and leg lesions are combined, one may propose to treat the leg arteries using an antegrade popliteal puncture. We have used this limb salvage procedure but it requires skill and experience. The puncture site is localized through “road mapping.” It may therefore be the only therapeutic access if surgery more proximally (e.g. femoropopliteal bypass graft) may not be performed and if the patient suffers from critical ischemia.
(c)
Figure 6.1 (a) Partial thrombosis of the right SFA; (b) result of desobstruction with Kensey catheter; and (c) results of angioplasty using the popliteal approach.
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Arterial access for endovascular interventions: popliteal access to peripheral procedures Techniques used The techniques used are as follows:
Table 6.1 Location of lesions Location
Number
Superficial femoral Ostial lesions (2–4 cm) Diffuse lesions > 15 cm Thromboses < 4 cm 4–8 cm > 8 cm Aneurysm Post-surgery chronic dissection Common femoral Stenoses (2–4 cm) Thromboses (4–6 cm) Superior anastomosis stenosis of a bypass graft
133 7 27 97 5 12 80 1 1 17 10 7 3
Authors’ personal experience A total of 153 patients under this group’s care have benefited from transluminal angioplasty using the percutaneous retrograde popliteal approach. During the same period, 5230 peripheral angioplasties of the legs were performed by the group, so transluminal angioplasties represent 2.8% of our procedures. These patients comprised 124 males and 29 females, with a mean age of 63 years (range 39–86 years). Risk factors were: diabetes (n = 29), hypertension (n = 76), smoking (n = 120), dyslipidemia (n = 84). Of these patients, 117 were in stage II of Fontaine’s classification, 24 in stage III, and 12 in stage IV. Lesion locations were as given in Table 6.1. Sixty-seven percent of the lesions were heavily calcified. Distal arterial runoff Distal arterial runoff was as follows: Three patent vessels: Two patent vessels: One patent vessel:
70 46 13 16 8
patients patients patients patients patients
(stage (stage (stage (stage (stage
IIb) IIc) III) III) IV)
Seventy-five patients underwent angioplasty through the popliteal access as first choice and 78 as second choice after failure of recanalization, either antegrade through the ipsilateral femoral despite the use of hydrophilic guidewires, laser fibers or other recanalization devices, or through brachial or contralateral access sites. Technical success Success of the popliteal access was as follows: No puncture failure Immediate success: Success of first choice: Success of second choice:
31
138/153 (90%) 69/75 (92%) 69/78 (88%)
The ankle brachial index increased from 0.52 ± 0.15 before the procedure to 0.92 ± 0.13 after the procedure. Failures occurred in 15/153 (10%) of cases and were mostly observed in long calcified lesions.
Laser recanalization: Recanalization with Kensey catheter: Simpson atherectomy device: Rotablator: Stent placement:
24 4 1 16 87
patients patients patient patients patients
(Palmaz, n = 36; Strecker, n = 2; nitinol stents, n = 28; covered stents, n = 26.) Several stents were implanted in the same patient. Complications Two hematomas were reported at the puncture site; they did not lead to compression symptoms and did not require surgery. Nine acute thromboses in the superficial femoral artery appeared at the angioplasty site during the first day; five required a bypass, two were successfully treated with mechanical thrombectomy (Hydrolyser) and/or thromboaspiration, and two patients who refused surgery were treated with drugs. Six thromboses appeared during the first month following the procedure; three were treated successfully with fibrinolysis and a new angioplasty, and three required a bypass graft. Six arteriovenous fistulas without hemodynamic consequences were also reported.
Discussion The popliteal access is still not often used, although it is reliable thanks to a good localization technique (e.g. road mapping, echo-Doppler). Indeed, in a series of 50 angioplasties, Tonnesen et al.1 reported results equivalent to ours, with an immediate success rate of 100%. Some contraindications must be respected (e.g. respiratory insufficiency, obesity) which would prevent obtaining a satisfactory ventral decubitus position. Other cases were also encountered where this approach could not be used, such as an inability to hyperextend the knee. Anatomical characteristics may also prevent popliteal access such as a thin popliteal artery, or a femoral or femoropopliteal obstruction near the puncture site. However, even when these contraindications are taken into account, this still is very often a usable approach. As a first-choice treatment, this approach competes with the contralateral femoral and brachial accesses. However, those are not always usable for anatomic reasons and certain techniques may be difficult to use through these two access sites, whereas the popliteal access allows nearly all endovascular techniques. All endoprostheses currently available may be implanted through popliteal access, especially covered stents, which allow the creation of internal bypass through a percutaneous access. The stent may be implanted very precisely at the femoral ostium through the popliteal access, whereas this is not always easy through contralateral access. The popliteal approach may be used to treat aneurysms in the leg arteries2,3 or for in situ fibrinolysis for limb salvage.4–6 This approach has high technical success rates and 88% of the antegrade femoral access failures could be recovered. Complications of this access are rare as long as a preprocedure echo-Doppler is performed to check the patency of
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(a)
(b)
(c)
(d)
(e) Figure 6.2 (a) Tight stenosis at the origin of the right external iliac artery; (b) partial thrombosis of the origin of the right superficial femoral artery; (c) laser recanalization of the right superficial femoral artery; (d) result of angioplasty of the right superficial femoral artery; and (e) result of angioplasty and placement of a Palmaz stent at the level of the right external iliac artery stenosis.
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Arterial access for endovascular interventions: popliteal access to peripheral procedures the artery and that there is no aneurysm at this level. Risk of thrombosis at the puncture site is rare, never having been observed by this group. The hematomas observed were without any consequence and new arterial-puncture-site closure devices should decrease the risk. Tonnesen et al.1 reports two popliteal hematomas in 50 cases, neither of which required surgery. These hematomas caused edema and pain for 2–3 months. There remains an unsolved problem: the arteriovenous fistulas, which seem to be frequent. They are, however, without any obvious hemodynamic consequence. Long-term results of the procedure do not depend on the approach but on the technique itself and on the lesions treated. The place of the popliteal access as compared to the contralateral and brachial approach ways is still debatable. The other two access sites allow manual compression remote from the treatment site, which is not associated with a decrease in flow related to the compression, which can result in the complication of thrombosis. Since the contralateral approach permits the use of large introducers, it thus also allows for procedures such as the “kissing” technique in the femoral bifurcation, which is not usable through the popliteal access.
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The brachial access, although useful, is limited by the diameter of the introducers. With preference, this group uses the popliteal access to treat superficial femoral lesions, which may not be treated at first or second choice, by an upper access. The antegrade popliteal approach enables treatment of popliteal lesions or threatening leg lesions.
Conclusion The popliteal access seems reliable and efficient, enabling the operator to recover numerous failures of the antegrade femoral access. However, because of the lack of familiarity with this technique, it has not been widely used in the treatment of peripheral arterial diseases. Its complication rate is low, as long as one adheres to a strict technique and locates the artery precisely. Its indications should be compared with those of the other access sites (i.e. contralateral and brachial). The popliteal approach accommodates all of the endovascular techniques and, by broadening the indications for angioplasty, it improves the success rate of the procedures. This approach should be better known and more frequently used by interventionists.
REFERENCES 1.
2. 3. 4. 5.
6.
7.
Tonnesen KH, Sager P, Karle A et al. Percutaneous transluminal angioplasty of the superficial femoral artery by retrograde catheterization via the popliteal artery. Cardiovasc Intervent Radiol 1988; 11: 127–31 Edwards H, Martin E, Nowygrod R. Nonoperative management of a traumatic peroneal artery false aneurysm. J Trauma 1982; 22: 323–6 McIvor J, Treweeke PS. Case report: direct percutaneous embolization of a false aneurysm with steel coils. Clin Radiol 1988; 39: 205–7 Perler BA, Osterman FA. Immediate postoperative urokinase infusion: extending the limits of limb salvage surgery. J Cardiovasc Surg 1990; 31: 184–8 Schroeder J. Catheter lysis and percutaneous transluminal angioplasty below the knee via the popliteal artery in a patient with femoral artery obstruction: technical note. Cardiovasc Intervent Radiol 1989; 12: 344–5 Weisman ID, Standchfield WR, Herzog CA Jr et al. Left ventricular thromboembolic occlusion of the popliteal artery treated nonoperatively with local urokinase infusion. A case report. Angiology 1988; 39: 179–86 Zeitler E, Richter EJ, Roth FJ et al. Results of percutaneous angioplasty. Radiology 1983; 146: 57–60
8. 9.
10. 11. 12. 13. 14.
Henry M, Amicabile C, Amor M et al. Angioplastie artérielle périphérique. Intérêt de la voie poplitée. A propos de 30 cas. Arch Mal Cœur 1993; 88: 463–9 (abstract) Henry M, Amor M, Henry I et al. Percutaneous transluminal angioplasty of peripheral arteries with retrograde catheterization through the popliteal artery: series of 63 cases. Radiology 1994; 193: 192 (abstract) Henry M, Amor M, Allaoui M et al. A new access site management tool: the AngioSeal haemostatic puncture closure device. J Endovasc Surg 1995; 2: 289–96 Henry M, Amor M, Ethevenot G et al. Percutaneous peripheral atherectomy using the Rotablator. J Endovasc Surg 1995; 2: 51–66 Henry M, Amor M. Stenting of femoral and popliteal arteries. In: Sigwart U, ed. Endoluminal stenting. WB Saunders: London, 1996; 476–86 Henry M, Amor M, Cragg A et al. Clinical experience with a new stent-graft for treatment of occlusive and aneurysmal peripheral arterial disease. Radiology 1996; 201: 717–24 Henry M, Amor M, Porte JM et al. La thrombectomie par le catheter Hydrolyser. A propos de 50 cas. Arch Mal Cœur (in press)
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Introducer sheaths, catheters, guiding catheters, and guidewires K Dougherty and Z Krajcer
Introduction Increased experience with endovascular techniques has caused an explosion of new technology. The number of vascular pathologies where surgical repair is the only option is rapidly decreasing. The endovascular specialist has a considerable assortment of commercially available sheaths, guidewires, and catheters to choose from. Choosing the correct equipment, however, can only be learned through hands-on experience.
Introducer sheaths Hemostatic introducer sheaths are generally used for all endovascular procedures. They establish a secure path from the skin to the vascular lumen. In addition to providing a safe port of access to the vascular system, they allow catheter instrumentation without ongoing blood loss or damage to the vessel wall. Sheath size is dependent upon the type of procedure and the outer diameter of the catheters or equipment used during the intervention. Most of the diagnostic peripheral procedures can be performed with 4-French sheaths. Smaller sheaths are particularly useful when performing diagnostic or interventional procedures on an outpatient basis. Catheter-directed thrombolysis should be performed with 4-French or 5-French sheaths to avoid the risk of bleeding around the sheath. Sheaths are generally 10–11 cm in length. Longer (30–100 cm) sheaths are used for a variety of purposes. This includes straightening out the tortuous iliac vessels, improving torque control and facilitating guide catheter, stent, and stent graft advancement. The Super Arrow-Flex introducer sheath (Arrow International Inc., Reading, PA) is popular for peripheral intervention because of its flexibility, and the numerous sizes and lengths. It is available from 40-cm to 100-cm lengths and from 5-French to 10-French diameters. It can provide all of the features of a guide catheter, with the added advantages of a builtin hemostatic valve and side-port. It incorporates a highly radio-opaque coil-wire design that allows it to flex at any point, in any direction, without kinking. This is particularly important for treating contralateral iliac, femoropopliteal and tibioperoneal lesions. A hydrophilic coating added to the tip allows successful negotiation through the tortuous peripheral anatomy. Many introducer sheaths can be used in place of guiding catheters for selective catheterization and visceral/branch artery intervention. Cook Endovascular has a variety of 34
peripheral introducer sheath sizes, lengths, and configurations to accommodate radial, brachial, axillary, or femoral access. The Flexor Check-FloII (Cook Inc., Bloomington, IN) introducer systems are thin-walled, with large lumens (Figure 7.1). The Flexor is equipped with a Tuohy–Borst side-arm that allows contrast injections, prevents blood reflux, and permits unimpeded catheter and guidewire introduction. It is kinkresistant with a hydrophilic coating and easily accommodates contralateral access. The Flexor Balkin Up and Over Contralateral Sheath (Cook Inc., Bloomington, IN) is frequently used for contralateral iliofemoral approach. The Flexor Shuttle Select (Cook Inc., Bloomington, IN) has a stiff proximal shaft with an atraumatic tip (Figure 7.2a). The lubricious hydrophilic coating promotes easier introduction but maximum pushability and support during endoluminal maneuvers in the supra-aortic vessels. The selective feature allows the sheath to be paired with the compatible 6.5-French Slip-Cath for selective engagement of the carotid vessels and is available in a variety of shapes (Figure 7.2b). The Beacon radio-opaque tip offers optimal visualization of catheter tip manipulation. The Flexor Shuttle Select has a Tuohy–Borst hemostasis valve with manual adjusting seal to allow unimpeded catheter or device introduction. Cook Endovascular also makes the Extra Large (14– 24-French) introducers. The 22- and 24-French sheath with Flexor Keller–Timmerman valve has a hydrophilic coating and is used to introduce large devices like endovascular stent grafts for abdominal aortic aneurysm exclusion (Figure 7.3). These sheaths range from 25 to 50 cm in length are equipped with a special hemostasis valve or Check-Flo valve that prevents blood reflux and allows flushing around the larger devices while they are positioned inside the sheath (Figure 7.2). The Pinnacle Destination (Terumo Corp, Tokyo, Japan) was developed as a renal guide sheath. There are three tip shapes, two detachable valve types and two French sizes to allow for procedural specific requirements. Like the Flexor Shuttle Select, the Destination is coil-reinforced and kink-resistant.
Angiographic catheters Diagnostic angiography is always performed prior to the endovascular intervention since it determines the complexity of the procedure, the access site, and the equipment that may be needed to successfully complete the intervention.
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Figure 7.1 The Flexor Check-Flo II (Cook Inc., Bloomington, IN) introducer systems are thin walled with large lumens and are equipped with a side-arm and hemostasis valve that allows contrast injections.
Angiographic catheters are constructed of polyethylene, polyurethane, nylon, Teflon, or a combination of these materials. Catheters made of polyethylene have a low coefficient of friction, can be torqued and have a good preshaped memory. Polyurethane catheters are softer and pliable, but have a higher coefficient of friction. Nylon catheters are stiffer and tolerate high flow rates and are generally used for aortography. Teflon is the stiffest material and is mainly used for sheaths and dilators. Many catheters are wire braided for extra torqueability. Others are coated with a hydrophilic polymer to improve trackability. Catheters vary in length and diameter. Outer diameter is designated by French size (3 French = 1 mm). Angiographic catheters are available in multiple shapes and sizes and can be divided into two basic categories: selective and non-selective. Non-selective catheters are usually designed with multiple side-holes, like the “pigtail” or “Omniflush” (AngioDynamics Inc., Queensbury, NY) and are used for angiography of large vessels, such as the aorta or vena cava (Figure 7.4). These non-selective shapes provide high flow and dispersion of a contrast agent without injuring the vessel wall. Angiography of high-flow vessels requires contrast injection by a power injector to obtain adequate opacification. These catheters typically come in either 4- or 5-French sizes, but are available in a wider range of 3–8 French. The “pigtail” catheter is designed to protect the vessel walls from the whipping effect during power-injected boluses of contrast. Calibrated marker “pigtail” catheters are used to determine accurate sizing of vessel lumen prior to endoluminal abdominal aortic aneurysm repair. This is particularly important during endoluminal intervention. Radio-opaque marker bands delineate a 20 cm segment, at 1 cm intervals, for precise measuring accuracy. When injecting into the pulmonary artery, stiffer catheters and higher flow rates maybe necessary. In these instances a Grollman or Montefore catheter may be more effective and both can easily manipulate through the cardiac chambers and into the pulmonary artery. Selective angiography catheter types and shapes are infinitely variable and choice is based on type and location of the lesion being treated (Figure 7.5). The standard inner diameters of a selective or flush catheter are 0.035 inches and 0.038 inches. Standard guidewires can be used to advance the catheters through the vasculature. Selective catheters are
35
(a)
(b) Figure 7.2 (a) The Flexor Shuttle Select (Cook Inc., Bloomington IN) has a stiff proximal shaft with an atraumatic tip. The lubricious hydrophilic coating promotes easier introduction but maximum pushability and support during endoluminal maneuvers in the supra-aortic vessels; (b) 6.5-French Slip-Cath for selectively engagement of the carotid vessels and is available in a variety of shapes. The Beacon radio-opaque tip offers optimal visualization of catheter tip manipulation.
preshaped to allow direct branch vessel engagement, pressure measurements, and contrast angiography. Specific catheters are recommended for specific anatomical locations and are designed to facilitate selective manipulation into branch vessels. It is best to have a variety of catheter shapes available for challenging anatomical situations. Precise knowledge of the
Figure 7.3 The 22- and 24-French sheath with Flexor KellerTimmerman valve has a hydrophilic coating and is used to introduce large devices like endovascular stent grafts for abdominal aortic aneurysm exclusion.
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Figure 7.4 Angiographic catheters are available in multiple shapes and sizes and non-selective catheters generally come with multiple side-holes to accommodate injections of large amounts of contrast.
type of catheter is very important for angiography so that appropriate and accurate information can be obtained prior to the intervention. Each company provides detailed product information on the catheters and their use. Hydrophilic catheters are useful for a selective approach of the carotid arteries, and to study the intra-cranial branches. Shorter length catheters (50 cm) are used for visceral, renal, or contralateral iliac artery injections. Catheters with side-holes should be avoided. Selective catheters generally have a single hole, located at the tip, through which all injected contrast exits. Because of the single end-hole flow rates are much lower than non-selective catheters and therefore power injectors should not be used. Furthermore, high-flow power injection through an end-hole catheter carries a considerable risk of vessel injury due to the end-hole jet effect. While catheter size or outer diameter is measured in French, catheter inner lumen diameter is measured in inches. Common sizes range from 0.018 to 0.038 inches. This inner
diameter measurement denotes the acceptable guidewire size for the catheter. A mismatch in sizes can cause problems; such as either the guidewire not fitting inside the catheter or blood leakage around the guidewire. Diagnostic catheter size and length range from 4 to 6 French, and from 50 to 125 cm, respectively. Most of these catheters are braided, with a soft tip, without braiding. Different catheter materials have specific functional characteristics such as stiffness or rigidity and kink-free torque control. Some catheters have inner and outer hydrophilic coating to reduce friction for ease of passage and manipulation.
Guide catheters Like diagnostic catheters, guiding catheters come in a variety of lengths and shapes designed to facilitate their manipulation into branch vessels. However, they differ from diagnostic catheters by having a substantially larger luminal diameter (Figure 7.6). Guiding catheters are sized like diagnostic catheters with the outer diameter in French and the inner diameter in inches. But, to allow passage of the endovascular instruments, guide catheters must have a lumen diameter at least twice that of a typical diagnostic catheter. Guide catheters are similar to sheaths in that they provide protection to the vasculature when passing multiple devices into the same vessel. Important guiding catheter characteristics include the ability to provide stable coaxial alignment between the catheter tip and the ostium of the vessel and kink-free torque control.
C1
C2
C3
MIK
HK 1.0
CONTRA 2
SHK 0.8
SHK 1.0
RC1
RC2
RDC
DUCK
CHGB
CHGC
CHG2.5
TRAIN
VAN
WEIN
H1
H3
MANI
BARN
BERN
H1H
H3H
JB1
JB2
JB3
ST
CK
SIM1
SIM2
SIM3
SIM4
GEN
HN1
HN2
HN3
HN4
HN5
Figure 7.5 Selective angiography catheter types and shapes are infinitely variable and choice is based on type and location of the lesion being treated.
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ALI MP1 Burke H1 HY1
Figure 7.6 Guiding catheters come in a variety of lengths and shapes designed to facilitate their manipulation into branch vessels. However, they differ from diagnostic catheters by having a substantially larger luminal diameter.
A properly selected guide catheter should also provide back-up support for balloon catheter advancement and withdrawal, reliable pressure monitoring, and adequate contrast delivery during injections. In comparison to diagnostic catheters, guiding catheters have reinforced construction and a much stiffer shaft to provide back-up support for the advancement of guidewires, balloons, and stents. Peripheral guiding catheters are generally 6, 7, or 8 French and range from 65 to 100 cm in length with internal diameters ranging between 0.064 and 0.088 inches.
Guidewires Guidewires permit safe transluminal navigation of catheters and devices. Basic guidewire construction affects handling characteristics. Design variables include tip configuration, length, diameter, stiffness, antifriction coatings, and radioopaque markers. Mastering guidewires involves observation of guidewire behavior under fluoroscopy and understanding the interaction between the guidewire leading edge and the lesion. The fundamental attributes of a guidewire include the ability to transmit torque, minimize friction, tip flexibility, and steerability. Guidewires should only be advanced under fluoroscopic guidance and never advanced when resistance is met. This will eliminate the risk of subintimal wire passage, vessel dissection, and perforation. Guidewire diameters are measured in inches. The standard range is 0.014–0.038 inches. The diameter of the guidewire should match the required diameter of the catheter. This provides better support of the catheter during manipulation and decreases the amount of leakage around the wire. Guidewires are either straight, angled, or have a J-shaped tip and have varying lengths of flexibility at the tip ranging from 3 to 20 cm. The J-tipped wire is the most commonly used guidewire for initial passage into the vessel because of its lowrisk of subintimal dissection. The main components of the traditional guidewire are the central core, which provides body, steerability, and torque control, and a tightly wound outer spring coil (Figure 7.7) and contains a forming ribbon for tip shaping and a Teflon outer coating to decrease friction.
Figure 7.7 The main components of the traditional guidewire are the central core, which provides body, steerability, and torque control, and a tightly wound outer spring coil.
Hydrophilic guidewires were developed to satisfy a wide variety of procedural requirements. The Glidewire guidewires, (Terumo, Somerset, NJ) use a unique design of a nitinol inner core, which is only minimally elastic, a markedly tapered distal tip that has a polyurethane outer surface instead of a spring coil, and a hydrophilic polymer coating. The hydrophilic coating is chemically bonded to the polyurethane jacket to reduce friction and thrombogenicity. They range in size from 0.018 to 0.038 inches in diameter and come in regular (180 cm) and exchange lengths (260 cm). The Magic Torque guidewire (Boston Scientific Corp, Natick, MA) has enhanced radio-opacity with distal platinum markers to facilitate accurate vessel measuring and device placement. It also has a hydrophilic coating on the distal 10 cm and PTFE on the distal 11–50 cm to help reduce access friction. Magic Torque is available in 0.035-inch diameter and is either 150 cm or 260 cm in length. The length of the wire is determined by its intended use. Most regular length guidewires are 145–175 cm long. Exchange length guidewires are 260–450 cm long and allow catheters, balloons, and other device exchanges while the guidewire is maintained in the distal position. The length of the guidewire will generally depend on the distance of the lesion from the access site and on the length of the catheter or the device that is being used. For diagnostic angiography procedures it is usually not necessary to use guidewires that are longer than 180 cm. However, during the interventional procedure it is generally recommended to use exchange length (260 cm) guidewires. This length is necessary to have adequate length of the guidewire to be able to remove the device without losing the wire position across the lesion. It is occasionally necessary to use longer wires when brachial access is used for an intervention of femoral, popliteal, and tibioperoneal arteries. In this circumstance a 400 cm Nitrex (ev3, Plymouth, MN) or a 450-cm-long Geenan and Zebra (Boston Scientific, Natick, MA) guidewire is very useful. When attempting to traverse severely stenotic lesions or occlusions of vessels it is essential to select a guidewire that is flexible and can be easily steered, yet has sufficient body stiffness. There are several products that are commonly used for this purpose. A 0.035-inch Super Stiff angled Glidewire (Terumo, Somerset, NJ), because of good steerability and sufficient support is the wire of choice when crossing occluded vessels. The 0.018-inch angled Glidewire Goldtip wire (Terumo, Somerset, NJ) is another guidewire that has a hydrophilic coating and can be of a great advantage for crossing severely stenotic or occluded tibioperoneal arteries. For neuro applications, the Glidewire Goldtip wire is available with an 8-cm floppy tip in sizes that range from 0.011 to 0.018 inches. One of the disadvantages of wires with a hydrophilic coating is their propensity to cause perforations of the vessels when not used with caution. For this particular reason it is not advisable to use these wires for renal or visceral interventions.
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Shorter guidewires are suitable for the renal and visceral interventions like the 0.014-inch Hi-Torque Spartacore 14 (Guidant Corp., Santa Clara, CA) with a 3- and 5-cm floppy tip for support. Several guidewires offer even more support and stiffness of the body than the Super Stiff Glidewire. For endoluminal repair of an abdominal aortic aneurysm (AAA) it is essential to have a sufficient support to advance a large-profile stent graft device across the iliac arteries. In this type of procedure a 0.035-inch Super Stiff Amplatz (Boston Scientific, Natick, MA) guidewire, a Nitrex (ev3, Plymouth, MN) or an even stiffer 0.035-inch Lunderquist (Cook Inc., Bloomington, IN) guidewire should be used. The 0.035-inch Super Stiff Amplatz guidewires are available with different lengths of the flexible segments at their distal ends. Some of the products are available with 3-mm J, 1-cm, 6-cm and 10-cm flexible-tip segments. The purpose of the flexible segment of the wire is to conform itself to the vessel anatomy, and avoid vessel trauma and spasm. The choice of length of the flexible segment will depend on the location of the vessel and the amount of support that will be needed to advancement the device. For endovascular abdominal aortic aneurysm repair, the 6-cm or 10-cm flexible-tip length should be used to advance the large-bore stent graft into the aorta. The Bentsen (Cook Inc., Bloomington, IN) wire is a 0.035-inch guidewire with a very soft body that allows easy tracking in a tortuous vessel. This wire is frequently used for advancing the catheter in the renal and other visceral vessels when other wires are not able to achieve this goal. It is also routinely used for advancing the vascular coils through the catheter for coil embolization. Deflectable tip wires are also available such as the Reuter Tip Deflecting Wire (Cook Inc., Bloomington, IN), which is used to deflect catheter tips. The Reuter wire is available in either 0.025-, 0.035-, or 0.038-inch diameters and are 110 cm or 145 cm in length and is not intended to exit the tip of the catheter it is deflecting. The Venture (St. Jude Medical, Minnetonka, MN) is a wirecontrol catheter which deflects at the tip up to 90∞. The wire control catheter is compatible with all 0.014-inch wires and is
an over-the-wire design to enable wire exchanges. The outside diameter is 0.022 inches and has an inside diameter of 0.017 inches. The Venture provides backup support for crossing total occlusions and a deflectable tip more precise steering capabilities.
Infusion wires and catheters Other specialty guidewires include infusion wires like the ProStream (Micro Therapeutics Inc., San Clemente, CA), the Katzen and the Cragg (Meditech, Boston Scientific Corp., Natick, MA) (Figure 7.2) which have an outside diameter of either 0.035 or 0.038 inches and range from 145 to 180 cm in length. Multiple side-holes with various infusion port lengths from 3 to 15 cm and/or an open end-hole allow pharmacological agents to be delivered over a predetermined distance or to distal vessels. This configuration also permits coaxial use through 5-French infusion catheters (Meiwissen, Boston Scientific Corp, Natick, MA). A smaller 2.9-French MicroMewi (Micro Therapeutics Inc., San Clemente, CA) infusion catheter is inserted over a 0.018-inch guidewire and permits coaxial infusion. The Meiwissen catheter is a 5-French infusion catheter, 150 cm long, that has an infusion length of either 5 or 30 cm.
Microcatheters Microcatheters are used when the target vessel is smaller than the conventional catheter and can be placed through the standard angiographic catheter. These catheters are generally used for therapeutic purposes, such as embolizing bleeding vessels, vascular malformations, and small aneurysms. The Echelon (ev3, Plymouth, MN) is a 2.1-French, 150-cm, braided nitinol and PTFE guidewire-supported microcatheter that tapers to 1.7-French. Microcatheters have allowed treatment of a number of vascular pathologies that were previously untreatable or could only be treated with microsurgery.
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Percutaneous transluminal angioplasty T Collins and PW McMullan Jr
Introduction Angioplasty is the mechanical alteration of a narrowed or occluded vessel lumen. The word derives from the roots “angio” or vessel and “plasticos” or fit for molding. Nowadays it is used to describe a variety of percutaneous vascular interventions. Percutaneous transluminal angioplasty (PTA) is used to describe angioplasty of vessels other than the coronary arteries. Charles Dotter, a vascular radiologist, introduced transluminal angioplasty in 1964. By using progressively increasing sizes of catheter he was able to dilate stenosed leg arteries. Andreas Gruentzig performed the first balloon angioplasty of a human peripheral artery in 1974. PTA has been most commonly used to treat iliac and leg arteries with atherosclerotic disease. The progression of expertise and equipment has expanded the use of PTA to all vascular beds, both venous and arterial. In many situations stenting has become the treatment of choice for completing percutaneous procedures; however, there remain clinical situations where PTA alone is acceptable if not preferred. Mechanism of PTA The application of peripheral balloon angioplasty exerts a centrifugal force from within the vessel lumen. This force is delivered via a balloon that is inserted percutaneously and inflated adjacent to the treatment area. The outward radial force, called hoop stress, stretches or separates the components of the vessel wall. This radial force is a product of the pressure applied and the area against which it is applied. The Laplace law describes this force as: Hoop stress = pressure × diameter Indications In general, the indications for percutaneous transluminal angioplasty in non-coronary arteries are prevention and/or reversal of ischemia. This broad classification includes preservation of function, restoration of function, improvement of quality of life, and end-organ salvage. Technique PTA is performed in an angiographic laboratory under fluoroscopic and cine-angiographic visualization. Arterial or venous access is gained most commonly by the modified Seldinger approach followed by insertion of a valved sheath which
prevents back-bleeding and allows repeated atraumatic entry into the vessel lumen. Through the sheath, an appropriately sized and shaped catheter is introduced over a leading wire. Once the vessel of interest is cannulated, angiography is performed in multiple orthogonal projections to delineate the diseased or abnormal portion and determine the severity of stenosis. Views should include the entire vascular bed to identify collateral arteries and the run-off vessels. Angiography of peripheral arteries is done optimally by digital subtraction angiography, which allows masking of bony structures, and this technique may be performed in an automated, stepwise fashion to capture the entirety of the distal aorta and lower extremities with a single injection of contrast from a power injector. Iso-osmolar contrast is used in order to maximize patient comfort. When the stenosis in question is of dubious severity or particularly difficult to image, catheter “pullback” to determine the pressure gradient across the lesion, intravascular ultrasound, or the use of a flow wire may assist in assessment. Numerous wires may be used to cross the diseased arterial segment. In general, wires range from 0.014 to 0.035 inches in diameter. The choice of wires is dependant upon the anatomy, stenosis versus occlusion, and balloon catheter to be utilized. The operator should be familiar with the available inventory prior to the procedure and plan appropriately.
Vascular territories Iliac vessels Roughly one-third of obstructive atherosclerotic disease affecting the patient with claudication is aortoiliac disease.1 In patients under the age of 40 with PAD, disease in the aortoiliac segment is the most common site of atherosclerosis.2 Reasons for intervention in the iliac vessels include lifestyle-limiting claudication, limb-threatening ischemia, and maintaining vascular access for procedures such as intraaortic balloon pump placement or coronary angiography.3 The TransAtlantic Inter-Society Consensus on Management of Peripheral Arterial Disease working group published an initial series of guidelines in 20004 for the direct management of PAD which were updated in January 2007 based on more current data.5 These guidelines recommend treatment with surgical versus percutaneous means based on lesion extent and morphology. Focal lesions (types A and B) are classified as likely responsive to PTA, whereas more complex or completely 39
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Textbook of peripheral vascular interventions Recommendation 36 Treatment of aortoiliac lesions TASC A and D lesions: Endovascular therapy is the treatment of choice for type A lesions and surgery is the treatment of choice for type D lesions [C]. TASC B and C lesions: Endovascular treatment is the preferred treatment for type B lesions and surgery is the preferred treatment for good-risk patients with type C lesions. The patient's co-morbidities, fully informed patient preference and the local operator's long-term success rates must be considered when making treatment recommendations for type B and type C lesions [C].
Figure 8.1 Lesions.5
TASC Recommendations for Treatment of Aortoiliac
occlusive lesions (types C and D) are considered surgical (Figures 8.1 and 8.2) Access for work in the iliac vessels is most commonly gained in the ipsilateral common femoral artery with a retrograde approach. Occasionally anatomy will require a crossover approach from the contralateral common femoral artery, in which case a braided, non-kinking 55-cm sheath with an inner
Type A lesions • Unilateral or bilateral stenoses of CIA • Unilateral or bilateral single short (≤3 cm) stenosis of EIA
Type B lesions: • Short (≤3cm) stenosis of infrarenal aorta • Unilateral CIA occlusion • Single or multiple stenosis totaling 3–10 cm involving the EIA not extending into the CFA • Unilateral EIA occlusion not involving the origins of internal iliac or CFA
Type C lesions: • Bilateral CIA occlusions • Bilateral EIA stenoses 3–10 cm long not extending into the CFA • Unilateral EIA stenosis extending into the CFA • Unilateral EIA occlusion that involves the origins of internal iliac and/or CFA • Heavily calcified unilateral EIA occlusion with or without involvement of origins of internal iliac and/or CFA
Type D lesions • Infra-renal aortoiliac occlusion • Diffuse disease involving the aorta and both iliac arteries requiring treatment • Diffuse multiple stenoses involving the unilateral CIA, EIA, and CFA • Unilateral occlusions of both CIA and EIA • Bilateral occlusions of EIA IIiac stenoses in patients with AAA requiring treatment and not amenable to endograft placement or other lesions requiring open aortic or iliac surgery
Figure 8.2
TASC Classification of Aortoiliac Lesions.5
diameter of 6 French or greater is used. Standard 0.035-inch Jwires or 0.035-inch hydrophilic wires are used to cross lesions after which it is common to change wires via a diagnostic catheter for a stiffer support wire. Over this wire, monorail, or over-the-wire peripheral balloons can then be inserted. Lesion dilation in the iliac vessels is performed very cautiously due to the risk of rupture, which causes lifethreatening retroperitoneal bleeding. A common method for balloon sizing is to perform angiography with a reference object in the field, measure the adjacent normal vessel with reference to the object, and choose a balloon size slightly smaller than the reference vessel. Common sizes are 6–8 mm. Upon inflation, the operator must be alert to any back or flank pain the patient experiences, which is a sign of vessel stretch. Dilatations beyond this point risk vessel dissection or rupture. Indications that balloon angioplasty has failed and stenting is required include a resultant dissection or a residual hemodynamic gradient of greater than 10 mmHg. Primary stenting is usually performed for treatment of a total occlusion.6 Compiled results of balloon angioplasty analyzed in 1989 reported the following: in 2697 iliac PTA procedures, the technical success rate was 92% with 2- and 5-year primary patency rates of 81 and 75%.7 Another meta-analysis performed in
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Percutaneous transluminal angioplasty 1997 based on 1473 procedures including 80% stenoses and 20% occlusions yielded a 91% technical success rated with primary patency rates of 74, 66, 61, and 58% at 1, 2, 3, and 4 years, respectively.8 Due to stent results which are generally superior (10–15% higher at each interval), the recently published ACC/AHA Guidelines for the Management of PAD9 list provisional iliac stent placement as a class I recommendation (level of evidence: B) for a suboptimal or failed result from balloon dilatation (persistent translesional gradient, residual diameter stenosis greater than 50%, or flow-limiting dissection). Primary stent placement is also listed as a class-I recommendation for the common iliac artery (level of evidence: B) and the external iliac artery (level of evidence: C).
Type A lesions Type B lesions
Type C lesions
Type D lesions
Superficial femoral and popliteal arteries In patients with PAD and claudication, superficial femoral artery (SFA) and popliteal disease is present in over 50% of cases.1 These vessels are characterized by a long course and often have diffuse segments of disease. When the muscles and joints of the lower extremity move, external forces of compression, torsion, shortening, and elongation act on the arterial wall. These arteries consequentially have very high rates of restenosis and remain a challenging area of treatment for the endovascular specialist. TASC guidelines divide SFA and popliteal disease into four categories, A–D.5 TASC A lesions are considered amenable to percutaneous intervention, whereas surgery is recommended for TASC D lesions. Lesions in the intermediate realm are categorized as TASC B and C (Figures 8.3–8.5). The ideal treatment for these lesions remains a topic of ongoing debate, and therapy favoring PTA versus surgery varies widely based on local practice. As in most areas of endovascular therapy, improvement in technology is allowing for more aggressive percutaneous approaches to femoropopliteal disease, and indications will evolve as data builds to support PTA. Factors that predict a favorable outcome in percutaneous treatment of SFA lesions include the presence of intermittent claudication, location in the proximal portion of the vessel, shorter stenosis length, lack of complete occlusion, adequate distal runoff, large diameter of treated artery, and a balloon result without significant residual stenosis.10,11 Access to the SFA and popliteal territories is most often gained in the contralateral common femoral artery in retrograde fashion. Crossover to the target limb is accomplished with an IMA or similarly curved catheter which directs passage Recommendation 37 Treatment of femoral popliteal lesions TASC A and D lesions: Endovascular therapy is the treatment of choice for type A lesions and surgery is the treatment of choice for type D lesions [C]. TASC B and C lesions: Endovascular treatment is the preferred treatment for type B lesions and surgery is the preferred treatment for good-risk patients with type C lesions. The patient's co-morbidities, fully informed patient preference and the local operator's long-term success rates must be considered when making treatment recommendations for type B and type C lesions [C].
Figure 8.3 TASC Recommendations for Treatment of Femoral Popliteal Lesions.5
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Single stenosis ≤10 cm in length Single occlusion ≤5 cm in length Multiple lesions (stenoses or occlusions), each ≤5 cm Single stenosis or occlusion ≤15 cm not involving the infra geniculate popliteal artery Single or multiple lesions in the absence of continuous tibial vessels to improve inflow for a distal bypass Heavily calcified occlusion ≤5 cm in length Single popliteal stenosis Multiple stenoses or oclusions totalling >15 cm with or without heavy calcification Recurrent stenoses or occlusions that need treatment after two endovascular interventions Chronic total occlusions of CFA or SFA (>20 cm, involving the popliteal artery) Chronic total occlusion of popliteal artery and proximal trifurcation vessels
CFA – common femoral artery; SFA – superficial femoral artery.
Figure 8.4 TASC classification of femoral popliteal lesions.5 Used with permission.
of a wire over the aortic bifurcation and down the common iliac. Following necessary focal angiography with this catheter, a stiff exchange-length wire is then employed for removal of the catheter and sheath and placement of a braided, nonkinking crossover sheath down to the level of the common femoral artery. Contralateral access may be impossible in certain cases due to the presence of an aortobifemoral graft or iliac occlusion. When necessary, ipsilateral antegrade common femoral or retrograde ipsilateral popliteal access is considered. Following insertion of the crossover sheath, uncomplicated lesions may frequently be crossed with the same straight, floppy-tipped stiff wire which then serves as a platform for balloon insertion. More complex lesions or total occlusions often require a more methodical technique with an angled 0.035-inch hydrophilic wire for initial approach delivered with the support of a 4-French catheter which can be angulated (IMA, JR4, MP) or hydrophilic for difficult-to-cross lesions. On occasion, a straight hydrophilic wire or a smaller 0.014–0.018-inch wire may facilitate lesion crossing. There are also newer devices designed for total occlusions which allow re-entry into the distal true lumen after initial wire passage creates a parallel dissection plane. Once the lesion is crossed, the stiff support wire is advanced, the catheter removed, and the balloon catheter inserted. Since injection through the sheath becomes difficult or impossible with the indwelling balloon catheter, it is important to establish bony landmarks on cine-angiography which correlate with the level of the lesion. Balloons of 4–6 mm in diameter are most often used in the SFA and popliteal arteries, and inflation is performed until the stenosis “waist” yields to the balloon (Figure 8.6). Following PTA, significant residual stenosis at the lesion site and flow-limiting dissection are indications for stent placement. Results of balloon angioplasty in the femoropopliteal arteries including initial technical success and durability are largely determined by lesion morphology. Early PTA data from the mid-1980s demonstrated that short, easily dilatable lesions had a 5-year patency of 75%, but lesions greater than 3 cm in
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Type B lesions: • Multiple lesions (stenoses or occlusions), each ≤5cm • Single stenosis or occlusion ≤15cm not involving the infrageniculate popliteal artery • Single or multiple lesions in the absence of continuous tibial vessels to improve inflow for a distal bypass • Heavily calcified occlusion ≤5cm in length • Single popliteal stenosis
Type C lesions • Multiple stenoses or occlusions totaling > 15cm with or without heavy calcification • Recurrent stenoses or occlusions that need treatment after two endovascular interventions
Type D lesions • Chronic total occlusions of CFA or SFA (>20 cm, involving the popliteal artery) • Chronic total occlusion of popliteal artery and proximal trifurcation vessels
Figure 8.5
TASC Classification of Femoral Popliteal Lesions.
length had markedly lower 1-year patency rates.12 Other series showed that PTA without stenting in lesions greater than 10 cm has a high initial technical success rate of over 90%, and cumulative patency rates at 18 months have been reported as high as 69%.13 The STAR registry, which was published in 2001 reported 5-year follow-up on 219 limbs in 205 patients. Primary patency for femoropopliteal PTA was 87% at 1 year, 80% at 2 years, and 55% at 4–5 years. The condition which was most predictive of occlusion was poor infrapopliteal runoff, defined as a single vessel with 50–99% stenosis or occlusion.14 In the modern era, devices which allow the operator to cross back into the distal true lumen following guidewire dissection are increasing operator aggressiveness in long segments of total occlusion. This yields higher initial technical success rates, but such results are often suboptimal with balloon therapy alone. Primary stenting in the femoropopliteal territory remains an ACC/AHA class III recommendation, but
stent placement is required in conditions of a suboptimal or failed balloon result.9 Improving stent technology is allowing for lower profile delivery systems, self-expanding nitinol designs, and exceptional fracture-resistant recoil properties. These advancements promise to make percutaneous therapy applicable to a broader variety of lesion subsets which have traditionally required surgery.
Tibioperoneal arteries In contrast to femoropopliteal lesions, the indication for angioplasty in the tibioperoneal vascular bed is generally not symptom-limiting claudication but rather chronic critical limb ischemia or limb salvage.5 Only 1.4% per year of patients with intermittent claudication progress to the degree of severity that ischemia at rest is a problem. Those who do are more prone to be diabetics and smokers.2 The goal of angioplasty in these patients is the establishment of inline flow to the level
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Figure 8.7 Left peroneal artery (a) before and (b) after balloon angioplasty. Figure 8.6 Left superficial femoral artery (a) before and (b) after balloon angioplasty.
of the foot in order to alleviate rest pain or promote healing of ulcers. Even though this initial patency may not be long lasting, the window of improved flow frequently allows wound healing prior to restenosis or reocclusion. Many of the technical methods employed in below-theknee angioplasty have been adopted from work in the coronary vasculature, a field which has rapidly evolved to deal with atherosclerosis in similarly sized vessels. Operators frequently use coronary equipment including guiding catheters, 0.014 specialty coronary guidewires, and small-diameter monorail coronary balloons. Retrograde access from the contralateral common femoral artery is possible with utilization of a crossover sheath followed by a guiding catheter. At times, antegrade access is necessary in order to deliver equipment to the distal vasculature due to equipment length constraints. Recently, balloons 1.5–4.0 mm in diameter have been developed with lengths as great as 120 mm specifically for use in the tibial vessels. These allow operators to treat the long diffuse
Figure 8.8
lesions that are typical in the tibial territory with a minimal number of balloon inflations (Figure 8.7). Results of tibioperoneal PTA are encouraging. In a large series of 235 patients, technical success of PTA in the tibioperoneal arteries was reported as 95%. A series of 284 critically ischemic limbs were treated with a success rate of 92% in a total of 529 lesions. Clinical success defined as the relief of rest pain or improvement of flow to the lower extremity was documented in 95%. A 5-year follow-up revealed a need for bypass surgery in 8% and significant amputations in 9%, yielding a 91% salvage rate.15 Renal arteries Etiologies for renal artery stenosis include atherosclerosis, fibromuscular dysplasia, arteritis, and radiation-induced injury, all of which cause renal hypo-perfusion and can induce elevated renin levels with resultant hypertension. Atherosclerosis is the most prevalent of these causes and most commonly affects the ostium of the renal artery so that bulky aortic plaque, which is
Right renal artery with fibromuscular dysplasia (a) before and (b) after balloon angioplasty.
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frequently calcified, extends into renal artery plaque. This phenomenon, coupled with the dilation-resistant nature of these lesions, produce a restenosis rate for balloon angioplasty approaching 50% due to recoil.16,17 Randomized trial data support routine stent placement for ostial atherosclerotic stenoses and produce a 6-month angiographic restenosis rate for stents of only 14%.18 Balloon angioplasty alone may be utilized for the other aforementioned types of lesions and has been studied extensively in fibromuscular dysplasia.19 Access for renal artery intervention is most often gained through the femoral artery, although brachial and radial access is sometimes the approach of choice. From the femoral approach, a 50-cm 6-French guiding catheter (hockeystick, renal double curve, or IMA) can be safely advanced over a 4-French diagnostic catheter (IMA or JR4) in telescopic fashion once a supporting 0.014-inch angioplasty wire has been advanced through the 4-French catheter for support. The 4-French catheter is then removed while leaving the guiding catheter and wire in place over which a monorail balloon (sizes range from 3 to 7 mm) is then advanced. Alternatively, a “no touch” technique may be used to position the angioplasty wire and guide catheter. In this technique a J-tipped wire is inserted into a guide catheter which is then positioned adjacent to the renal ostium with the J-wire extending out of the end of the catheter. An angioplasty wire is then manipulated into the renal artery and the J-wire is removed while advancing
the guide to the ostial position. Angiography should allow visualization of the entire renal cortex to avoid missing an accessory renal artery prior to angioplasty and to ensure visualization of wire perforation or poor reflow following angioplasty. Fibromuscular dysplasia is typically responsive to balloon therapy since it produces a tearing of the fibrous band or curtain which impedes flow (Figure 8.8).19 Rates of restenosis following PTA have been reported as 7–27% over follow-up periods ranging from 6 months to 2 years.17,20–22 Likelihood of a favorable clinical response to PTA correlates with an age of less than 57, lack of concomitant disease in the carotid and coronary vessels, and presence of hypertension for less than 9 years.23
Conclusion PTA in peripheral vessels has evolved dramatically in the four decades since its inception and now offers thousands of patients annually relief from ischemia without the necessity of surgical intervention. While many procedures in the periphery now include the use of stents, there remains a significant role for balloon angioplasty alone. As advancing technology puts new tools in the hands of increasing numbers of well-trained operators, the future of the endovascular field holds great promise.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.
10. 11.
Henry M, Rath PC, Klonaris C et al. Peripheral vascular diseases: an update on endovascular therapy. Indian Heart J. Nov-Dec 2005; 57(6): 747–66 Bittl JA, Hirsch AT. Concomitant peripheral arterial disease and coronary artery disease: therapeutic opportunities. Circulation. Jun 29 2004; 109(25): 3136–44 Ansel G. Primary stenting of the iliac artery. Endovascular Today. 2005; 5: 39–42 TransAtlantic Inter-Society Consensus (TASC) on Management of Peripheral Arterial Disease (PAD). Journal of Vascular Surgery. 2000; 31S: 1–296 Norgren L, Hiatt WR, Dormandy JA et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg. Jan 2007; 45(1 Suppl): S5–S67 Bates MC, Aburahma AF. An update on endovascular therapy of the lower extremities. J Endovasc Ther. Dec 2004; 11 Suppl 2: II107–127. Becker GJ, Katzen BT, Dake MD. Noncoronary angioplasty. Radiology. Mar 1989; 170(3 Pt 2): 921–40 Bosch JL, Hunink MG. Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease. Radiology. Jul 1997; 204(1): 87–96 Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. J Am Coll Cardiol. Mar 21 2006; 47(6): 1239–1312 Johnston KW. Femoral and popliteal arteries: reanalysis of results of balloon angioplasty. Radiology. Jun 1992; 183(3): 767–71 Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty. Factors influencing long-term success. Circulation. Feb 1991; 83(2 Suppl): I70–80
12. 13.
14. 15.
16.
17. 18. 19. 20. 21.
22. 23.
Krepel VM, van Andel GJ, van Erp WF et al. Percutaneous transluminal angioplasty of the femoropopliteal artery: initial and longterm results. Radiology. Aug 1985; 156(2): 325–28 Murray JG, Apthorp LA, Wilkins RA. Long-segment (> or = 10 cm) femoropopliteal angioplasty: improved technical success and long-term patency. Radiology. Apr 1995; 195(1): 158–62 Clark TW, Groffsky JL, Soulen MC. Predictors of long-term patency after femoropopliteal angioplasty: results from the STAR registry. J Vasc Interv Radiol. Aug 2001; 12(8): 923–33 Dorros G, Jaff MR, Dorros AM et al. Tibioperoneal (outflow lesion) angioplasty can be used as primary treatment in 235 patients with critical limb ischemia: five-year follow-up. Circulation. Oct 23 2001; 104(17): 2057–62 Sos TA, Pickering TG, Sniderman K et al. Percutaneous transluminal renal angioplasty in renovascular hypertension due to atheroma or fibromuscular dysplasia. N Engl J Med. Aug 4 1983; 309(5): 274–79 Plouin PF, Darne B, Chatellier G et al. Restenosis after a first percutaneous transluminal renal angioplasty. Hypertension. Jan 1993; 21(1): 89–96 van de Ven PJ, Kaatee R, Beutler JJ et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomised trial. Lancet. Jan 23 1999; 353(9149): 282– 86 Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med. Apr 29 2004; 350(18): 1862–71 Jensen G, Zachrisson BF, Delin K et al. Treatment of renovascular hypertension: one year results of renal angioplasty. Kidney Int. Dec 1995; 48(6): 1936–45 Klow NE, Paulsen D, Vatne K et al. Percutaneous transluminal renal artery angioplasty using the coaxial technique. Ten years of experience from 591 procedures in 419 patients. Acta Radiol. Nov 1998; 39(6): 594–603 Baumgartner I, Triller J, Mahler F. Patency of percutaneous transluminal renal angioplasty: a prospective sonographic study. Kidney Int. Mar 1997; 51(3): 798–803 de Fraissinette B, Garcier JM, Dieu V et al. Percutaneous transluminal angioplasty of dysplastic stenoses of the renal artery: results on 70 adults. Cardiovasc Intervent Radiol. Jan-Feb 2003; 26(1): 46–51
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Cutting balloon angioplasty S Tyagi
Introduction Balloon angioplasty is an established revacularization procedure for coronary and non-coronary vascular stenosis. However, conventional balloon dilatation results in application of force in a random manner to the components of the stenosis. This circumferential shear stress often causes irregular intimal tear, splits, and stretches. Vessel wall trauma can cause dissection, intimal proliferative response, and restenosis.1 Elastic recoil also limits response to balloon angioplasty. Some lesions either in native vessels or grafts may be difficult to dilate with conventional balloon angioplasty. This may be as a result of the simultaneous presence of atherosclerosis, fibrosis, and calcification. To overcome these limitations, Barath et al.2 designed a hybrid device, a cutting balloon (CB), that has tiny razor-sharp blades mounted on its surface. It is designed to minimize the vessel wall trauma that is traditionally associated with conventional balloon angioplasty. The concept of the CB is to cut first and dilate next, and the balloon pressure serves primarily to propagate the incisions.3 Use of the CB has been explored mainly in coronary arteries. Initial studies suggests its usefulness in treatment of concentric lesions, ostial lesions, small vessels, and long diffuse lesions.1,3,4 Long-term effectiveness of balloon angioplasty is limited by restenosis. Pathogenesis of restenosis is mainly intimal hyperplastic reaction in response to vessel injury. CB angioplasty reduces the force needed to dilate an obstructive lesion thereby minimizing barotrauma to the vessel.4 This was supposed to reduce restenosis. However, the proposed mechanism has not been found to be effective for prevention of restenosis in coronary arteries.5,6 Pathology of in-stent restenosis is different: it results from smooth muscle cell proliferation. CB offers a simple, safe, and effective option for treatment of in-stent restenosis in coronary arteries. Initial reports suggest that it may achieve a better result than conventional percutaneous transluminal coronary angioplasty (PTCA), by making the tissue more amenable to being pushed outward through the stent struts.1,7–10 Experience with CB angioplasty in peripheral arteries is presently limited. However its use is being explored in number of situations.
Device description and mechanism of cutting balloon angioplasty The CB (Boston Scientific, Natick, MA) features a noncompliant balloon with three or four Atherotomes (microsurgical blades) depending on balloon diameter, mounted
longitudinally on the outer surface. The Atherotomes are microtome-grade blades, approximately three to five times sharper than surgical scalpel blades. When the CB is inflated the Atherotomes are exposed (Figure 9.1). As inflation continues and the balloon expands, the blades concentrate the dilation force upon an extremely small area along the entire length of the Atherotome. The hoop strength of the vessel is overcome and a cut occurs along the line of the Atherotome. These incisions facilitate dilatation of the target lesion with less dilating force, thus minimizing trauma to the vessel. This should decrease the inflammatory response and in turn restenosis.11 Concentration of dilating force enables more resistant stenosis to be overcome. The device available for small vessels has a 2–4-mm-diameter balloon on a monorail or over-the-wire 139-cm shaft, for use on 0.014-inch guidewire through a 5- to 6-French sheath. Coronary CBs have a 6-, 10-, or 15-mm-long Atherotome while the peripheral CB has a 15-mm-long Atherotome and a 0.127-mm working height. The larger peripheral CB is available in 5–8-mm diameter for use on 0.018-inch guidewire as an over-the-wire system through a 7-French sheath. Each of these balloons has four Atherotomes of 1-cm length and 50-, 90-, or 135-cm working catheter length.
Technical aspects of cutting balloon angioplasty The CB has a special folding manufactured into the balloon to protect the three or four blades from being exposed; therefore only a negative prep should be used. No air or fluid should be introduced into the CB until the first inflation of the lesion. Dilation as well as deflation should be performed in a slow manner to allow extrusion and refolding of the blades. The metal blades on the CB make it stiffer and somewhat larger than the regular balloons. For successful advancement of the balloon across the lesion the guiding catheter should be coaxial and should provide a strong back-up. The guidewire should be stiff to allow the CB to be advanced smoothly to the stenotic area. Rigidity of the CB affects navigation across steep bifurcations in contralateral use. In a tortuous/angled vessel or in a diffuse, tight stenosis a shorter balloon would provide better trackability and crossability. A CB is selected with a diameter equal to the diameter of the adjacent normal segment of the artery. Balloon pressure should be increased gradually stepwise (1 atmosphere per second) up to 6 atmospheres to reach nominal size. If an indentation is still noted, pressure is gradually increased 45
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AtherotomeTM
Figure 9.1 Illustration of inflated cutting balloon with Atherotome (blades) and depiction of protection of blade by fold of balloon when deflated.
to 8 atmospheres. If further dilatation is needed, adjunctive balloon angioplasty with a standard angioplasty balloon of appropriate size can be performed. If the lesion is longer than the length of the CB, inflate the CB in the distal portion of the lesion first and move proximal with further inflations.
Clinical experience Aortoarteritis (Takayasu’s disease) Stenotic lesions in aortoarteritis often require high inflation pressure (> 10 atmospheres) for dilatation and residual
(a)
stenosis is not uncommon.12 This is because the stenosis is caused by dense transmural fibrosis. We evaluated the use of CB in dilating stenotic arterial lesions at various sites in this condition. In 22 patients, aged 7–45 years (mean 14.6 ± 7.5 years), 29 stenotic lesions (≥ 75%) were treated by CB. Twenty-one lesions were in the renal, two in the carotids, two in the subclavian, one in the axillary artery and three in the aorta. Of the 21 lesions in the renal artery, 17 were de novo and 4 had in-stent restenosis. For renal angioplasty, CB 4–5 mm in diameter with an Atherotome length of 10–15 mm was passed through an 8-French coaxial guiding catheter or a 7-French sheath over 0.014–0.018-inch diameter, extrasupport guidewire. Femoral approach was used in 15 patients and a high-brachial approach in 3 patients with severe caudal angulation of renal artery. The balloon could be negotiated through stenosis with ease in all patients. In patients with de novo lesions inflation of the balloon at 6–8 atmospheres could eliminate “waste” on the CB in 14 of 17 (82.3%) lesions. Adjunctive balloon angioplasty to further enlarge the lumen was performed in 17 lesions using a 5–6-mm conventional balloon. The stenosis decreased from 87.5 ± 7.8% (mean ± SD) to 28.2 ± 9.3% (mean ± SD) after CB and further reduced to 14.2 ± 4.9% (p < 0.001) after further dilatation/stent implantation (Figure 9.2). There was no complication. Failure to abolish “waste” in CB in three patients could be due to the inability of the 0.127-mm working height of the blade to reach the dense fibrosis in the media through markedly thickened intima, which is often the pathology.13 Follow-up angiographic restudy performed after 6–24 months in 14 lesions showed restenosis in two patients (14.3%). Both of these underwent redilation. CB was found to be especially effective in dilating four lesions with in-stent renal artery restenosis. Good dilatation with smooth lumen could be achieved at low pressure (5–6 atmospheres) in these patients (Figure 9.3). Follow-up angiogram after 6–12 months showed no evidence of restenosis in these four patients. Studies have shown that in-stent restenosis results from smooth muscle cell proliferation9
(b)
Figure 9.2 (a) Aortogram showing severe bilateral renal artery stenosis due to aortoarteritis in a young girl with severe hypertension and congestive heart failure; and (b) good dilatation of both renal arteries after CB angioplasty. Patient had marked improvement in hypertension and congestive heart failure after angioplasty.
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(a)
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(b)
Figure 9.3 (a) Severe in-stent restenosis (arrow) of the proximal segment of upper left renal artery in a young girl with aortoarteritis; and (b) good dilatation of the stenosed segment after 4 × 10 mm CB angioplasty with relief in hypertension.
which can be easily sliced by CB. Stenosis at other sites – aorta, carotid, subclavian, or axillary – could also be relieved effectively by CB angioplasty without any complication. Our experience, along with a few case reports in literature15,16 on CB angioplasty in aortoarteritis show that the procedure is safe and permits dilatation at lower pressure in a number of patients, with less dissection, reducing the need for stent implantation. However, some patients may still have residual “waste” on the balloon due to dense transmural fibrosis. Lower extremity arteries Angioplasty of long stenotic lesions or chronic total occlusions in the superficial femoral (SFA), popliteal, and tibial arteries may be suboptimal. Implantation of stent in this region has a high restenosis rate. Changes in arterial flexion with daily activity can result in fatigue and fracture of metallic stents in the femoropopliteal arterial system.16,17 Angioplasty with a
(a)
(b)
CB may cause less barotrauma and dissection reducing the need for stent implantation and therefore may be an attractive option for such patients. Ansal et al.18 reported initial technical success with the use of CB in 89% of 73 patients with popliteal or crural obstruction. At 1-year mean follow-up 89.5% of treated limbs were salvaged. They concluded that CB angioplasty is a safe and feasible option for the treatment of popliteal and infrapopliteal vessels.17 Our experience and a few other reports19 also show promising results with CB for treatment of atherosclerotic disease of SFA and crural arteries (Figure 9.4). However there are no randomized control trials comparing percutaneous transluminal angioplasty (PTA) with CB for peripheral arteries. Lower-limb vein bypass graft Recurrent stenotic lesions associated with vein bypass grafts are often fibrous and smooth. Unlike de novo atherosclerotic lesions,
(c)
Figure 9.4 (a) Severe stenosis (arrow) of femoral artery; (b) good dilatation of the stenosed segment after 4 × 10 mm CB angioplasty; and (c) further improvement in femoral artery lumen after adjunctive balloon angioplasty. There was no dissection and no need of stent implantation.
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they respond poorly to balloon angioplasty and may often result in a dissection requiring stent placement to avoid early recurrent thrombosis or open repair for residual stenosis. Recent reports have found CB angioplasty to be an acceptable option for focal infrainguinal vein graft stenosis.20,21 This technique reduces the requirement for bail-out stenting or conversion to open surgery in this situation. In-stent restenosis of peripheral arteries In-stent restenosis (ISR) occurs in up to 5% of cases of carotid angioplasty and stenting,22,23 and between 9–24% in patients undergoing renal angioplasty and stenting.24 ISR lesions tend to be more resistant than de novo lesions because of the presence of more smooth muscle and proliferative cells, and fewer macrophages, collagen, and tissue factor.25 There is a rationale for using CB in ISR as it has an ability to achieve acute luminal gain with minimum tissue injury. The longitudinal blades of the CB concentrate the dilation force, creating radially directed fissures and enabling more resistant stenosis to be overcome and thus achieving more acute luminal gain compared to conventional balloon angioplasty. Better lumen gain after dilation may be related to the extrusion of the fibrous residual neointimal plaque from the stent struts, which results in less tissue injury compared with other revascularization modalities. There are few case reports regarding the successful use of CB in ISR of renal26 and carotid arteries.27 Cutting balloon angioplasty for resistant venous stenosis of a hemodialysis fistula Venous stenosis in a hemodialysis shunt is often resistant to high-pressure balloon dilatation.28 This could be due to dense fibrous strands incorporated in the venous neointimal layer or caused by scar tissue developing from recurrent puncture trauma to the venous wall in hemodialysis shunts. Vorwerk et al.29 performed CB angioplasty in 19 stenosed hemodialysis fistulas and grafts. In seven patients, CB angioplasty was followed by conventional balloon angioplasty to achieve the desired diameter without residual stenosis. The balloon expanded completely in all patients and no balloon waste remained. The degree of stenosis decreased from 65 ± 15% (mean ± SD) to 14 ± 9% (mean ± SD). Primary patency rates were 94 ± 6% after 1 month, 86 ± 9% after 2 and 3 months, and 64 ± 15% after 6 and 9 months. No major complications occurred; there was only one case of dislodgement of a microtome from the CB, which occurred while retrieving the CB. CB increased the technical success of balloon dilatation of hemodialysis fistulas and grafts. Other studies30,31 have also reported good initial success and primary-assisted patency at 6 months. A recently published prospective, randomized trial reported more sobering results in that CB and standard balloon angioplasty had equivalent 6-month patency rate for stenotic or thrombosed hemodialysis grafts.32 Severe peripheral pulmonary stenosis Pulmonary artery stenosis presents a therapeutic challenge, given the variety in its presentation and severity, because surgical access to the lesions is difficult. It can present as an
isolated lesion, affecting one of the main branches of the pulmonary artery, or multiple lesions affecting smaller, peripheral branches. In peripheral pulmonary stenosis, if prolonged dilation does not lead to a morphologically and/or hemodynamically satisfying result, stent placement would be the next logical step. However, stent placement in a child or adolescent is undesirable, because growth of the pulmonary artery can leading to relative stenosis in the stented segment. Recent studies have shown usefulness of CBs in treatment of branch pulmonary artery stenosis and angioplasty-resistant pulmonary artery stenosis. Butera et al.33 successfully treated eleven peripheral pulmonary artery stenoses in four patients. The main vessel diameter increased by 81% (p < 0.001) and RV/LV pressure ratio decreased from 1.15 to 0.75 (p = 0.05). There was no intraprocedural or late complication. Results were stable on 18 months of follow-up. Bergersen et al.34 performed CB angioplasty of 79 vessels in 29 patients for relieving stenoses in small pulmonary arteries. Minimal luminal diameter increased from 1.5 ± 0.8 to 3 ± 1.1 mm (p < 0.001). On follow-up 79% of patients showed sustained improvement. These results suggest that CB angioplasty is a promising technique for the treatment of highly challenging pathologies such as small-vessel pulmonary artery stenosis and intra-stent restenosis. However, further studies with longer follow-up are needed to confirm these initial results. Recently CB has also been used in palliative treatment in tetralogy of Fallot.35 Pulmonary vein stenosis After radio-frequency ablation for atrial fibrillation, patients may develop pulmonary vein stenosis requiring stent angioplasty. Cook et al.36 compared CB angioplasty with standard angioplasty in 21 patients with pulmonary vein in-stent stenosis. Although initially both the techniques significantly improved the lesion diameter, on follow-up, restenosis was seen more often in angioplasty alone group (4/6 vessels) as compared to the CB group (2/15 vessels) showing superiority of CB angioplasty in this situation. In a recent report, Seale et al.37 found CB angioplasty to be safe in palliation of pulmonary vein stenoses. It gave good acute relief but often needed to be repeated. Complications of cutting balloon angioplasty Use of the CB requires caution to prevent complications because of its specific design. Rupture of the balloon, aneurysm formation, and (rarely) rupture of the artery after CBA has been reported in a few cases and is an area of concern.38,39 Rated burst pressure should not be exceeded as balloon rupture can lead to microtome dislodgement during balloon retrieval. Balloon rupture and entanglement with stent struts during dilatation for ISR has also been reported.
Conclusion CB angioplasty in peripheral arteries is safe, easy to use and has the potential to improve the efficacy of balloon angioplasty in resistant stenotic lesions. Previously, the maximum available
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Cutting balloon angioplasty diameter of 4-mm CB limited the use of this balloon to small arteries and veins. However with the availability of 5–8-mm CB, larger vessels can now be treated. It has proved useful in several clinical indications such as peripheral arterial stenosis in native arteries below the inguinal ligament, resistant stenosis of dialysis fistulas and grafts, and neointimal hyperplasia in the infrainguinal arterial bypass graft salvage. Efficacy has also been reported in fibrotic lesions of aortoarteritis and in-stent restenosis of carotid and renal arteries. The more-than-theoretical
49
advantage is that the CB can “focus” the force, overcome fibrous stenosis, create less wall injury, and could decrease the need for adjunctive stent placement in most cases.
Acknowledgments The author thanks Dr Girish MP and Dr Mohit D Gupta for their help in preparation of this manuscript.
REFERENCES 1. 2. 3. 4. 5.
6. 7. 8. 9.
10. 11.
12.
13. 14. 15. 16. 17. 18. 19. 20.
Yamaguchi T, Nakamura M, Nishida T et al. Update on cutting balloon angioplasty. J Interven Cardiol 1998; 11 (Suppl.1): S114–9 Barath P, Fishbein MC, Vari S, Forrester JS. Cutting balloon: A novel approach to percutaneous angioplasty. Am J Cardiol 1991; 68: 1249–52 Cejna M. Cutting balloon: Review on principles and background of use in peripheral arteries. Cardiovasc Intervent Radiol 2005; 28: 400–8 Voigt B, Pfitzer P, Weismueller P et al. Cutting balloon angioplasty: An alternate way in the treatment of complex coronary lesions. J Am Coll Cardiol 2000; 35(Suppl A): 1062–78 Bittl JA, Chew DP, Topol EJ, Kong DF, Califf RM. Meta-analysis of randomized trials of percutaneous transluminal coronary angioplasty versus atherectomy, cutting balloon atherotomy, or laser angioplasty. J Am Coll Cardiol 2004; 43: 936–42 Mauri L, Bonan R, Weiner BH et al. Cutting balloon angioplasty for the prevention of restenosis: results of the cutting balloon global randomized trial. Am J Cardiol 2002; 90: 1079–83 Albiero R, Nishida T, Karvouni E et al. Cutting balloon angioplasty for in stent restenosis. Catheter Cardiovasc Interv 2000; 50: 452–9 Kurbaan AS, Foale RA, Sigwart U. Cutting balloon angioplasty for in-stent restenosis. Catheter Cardiovasc Interv 2000; 50: 480–8 Cin VG, Pekdemir H, Akkus MN et al. Cutting balloon angioplasty for the treatment of in-stent restenosis in diabetics: A matched comparison of 6 months’ outcome with conventional balloon angioplasty. Angiology 2006; 57(4): 445–52 Tsetis D, Morgan R, Belli AM. Cutting balloons for the treatment of vascular stenoses. Eur Radiol 2006; 16: 1675–83 Inoue T, Sakai Y, Hoshi K et al. Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty. Circulation 1998; 97: 2511–8 Tyagi S, Verma PK, Gambhir DS et al. Early and long term results of balloon angioplasty in aortoarteritis (Takayasu Disease): Comparison with atherosclerosis. Cardiovasc Intervent Radiol 1998; 21: 219–4 Hotchi M. Pathological studies on Takayasu arteritis. Heart Vessels 1992; Suppl 7: 11–7 Henry M, Rath PC, Lakshmi G, Henry I, Hugel M. Percutaneous transluminal angioplasty using a new peripheral cutting balloon for stenosis of arch vessels in aortoarteritis. Int Angiol 2004; 3: 403–9 Rath PC, Lakshmi G, Henry M. Percutaneous transluminal angioplasty using a cutting balloon for stenosis of the arch vessels in aortoarteritis. Indian Heart J 2004; 56: 54–7 Wensing PJ, Scholten FG, Buijs FC et al. Arterial tortuosity in femoralpopliteal region during knee flexion: a magnetic resonance angiographic study. J Anat 1995; 187: 133–9 Diaz JA, Villegas M, Tamashiro G et al. Flexions of the popliteal artery: dynamic angiography. J Invas Cardiol 2004; 16: 712 Ansel GM, Sample NS, Botti III Jr CF et al. Cutting balloon angioplasty of the popliteal and infrapopliteal vessels for symptomatic limb ischemia. Catheter Cardiovasc Interv 2004; 61: 1–4 Rabbi JF, Kiran RP, Gersten G, Dudrick SJ, Dardik A. Early results with infrainguinal cutting balloon angioplasty limits distal dissection. Ann Vasc Surg 2004; 18: 640–3 Kasirajan K, Schneider PA. Early outcome of “cutting” balloon angioplasty for infrainguinal vein graft stenosis. J Vasc Surg 2004; 39: 702–8
21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
34. 35. 36. 37. 38.
39.
Muller-Hulsbeck S, Order BM, Jahnke T. Interventions in infrainguinal bypass grafts. Cardiovasc Intervent Radiol 2006; 29: 17–28 Levy EI, Hanel RA, Lau T et al. Frequency and management of recurrent stenosis after carotid artery stent implantation. J Neurosurg 2005; 102: 29–37 Bendok BR, Roubin GS, Katzen BT et al. Cutting balloon to treat carotid in-stent stenosis: technical note. J Invasive Cardiol 2003; 15: 227–32. Van de Ven PJ, Kaatee R, Beutler JJ et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomized trial. Lancet 1999; 353: 282–6 Kearney M, Pieczek A, Haley L et al. Histopathology of in-stent restenosis in patients with peripheral artery disease. Circulation 1997; 95: 1998–2002 Munneke GJ, Engelke C, Morgan RA, Belli AM. Cutting balloon angioplasty for resistant renal artery in-stent restenosis. J Vasc Interv Radiol 2002; 13(3): 327–31 Tamberalla MR, Yadav JS, Bajzer CT, Bhatt DL, Chebl AA. Cutting balloon angioplasty to treat carotid instent restenosis. J Invas Cardiol 2004; 16: 133–5 Trerotola SO, Kwak A, Clark TW et al. Prospective study of balloon inflation pressures and other technical aspects of hemodialysis access angioplasty. J Vasc Interv Radiol 2005; 16: 1613–8 Vorwerk D, Adam G, Muller-Leisse C, Guenther RW. Hemodialysis fistulas and grafts: Use of cutting balloon to dilate venous stenosis. Radiology 1996; 201: 864–7 Singer-Jordan J, Papura S. Cutting balloon angioplasty for primary treatment of hemodialysis fistula venous stenoses: preliminary results. J Vasc Interv Radiol 2005; 16: 25–9. Carrafiello G, Lagana D, Mangini M et al. Cutting balloon angioplasty for the treatment of hemodialysis vascular accesses: midterm results. Radiol Med 2006; 111: 724–32 Vesely TM, Siegel JB. Use of the peripheral cutting balloon to treat hemodialysis-related stenoses. J Vasc Interv Radiol 2005; 16: 1593–603 Butera G, Antonio LT, Massimo C, Mario C. Expanding indications for the treatment of pulmonary artery stenosis in children by using cutting balloon angioplasty. Catheter Cardiovasc Interv 2006; 67: 460–5 Bergersen L, Jenkins KJ, Gauvreau K, Lock JE. Follow-up results of Cutting Balloon angioplasty used to relieve stenoses in small pulmonary arteries. Cardiol Young 2005; 15: 605–10 Carlson KM, Neish SR, Justino H et al. Use of cutting balloon for palliative treatment in Tetralogy of Fallot. Catheter Cardiovasc Interv 2005; 64: 507–12 Cook AL, Prieto LR, Delaney JW, Rhodes JF. Usefulness of cutting balloon angioplasty for pulmonary vein in-stent stenosis. Am J Cardiol 2006; 98: 407–10 Seale AN, Daubeney PE, Magee AG, Rigby ML. Pulmonary vein stenosis: initial experience with cutting balloon angioplasty. Heart 2006; 92: 815–20 Oguzkurt L, Tercan F, Gulcan O, Turkoz R. Rupture of the renal artery after cutting balloon angioplasty in a young woman with fibromuscular dysplasia. Cardiovasc Intervent Radiol 2005; 28: 360–3 Murakami R, Tajima H, Kumita S. Cutting balloon-associated hemodialysis fistula rupture after failed standard balloon angioplasty. Kidney Int 2006; S70(5): 825
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SilverHawk® atherectomy device RS Gammon and JR Nelson
Introduction Successful treatment of infrainguinal peripheral arterial disease (PAD) has proven to be one of the greatest challenges in vascular intervention. Some of this is explained by the disease characteristics: diffuse involvement with long lesions and multi-level disease, propensity to calcification and total occlusions, and high resistance or low flow states. This is further compounded by the unique mechanical characteristics of the arteries, including extension, contraction, rotation, compression, and extreme flexion especially within the joint spaces. These mechanical challenges contribute to stent failure both in terms of restenosis and stent fracture. Disappointing results with angioplasty and stenting have led to the development of many alternative devices in search of more consistent and durable results. The most intuitive solution in the treatment of vascular disease is plaque removal, or atherectomy. The concept was introduced in the 1980s and many devices following that successfully removed plaque by one means or another.1–13 Unfortunately, most of these devices were relatively inefficient at addressing the large plaque burden present. Furthermore, they often induced vessel injury and embolization as they could not effectively collect the majority of plaque liberated from the vessel wall. Trials of coronary atherectomy have shown that suboptimal atherectomy does not significantly reduce restenosis compared to angioplasty, whereas more aggressive, or “optimal,” atherectomy does.14–21 The SilverHawk® system received Food and Drug Administration (FDA) approval in 2003 for the treatment of peripheral arteries, including Femoropopliteal and tibioperoneal vessels.22 It provides a unique approach to removing plaque from de novo or restenotic lesions of any length. Both calcified and non-calcified lesions are treatable with the device. Because the cutter is apposed to the plaque mechanically, the catheter excises large amounts of plaque without causing significant barotrauma to the arterial wall. The device can also remove eccentric plaque and create a more optimal environment for laminar flow. By excising plaque and avoiding stretch, the chance of dissection is minimized, and the signals that initiate intimal hyperplasia are postulated to be minimized. SilverHawk® atherectomy, or plaque excision, may also offer the opportunity to learn more about underlying atherosclerotic disease processes. Histological analyses can identify inflammatory cell infiltration, the presence of thrombus, calcification, or fibrosis, the degree of smooth muscle cell proliferation, and the lipid content of the plaque removed. Genomic and proteomic analyses of the excised tissue also provide further insight into 50
the pathophysiology of restenosis and identify predictive markers of restenosis and cardiovascular risk. The SilverHawk® device is a 0.014-inch-based monorail catheter designed for single-operator use (Figure 10.1). It consists of a motor drive unit that contains a battery pack and a thumb switch to activate the cutter. The working end consists of a hinged housing unit containing a carbide cutting blade. The blade is activated from the motor drive unit at a rate of 8,000 rpm, and the catheter is then advanced into an area of plaque. With each pass, the cutter is used to pack the tissue into the distal tip of the nosecone to maximize collection capacity. The length of each pass is limited to the length of the remaining empty portion of the collection chamber to avoid embolization of excess material after a pass through the lesion. The device can then be either removed or rotated to treat a different quadrant in the same lesion or other lesions. A single device can be used to treat multiple lesions and/or multiple vessels. A variety of cutter sizes exist (Table 10.1) which allows treatment of vessels ranging from 2.0 to 7.0 mm diameter. Different length collection chambers may allow more extensive tissue storage before needing to remove the device to empty plaque. Immediate gross assessment of lesion composition is possible while emptying the device (e.g. presence of thrombus) and may impact treatment decisions and dictate adjunctive therapy. The device can be used from either antegrade or contralateral approach, typically through a 6-French or 7-French sheath.
Clinical outcomes The TALON (Treating Peripherals with SilverHawk®: Outcomes Collection) Study23 was a prospective, multi-center, non-randomized, observational outcomes registry that enrolled consecutive patients undergoing plaque excision for lower extremity PAD. In addition to demographics, risk factors, and procedure characteristics, TALON collected acute, 6-, and 12-month outcome data. Tissue and blood samples were collected from consenting participants. The registry enrolled 728 patients with 906 limbs involved. A total of 1517 lesions were treated in 1001 procedures. Demographics were typical of peripheral series, with an average age of 70: 50% were diabetics, and 66% had a history of, or were currently, smoking. The majority or patients had claudication, but 275 (30.6%) had critical limb ischemia (CLI) as defined as a Rutherford–Becker24 score of 4 or 5. Lesion locations included iliac (68 or 4.5%), common femoral/profunda (102 or 6.7%), superficial femoral
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(b)
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(d) Figure 10.1 (a) SilverHawk® device; (b) SilverHawk® magnified to show cutting unit. The carbide coated disc spins at 8,000 rpm; (c) SilverHawk® devices shown with motor dive units; and (d) SilverHawk® under fluoroscopy within the common femoral artery.
(730 or 48.1%), popliteal (226 or 14.9%), tibioperoneal/ peroneal (183 or 12.1%), anterior or posterior tibial (198 or 13.1%), and dorsalis pedis/calcaneal (10 or 0.7%). Average lesion length for the series was 58 mm, with average superficial femoral artery (SFA) lesion length of 82 mm. Moderate or severe calcification was reported in 62.9% of lesions, and 28.6% of lesions were total occlusions. The majority of lesions (87.5%) were de novo, but 12.5% represented restenosis, including in-stent restenosis. This series represented a realworld, “all-comers” patient cohort with a large PAD burden. Procedural characteristics were recorded in this early experience with the device. Average SilverHawk® procedure time was 27.5 minutes. This is notable considering that 40.7% of procedures involved the treatment of more than one lesion, and the early generation devices available at that time were considerably less efficient than current devices. Adjunctive therapy was used in 26.5% of cases and was primarily balloon angioplasty, with stents deployed in only 6.1% of cases.
Twelve-month outcome data are available on 335 patients with 658 lesions. Patency was defined as freedom from target lesion revascularization (TLR). At 1 year, 79% of these lesions were free from revascularization. For patients with claudication, defined as a Rutherford–Becker score of less than 4, the patency rate was 85%. Remarkably, there was no significant difference between diabetics and non-diabetics, with patency rates of 82 and 78%, respectively. Zeller et al. published the earliest experience with the SilverHawk® device from Europe, reporting the 6-month patency rates of infrapopliteal atherectomy as determined by duplex ultrasound.25 Balloon predilation was frequently used to allow passage of first-generation cutters. Adjunctive balloon angioplasty was performed in 29% of cases. The mean ankle–brachial index for the group improved from 0.46 to 0.80 before discharge and remained improved during follow-up. The restenosis rate, defined as 70% or greater stenosis by duplex ultrasonography, was 14% at 3 months and 22% at 6 months.
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SilverHawk® devices available for use
SilverHawk® type LS: Large vessel standard tip LX: Large vessel extended tip MS: Medium vessel standard tip SX: Small vessel extended tip SS+: Small vessel standard tip DS: Distal vessel standard tip
Vessel diameter (mm) 4.5–7.0 4.5–7.0 3.5–5.0 3.0–3.5 3.0–3.5 1.5–2.0
Zeller et al. also reported 2-year results of SilverHawk® atherectomy for infrapopliteal lesions. 25 Forty-nine lesions in 36 lower limbs were treated, 19 (53%) of these patients had CLI, and 11 (22%) lesions were total occlusions. Mean lesion length was 48 mm, and nine lesions (18%) were in-stent restenoses. Sixteen (33%) lesions were treated with predilation and 19 (39%) with post-dilation. Two of these lesions were stented. A residual stenosis < 30% was achieved in 48 (98%) lesions. The mean ankle–brachial index increased from 0.48 to 0.81 by discharge. Primary and secondary patency rates were 67% and 91% after 1 year and 60% and 80% after 2 years, respectively. In the US, Keeling et al.26 reported their early experience with the SilverHawk® catheter in patients with claudication or CLI, including clinical and duplex follow-up. Sixty-six limbs of 60 patients underwent 70 atherectomy, or plaque excision, procedures. Twenty-three of the 70 procedures (33%) were done for claudication but two-thirds of patients had CLI. Of the CLI patients, 22 of 70 (31%) had rest pain, and 25 of 70 (36%) had minor or major tissue loss. All of the patients had femoropopliteal lesions treated and 17 patients required plaque excision of tibial vessels. Mean lesion length was 8.8 cm, and femoropopliteal TASC27 criteria included 5 TASC A lesions, 14 TASC B lesions, 32 TASC C lesions, and 19 TASC D lesions. Adjunctive therapy was used in 17 procedures (24.3%), consisting of 14 balloon angioplasties and 3 stents. The mean increase in ankle–brachial index was 0.27. Duplex ultrasound surveillance was performed at 1, 3, and 6 months and annually. One-year primary, primary-assisted, and secondary patency was 61.7, 64.1, and 76.4%, respectively. Restenosis or occlusion was significantly more common in patients with TASC C and D lesions. Similar findings were seen in the TALON registry.23 Predictors of target lesion revascularization included increasing Rutherford–Becker score (HR 1.84, 95% CI 1.28 to 2.65, p = 0.0003) and multiple lesions (HR 1.37, 95% CI 1.11 to 1.70, p = 0.0019). Lesion lengths > 50 mm were associated with a 2.9-fold increased risk for TLR and lesion lengths > 100 mm were associated with a 3.3-fold increase in TLR. SilverHawk® for limb salvage CLI is usually caused by diffuse multi-level disease, often involving infrapopliteal vessels. These features might favor a strategy of plaque excision over plaque-displacement approaches. Yancey et al.28 described the outcome of 18 consecutive procedures in 17 limbs, all of whom had severe CLI and multi-level disease. All patients had femoropopliteal involvement with TASC C disease present. The clinical indication was tissue loss
Sheath compatibility (French) 7-F/8-F 8-F 7-F/8-F 7-F 7-F 6-F
in thirteen limbs and rest pain in four. Initial resolution of symptoms or complete healing was achieved in twelve limbs, and partial healing was achieved in two others. Early amputation was necessary in the remaining three patients, but this was felt most likely due to severe inframalleolar disease and advanced forefoot ischemia at the time of presentation. The mean ankle–brachial index improved from 0.39 to 0.75 postprocedure. However, at 6 months it had fallen to 0.48, and at 12 months, stenosis-free patency of the femoropopliteal segment was only 22%. Two patients required late amputation. A multi-center experience using SilverHawk® plaque excision for limb salvage was published by Kandzari et al.29 The study enrolled 69 patients with 76 ischemic limbs from 7 different institutions. A particularly severe cohort was selected, with all patients having tissue destruction, as defined as a Rutherford–Becker score of 5 or 6. Remarkably, amputation was already planned in 63% of patients prior to any attempt at salvage. Seventy-eight percent of patients had diabetes and 47% had renal impairment. All patients had multi-vessel and multilevel involvement. SilverHawk® plaque excision was performed in all patients, with procedural success of 98.7%. Adjunctive angioplasty was used in 13%, and 6% received stents. At 6 months, three patients required below-the-knee and three patients above-the-knee amputation. Eighty-two percent of patients had either avoided amputation completely or underwent lesser amputation than originally planned. Target lesion revascularization was 4% at 6 months. At our center, we reported on 57 consecutive patients with CLI treated with plaque excision.30 Forty-three patients (75%) had multi-level disease. An average of two lesions were treated per procedure. All patients had plaque excision. Adjunctive therapy was used in 20%, including angioplasty (16.5%), stent (1%), stent and angioplasty (2.5%), and rotational atherectomy and angioplasty (1%). Patients were followed up to 24 months, with a mean of 11 months (Table 10.2). The average Rutherford–Becker score was markedly improved at 6 months and 12 months. Of limbs with tissue loss, 80% showed visible healing; rest pain had resolved in 90% of patients with a Rutherford–Becker score of 4. One patient required above-the-knee and three required below-the-knee amputations. Overall, the limb salvage rate was 93%.
Special applications An argument for SilverHawk® plaque excision as the default strategy for most infrainguinal interventions is difficult until
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Table 10.2 Austin Heart PA single-center, critical limb ischemia experience. Data representative of 57 consecutive patients presenting with Rutherford–Becker (RB) scores ≥ 4. Of the five patients that did not show visible healing or resolution of rest pain; one went on to receive above-knee-amputation (AKA) and three below-knee-amputation (BKA). Furthermore, three patients died before 12-month follow-up Critical limb ischemia follow-up data
Preprocedure
6-month
12-month
Average RB score Limbs that showed visible healing Limbs with resolution of rest pain
4.45 ± 0.09 n = 33 (80% of those with RB < 4) n = 19 (90% of those with RB = 4)
1.45 ± 0.24
1.17 ± 0.35
Amputation AKA BKA Metatarsal or partial toe amputation
n n n n
= = = =
10 1 3 6
randomized data comparing it to other strategies are available. However, certain lesion locations are notoriously difficult to treat using plaque displacement technology. SilverHawk® plaque excision may offer a clear advantage in certain lesion subsets.31 Common femoral artery Endovascular treatment of common femoral lesions presents numerous challenges. Naturally, the lesions occur in a joint space making stenting unfavorable. They also often involve the bifurcation, and frequently are calcified and/or totally occluded. Access to reach the lesions may be difficult, and stent placement may prevent future access from this site. The frequent use of closure devices may have accelerated the prevalence of disease at this site. These challenges have made surgical endarterectomy often the best option to treat disease at this location, though this may also complicate future access. SilverHawk® plaque excision has the potential to perform as an “endovascular endarterectomy” in common femoral lesions.32 A vessel size of approximately 7 mm is easily treated with the LS device, the largest diameter cutter (see Table 10.1). As opposed to plaque displacement technologies, plaque excision does not compromise important branches. Instead, selectively choosing to place the wire in either the superficial or profunda femoral artery can facilitate delivery of the device to each wall to optimize plaque removal. The risk of major dissection (possibly leading to stent placement in this location) is minimized, especially compared to techniques like kissing balloons previously advocated. A specific indication for SilverHawk® may be in treating iatrogenic lesions created by femoral closure devices.33,34 Use of these closure devices has been associated with both acute limb ischemia, and subsequent claudication. Suturemediated closure devices can disrupt plaque within the femoral artery. Devices such as Angioseal (St. Jude, St. Paul, MN) may cause plaque disruption from the foot-plate, or the collagen plug may be inadvertently deployed within the artery. SilverHawk® plaque excision appears to be effective in treating either scenario. At our institution we have used SilverHawk® plaque excision to treat nine lesions with either stenosis or
17.5% 2% 5% 10.5%
occlusion 1 hour to 2 weeks following Angioseal deployment (Figure 10.2). The LS SilverHawk® platform was used in all cases. All procedures were technically successful and without complication. No patient has developed recurrent stenosis with more than 2 years follow-up including routine duplex surveillance. Profunda femoral artery The SilverHawk® device has performed well in ostial lesions, and is capable of treating profunda lesions of this type. A common scenario is the patient with SFA occlusion and stable claudication, who converts to severe symptoms with the development of an ostial profunda lesion. These resilient lesions exhibit recoil after dilation (even with cutting balloons) and stenting is discouraged because of the location. However, SilverHawk® plaque excision has proven effective for this lesion. The true reference vessel size may be difficult to estimate due to ostial location, early branching, and frequent post-stenotic dilation. The angle of the vessel take-off may also create the possibility of deep wall cuts. For these reasons we do not attempt to achieve angiographically “perfect” results (Figure 10.3). Postdilation is performed with greater frequency relative to other lesions. Even with low-pressure inflations, less recoil is evident after the lesion is “scored” with atherectomy. Popliteal artery The popliteal artery presents challenges to interventional therapy as it crosses a joint space that may experience extreme flexion. Stent placement with current stent technology is generally avoided. Distally, the trifurcation of the vessel presents further challenges, and tibial vessels may be compromised by angioplasty or stenting. Covered stents in particular may present risk as they occlude genicular collaterals, which may become critical if the intervention subsequently fails. Plaque excision is often capable of achieving technical success in popliteal lesions without the need for stenting and without compromising dependant branches (Figure 10.4). In some cases, rather than occluding important branches or collaterals, plaque excision may actually expose ostia to branches that previously had poor flow.
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(b)
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(e) Figure 10.2 (a) This patient underwent an angiographic interventional procedure via left common femoral access. The access site for this intervention was closed with an 8-French Angioseal; (b) four days later, the patient returned to the physician’s office with significantly elevated left-leg claudication and paresthesias. Angiographic results showed a total occlusion of the left common femoral artery at the previous arterial access site. A SilverHawk® atherectomy device was used to treat the lesion and provided excellent removal of thrombus and collagen material; (c) gross tissue samples removed from the SilverHawk® device were processed for histological analyses; (d) intimal plaque with collagen material removed from SilverHawk® device; and (e) collagen materials after collagen-specific stain. (See Color plates.)
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(a) Figure 10.3 alone.
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(b)
(a) Complex CFA stenosis involving the ostia of both the SFA and PFA; and (b) result after SilverHawk® plaque excision
In-stent restenosis In-stent restenosis in the lower extremities is often a diffuse proliferative process that responds poorly to repeated intervention. The SilverHawk® device is capable of excising a large amount of this tissue and may avoid repeated barotrauma. Although the device is not approved for this indication, we have found it to be invaluable in treating this common and difficult disease. Extremely large amounts of tissue may be removed in some cases (Figure 10.5) and adjunctive therapy is usually not necessary. Long-term patency may still be suboptimal in this difficult disease. Zeller et al. reported 1-year results of femoropopliteal lesions treated with SilverHawk® and compared de novo lesions to in-stent restenosis as well as non-stent restenosis. 35 Primary patency was defined as freedom from > 50% restenosis as defined by duplex ultrasound (proximal systolic peak flow velocity ratio > 2.4). Primary patency was 84% in the de novo lesions and 54% in the in-stent restenosis lesions (p = 0.002). Some of this difference may be explained by lesion length in that the mean lesion length was 43 mm in de novo lesions and 105 mm in in-stent restenosis lesions. The difficulty of treating in-stent restenosis remains one of the arguments against widespread use of stents for infrainguinal lesions.
Complications Device-related complications with SilverHawk® plaque excision are low. Major dissection, acute thrombosis, perforation, or late aneurysm formation occur in < 1% of cases in experienced hands.23 The complication that has received the most attention is distal embolization. Distal embolic protection devices catch debris in almost all peripheral interventions,36 including plaque excision.37 The clinical significance of these embolic particles is often inconsequential in the relatively tolerant peripheral bed as opposed to the cerebral or
coronary circulation. Furthermore, the incidence of embolization is probably directly related to operator experience and technique. For instance, in Zeller’s35 first eight SilverHawk® procedures, embolization was observed in five cases. However, the embolus was easily aspirated in each case without clinical sequelae. With further experience, using slower passes and taking care not to over-fill the collection chamber, there were no apparent emboli in the next 123 lesions treated. Clinically significant embolization has been a rare event in the 2000-plus lesions we have treated. We use embolic protection in less than 1% of cases, usually reserved for lesions with known thrombus, recent total occlusion, “coral reef ” calcification, or Angioseal occlusion. Patients with CLI and single-vessel run-off should be considered for embolic protection due the potential consequence of embolization and lack of reserve flow. Even in these higher-risk scenarios, the additional cost of the filter and technical challenges presented must be weighed against the risk of major embolization. Unfortunately, much of the argument for embolic protection has come from users with minimal device experience. With good operator technique (slow passes, frequent packing, avoiding over-packing), the risk of clinically significant embolization is low.
Future studies As with any new device, the first studies with the SilverHawk® device have attempted to define performance characteristics and outcomes across a broad range of clinical and lesion presentations. While these registry reports provide valuable information, trials randomizing SilverHawk® plaque excision against other strategies and employing rigorous core laboratory adjudication are needed. Design of these trials has been difficult as suitable control arms are lacking. Many investigators
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Figure 10.4 (a)–(d): Long superficial femoral artery occlusion (a) along with below the knee outflow (b) prior to treatment. Images were repeated at the prior site of occlusion (c) and below the knee (d) immediately following treatment with SilverHawk® athererctomy.
dismiss angioplasty as a suitable, or even ethical, control in long lesions and total occlusions. Approval from the FDA for a stent control arm is difficult as the stents currently favored by clinicians for femoropopliteal use are only approved for biliary use. Likewise, those often favored for infrapopliteal use are only approved for coronary use. The recent approval of standardized performance goals and endpoint assessments for evaluation of new devices in femoropopliteal intervention provides accepted benchmarks for comparison.38 A multi-center trial with the SilverHawk® in femoropopliteal lesions should commence soon. Follow-up will include meticulous clinical and duplex assessment for greater than 1 year. Arteries that appear to have restenosis by duplex ultrasound will undergo conventional or computed tomography angiography to confirm. All studies will have core lab adjudication.
A randomized multi-center study is currently enrolling patients with CLI and infrapopliteal disease. Many believe that distal bypass using a venous conduit is the accepted “goldstandard” for treating critical limb ischemia. The PROOF, (Plaque Removal Versus Open Bypass Surgery for Critical Limb Ischemia), study will enroll 304 patients at approximately 40 sites across the US. Patients with CLI are randomized to SilverHawk® plaque excision versus surgical bypass. SilverHawk® plaque excision provides the unique ability to readily remove and analyze plaque from multiple sites along with the freedom to provide subsequent treatments. Gross and histological information gained may impact clinical decisionmaking. Proteomic and genomic evaluation of the tissue has the potential to deepen the understanding of atherosclerosis. What are the characteristics of plaque and the features that predict recurrence? Within the same patient, how much
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or inter-patient plaque variability? What proteomic and gene expression changes can be measured when new systemic medications are started, and how soon do these changes occur? Most importantly, do these findings within plaque predict clinical success of the drug, leading to a markedly accelerated and more accurate pathway for drug development?
Summary
Figure 10.5 Tissue removed from SFA in-stent restenosis. A glistening white appearance and rubbery consistency are typical. (See Color plates.)
variability exists in plaque from one lesion to the next, from one vessel to the next, from one month to the next? Are there circulating biomarkers that correlate with either intra-patient
The SilverHawk® device offers a fundamentally different and more intuitive approach to solving the challenges presented by lower-extremity atherosclerosis. The mechanism of the device reduces barotrauma and achieves effective plaque excision that renders comparison to previous forms of atherectomy irrelevant. The device has particular utility in certain lesion subsets that have been notoriously difficult to treat with plaque-displacement technology. Results from single and multi-center registries are encouraging, but proof that SilverHawk® plaque excision should be the default strategy for infrainguinal disease needs to come from multi-center, randomized trials with operators skilled in using the device.
REFERENCES 1. 2. 3.
4.
5. 6. 7. 8.
9. 10. 11. 12. 13. 14.
15.
Agmon M, Scheinowitz M, Beitner S et al. The Bard Rotary Atherectomy System (BRAS): initial experience in patients with peripheral vascular disease. J Intervent Cardiol 1993; 6(1): 51–9 Mazur W, Ali N, Rodgers G et al. Directional atherectomy with the Omnicath: a unique new catheter system. Cathet Cardiovasc Diagn 1994; 31(1): 79–84 Dorros G, Iyer S, Lewin R et al. Angiographic follow-up and clinical outcome of 126 patients after percutaneous directional atherectomy (Simpson AtheroCath) for occlusive peripheral vascular disease. Cathet Cardiovasc Diagn 1991; 22(2): 79–84 Vroegindeweij D, Kemper F, Tielbeek A et al. Recurrence of stenoses following balloon angioplasty and Simpson atherectomy of the femoro-popliteal segment: A randomised comparative 1-year follow-up study using colour flow duplex. Eur J Vasc Surg 1992; 6(2): 164–71 Williams D, Fahrenbach M. Directional coronary atherectomy: but wait, there’s more. Circulation 1998; 97(4): 309–11 Thorpe P. Atherectomy tools for arterial treatment. Admin Radiol 1992; 11(2): 23, 25–88 Saland K, Cigarroa J, Lange R et al. Rotational atherectomy. Cardiol Rev 2000; 8(3): 174–9 Goldberg S, Berger P, Cohen D et al. Rotational atherectomy or balloon angioplasty in the treatment of intra-stent restenosis: BARASTER multicenter registry. Catheter Cardiovasc Interv 2000; 51(4): 407–13 Osula S, Ramsdale D. “Cutting Balloon and the Three Burrs”: treatment for ostial left anterior descending artery in-stent restenosis. J Invasive Cardiol 2002; 14(2): 93–5 Payne J. Alternatives for revascularization: peripheral atherectomy devices. J Vasc Nurs 1992; 10(1): 2–8 Kuan P. Clinical efficacy of transluminal extraction coronary atherectomy. J Formos Med Assoc 1992; 91(3): 323–8 Myers K, Denton M. Infrainguinal atherectomy using the Auth Rotablator: patency rates and clinical success for 36 procedures. J Endovasc Surg 1995; 2(1): 67–73 Sketch MH, Phillips HR, Stack RS et al. Coronary transluminal extraction-endarterectomy. J Invasive Cardiol 1991; 3(1): 13–8 Topol E, Leya F, Pinkerton C et al. A comparison of directional atherectomy with coronary angioplasty in patients with coronary artery disease: The CAVEAT Study Group. New Eng J Med 1993; 329(4): 221–7 Holmes DJ, Topol E, Califf R et al. A multicenter, randomized trial of coronary angioplasty versus directional atherectomy for patients
16.
17. 18.
19. 20.
21. 22. 23. 24. 25.
26. 27. 28.
with saphenous vein bypass graft lesions. CAVEAT-II Investigators. Circulation 1995; 91(7): 1966–74 Adelman A, Cohen E, Kimball B et al. A comparison of directional atherectomy with balloon angioplasty for lesions of the left anterior descending coronary artery. New Engl J Med 1993; 329(4): 228–33 Baim D, Cutlip D, Sharma S et al. Final results of the Balloon vs. Optimal Atherectomy Trial (BOAT). Circulation 1998; 97(4): 322–31 Lansky A, Mintz G, Popma J et al. Remodeling after directional coronary atherectomy (with and without adjunct percuta-neous transluminal coronary angioplasty): a serial angiographic and intravascular ultrasound analysis from the Optimal Atherectomy Restenosis Study. J Am Coll Cardiol 1998; 32(2): 329–37 Simonton C, Leon M, Baim D et al. ‘Optimal’ directional coronary atherectomy: final results of the Optimal Atherectomy Restenosis Study (OARS). Circulation 1998; 97(4): 332–9 Lansky A, Popma J, Cutlip D et al. Comparative analysis of early and late angiographic outcomes using two quantitative algorithms in the Balloon versus Optimal Atherectomy Trial (BOAT). Am J Cardiol 1999; 83(12): 1611–6 Tsuchikane E, Sumitsuji S, Awata N et al. Final results of the Stent versus directional coronary atherectomy randomized trial (START). J Am Coll Cardiol 1999; 34(4): 1050–7 Gammon R. Plaque excision treatment of infrainguinal PAD. Endovasc Today 2005; 6: 70–4 Ramaiah V, Gammon R, Kiesz S et al. Midterm outcomes from the TALON registry: Treating peripherals with SilverHawk®: Outcomes collection. J Endovasc Ther 2006; 13(5): 592–602 Rutherford RB, Beaker JD. Recommended standards for reports dealing with lower extremity ischemia: Revised version. J Vasc Surg 1997; 26(3): 517–38 Zeller T, Rastan A, Schwarzwalder U et al. Midterm results after atherectomy-assisted angioplasty of below-knee arteries with use of the Silverhawk device. J Intervent Radiol 2004; 15: 1391–97 Keeling W, Shames M, Stone P, et al. Plaque excision with the SilverHawk catheter: Early results in patients with claudication or critical limb ischemia. J Vasc Surg 2007; 45(1): 25–31 TransAtlantic Inter Society Consensus (TASC). Management of peripheral arterial disease (PAD). J Vasc Surg 2000; 30: 1–296 Yancey A, Minion D, Rodriguez C et al. Peripheral atherectomy in transatlantic intersociety consensus type C femoropopliteal lesions for limb salvage. J Vasc Surg 2006; 44(3): 503–9
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35. 36.
37. 38.
Zeller T, Rastan A, Sixt S et al. Long-term results after directional atherectomy of femoro-popliteal lesions. J Am Coll Cardiol 2006; 48(8): 1573–78 Wholey M, Toursarkissian B, Postoak D et al. Early experience in the application of distal protection devices in treatment of peripheral vascular disease of the lower extremities. Catheter Cardiovasc Interv. 2005; 64(2):227–35 Suri R, Wholey MH, Postoak D et al. Distal embolic protection during femoropopliteal atherectomy. Catheter Cardiovasc Interv 2006; 67(3): 417–22 Rocha-Singh K, Jaff M, Crabtree T et al. Performance goals and endpoint assessments for clinical trials of femoropopliteal bare nitinol stents in patients with symptomatic peripheral arterial disease. Catheter Cardiovasc Interv 2007; 69(6): 910–9
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I Henry, M Henry, and M Hugel
Introduction Balloon angioplasty alone or completed with stent implantation is the most effective procedure to treat peripheral arterial diseases. However, this technique is still limited by the complexity of certain lesions (e.g. calcified, long, bifurcated, diffuse, and those in small vessels). High-speed rotational ablation has been developed as a means of removing rather than simply displacing the occluding atherosclerotic material. It was postulated that this debulking process would improve results as compared to balloon dilatation. The RotablatorTM (Boston Scientific, Natick, MA) was developed by David Auth and used for the first time in humans by Zacca.1
Technique Description The Rotablator is a flexible, non-radio-opaque catheter fitted with a diamond-encrusted metal burr that selectively cuts away inelastic tissue during high-speed rotation. The catheter, which tracks coaxially over a 0.009-inch (0.23 mm) guidewire to prevent deflection, is encased in a 4.3-French sheath that protects the vessel wall during drive shaft rotation. Saline is infused through this sheath to lubricate and cool the catheter, burr, and guidewire. The drive shaft is connected to a compressed air turbine that rotates the burr at speed varying from 50,000 to 200,000 rpm. The diameters of available burrs range from 1.5 to 4.5 mm. Patient preparation On the day prior to the procedure, patients receive ticlopidine (500 mg) or clopidogrel (75 mg), aspirin (250 mg) and vasodilators (180 mg diltiazem and/or 60 mg nifedipine). In addition to the standard preangioplasty baseline testing, measurements of free hemoglobin (blood and urine), haptoglobin, and lactic dehydrogenase are made to monitor hemolysis that may be provoked by rotational ablation. During the procedure 5000 to 10,000 units of heparin are given. Approach techniques All procedures are carried out under local anesthesia and neuroleptanalgesia. The most frequently used access technique to
treat femoral, popliteal, or distal artery lesions is the ipsilateral antegrade femoral approach. An introducer is selected to accommodate the maximum size of the burr to be used (maximum size of the burr multiplied by 3 equals the French size of the introducer). For the percutaneous access, a 9-French is usually the largest sheath used in our facility (allows passage of a 3-mm burr). Once the introducer is in place, baseline imaging is conducted, including control angiography as well as endovascular ultrasound and/or angioscopy. The 0.009-inch guidewire is carefully passed through the lesion site(s) as far as possible down the artery so that any complications (spasm, distal embolism) may be dealt with promptly. If the femoral artery is tortuous or if there is a stenosis at the origin of the anterior tibial artery, a straight or angled 4-French catheter can be used to cross the proximal obstacles and/or to strengthen the guidewire. When selecting the first burr, the diameter is usually 75–85% of the arterial diameter below the stenosis. With the guidewire positioned, this burr is slowly advanced along the wire to about 1 cm above the stenosis (because the burr advances spontaneously when rotation begins). The rotational speed should not be allowed to dip below 2000–5000 rpm, and ablation sequences must be short (15–30 seconds) to reduce heat accumulation and ensure appropriate downstream dispersion of the particles produced. The total rotation time depends on the lesion (15–450 seconds in our experience), but a note of caution is warranted. Inasmuch as the total ablation time has a major influence on hemolysis, spasm frequency, and distal embolism, rotation time must be strictly limited. Once the lesion has been cleared with the Rotablator, the burr is withdrawn, and angiography is used to evaluate the results. If the remaining stenosis is > 50%, a larger burr is used. If < 20% luminal narrowing remains, the procedure is stopped. Residual stenoses between 20 and 50% are always treated by adjunctive balloon dilatation. As a rule the results of Rotablator therapy in the femoral segment are always insufficient, whereas in the distal arteries the outcome is almost always adequate. If a complementary dilatation is necessary, the balloon chosen is equal in diameter to the size of the nondiseased artery, and the inflation pressure must remain below 4–5 atmospheres. This low pressure is sufficient to remove the residual stenosis while avoiding a dissection. A completion angiogram documents the final results at the treatment site(s) as well as the distal run-off. If no thrombogenic incident occurred during the procedure, the introducer is immediately withdrawn, and 59
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the post-operative care of the patient ensues as for other peripheral angioplasties. However, in addition to clinical and Doppler surveillance, the hematologic tests must be repeated to check for hemolysis. If this occurs, the patient is hydrated, and a bicarbonate solution is infused. Other approach techniques may sometimes be used with the Rotablator. For example, the retrograde femoral procedure is required to treat iliac lesions. However, the size of this artery requires large burrs and introducers that increase procedural complications. The retrograde popliteal approach, on the other hand, is excellent for treating common femoral artery lesions and stenoses at the origin of the superficial femoral approach. In this technique, a 7-French or 8-French introducer is inserted to accommodate up to a 2.5 mm burr if long, calcified femoral lesions are to be treated. The procedure is the same as the one described above. Alternatively, the contralateral femoral approach can be used to treat lesions at the femoral bifurcation, in the common femoral artery, or at the origin of the SFA or profunda. An 8French or 9-French guiding catheter may assist in crossing the aortic bifurcation. The guidewire is placed far into the contralateral SFA or profunda, and the burr is gently advanced along the guidewire. In particular, this approach allows access to sites (e.g. femoral bifurcation) that were heretofore unapproachable by other standard techniques except surgery. The popularity of the radial or the brachial approach for balloon dilatation would appear feasible for rotational atherectomy treatment.
on the other hand, are always treated sequentially with a few days interval between treatments to minimize the side effects. In the case of an arterial occlusion, it is generally impossible to pass the Rotablator guidewire, and a channel must first be created through the obstruction. Currently, in 70–90% of cases, it is possible to recanalize with a hydrophilic guidewire, certain laser devices, or other recanalization devices. After creating a channel, the Rotablator guidewire can be inserted using a 4-French or 5-French catheter. Because even a recanalized calcified occlusion may not respond to balloon dilatation, the Rotablator can effectively debulk the lesion, reducing the delamination risk and possibly avoiding the need for a stent. It is preferable to use incrementally sized burrs to progressively pulverize the atheroma, and there should be no hesitation in using smaller burrs if resistance is encountered. Whereas recanalization of SFA occlusion remains controversial, the evolving Rotablator techniques for distal lesions require that the SFA remain open for access to these distal arteries. The immediate use of the Rotablator after angioplasty failure has not been investigated thoroughly. Poor radiological visibility may predispose to a high risk of complications, for example, dissection extension, perforation, or plaque embolism. Intraluminal imaging techniques, such as angioscopy or intravascular ultrasound, may assist in the decision to perform a simultaneous procedure; however, when there is doubt, it is preferable to wait until the lesion has healed before using this technique.
Special treatment scenarios Multilevel disease (Figure 11.1) in the femoropopliteal and distal segments may be treated concurrently with endovascular techniques. The Rotablator guidewire is placed down the leg artery, and proximal lesions are treated first. Bilateral lesions,
Personal experience
(a)
(b)
We have a large series of patients treated with Rotablator. Then we can draw some conclusions about indications, results, complications, and mid-term results of this technique.
(c)
Figure 11.1 (a) Arteriogram showing a very tight popliteal stenosis; (b) arteriogram at the origin of the anterior tibial artery; (c) after treatment with the Rotablator and balloon dilatation, both lesions show satisfactory flow.
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Percutaneous peripheral atherectomy using the Rotablator Table 11.1
Patient characteristics
Characteristics parameters
No. of patients
Risk factors: Diabetes Multivascular diseases (cerebral, coronary, renal, abdominal aorta) Previous vascular surgery Clinical stage: Moderate claudication Severe claudication Rest pain Minor tissue loss, no healing ulcer Run-off status: Number of occluded arteries: 3 2 1 0 Number of stenosed arteries (≥ 50%): 3 2 1 0
48 (32%) 128 (85%) 32 (21%) 16 (11%) 98 (65%) 28 (24%) 8 21 40 40 49 76 28 18 28
150 patients; mean age (years): 73 ± 1 (range 42–90) 94 male; mean age (years): 68 ± 1 (range 42–86) 56 female; mean age (years): 77 ± 1 (range 61–90)
Patient information A total of 150 patients (94 males, 56 females; mean age 73 ± 1 year, range 42–90) were candidates for percutaneous rotational ablation in the lower limbs. Details of the patient population are shown in Table 11.1. Thirty-two percent of the patients were diabetic, 85% had other atherosclerotic disease (cerebrovascular, coronary, renal). Twenty-one percent had undergone previous vascular surgery. Sixty-five percent had severe claudication, and one-quarter of the patients had rest pain and/or ulceration. Adequate run-off (no stenosis > 50% in three vessels) was present in only 28 patients (19%) and 51% of the patients had flow-limiting disease in all three distal arteries. Eighty-nine patients (59%) were being evaluated for failure to show improvement with other techniques (angioplasty, surgery, medical treatment), 39 patients (26%) for symptom progression or limb salvage, and the remainder for angioplasty restenosis or for the treatment of distal lesions in multilevel endovascular procedures. Techniques All 150 patients underwent rotational atherectomy using the Rotablator according to the methods described above. A total
Table 11.2
of 212 lesions were attempted in the iliac, femoral, popliteal, or distal arteries (Tables 11.2–11.4). There were 193 stenoses (91%) and 19 chronic occlusions; 93% were calcified, and 63% were located at important bifurcations or collateral branch origins. Fifty percent of the lesions were located below the knee. The length of the lesions varied from 1 to 20 cm, 17% of the treated lesions were longer than 7 cm, 25% were between 4 and 6 cm, and 58% were smaller than 3 cm. The lesions at the femoral level were significantly longer than those in other segments (5.70 ± 0.40 cm vs. 2.97 ± 0.30 cm) (p < 0.001). The maximum number of lesions treated in one patient was four. There was no difference between the male and the female population regarding the characteristics or location of the lesions, but the average number of treated lesions was lower in males (1.35 lesion per patient) than in females (1.53 per patient). The approach techniques used and incidences of concomitant procedures are listed in Table 11.5. One lesion in an anterior tibial stenosis was excluded when a guidewire failed to pass successfully. Rotational ablation alone was used to treat 16 patients (19%) at the femoral level, 9 (47%) at the popliteal level and 92 (87%) at the distal artery level. Adjunctive dilatation was necessary in 70 patients (81%) at the femoral level, 10 (53%) at the popliteal level, and 14 (13%) at the distal leg artery level (Figure 11.2). Figures 11.1 and 11.3–11.6 show some results at different locations. Procedural success Seven procedures failed subsequent to intra-procedural complications (see below). Therefore, the immediate technical success by lesion was 97% (95% by patient). Figure 11.7 summarizes the percentage stenosis before and after Rotablator and following adjunctive dilatation at the femoral, popliteal, and distal arterial levels. Residual stenosis after Rotablator was higher at the femoropopliteal levels (44%) than in the distal segment (p < 0.01), due to the burr-to-vessel diameter ratio, which was 80.8 ± 1.6% at the distal level but only 61.1 ± 2.6% at the femoropopliteal levels (p < 0.001). Complications There were 37 intra-procedural complications (25%) related to the Rotablator treatment (Table 11.6). Among these, arterial spasm (17 cases; 11%) comprised the majority of these events. It occurred more frequently in the distal arteries (15; 88%) than in the femoropopliteal segment (p < 0.02), but it was successfully treated in most patients (16/17). Twelve thromboses (8%) were encountered; eight were successfully treated by fibrinolysis. Dissections and perforations occurred
Lesion characteristics
Bifurcation or branches Calcified Occluded Stenosed
No.
Percent
134 192 19 193
63 93 9 91
61
Above knee (%) 62 98 14 86
Below knee (%) 64 87 4 96
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Lesion characteristics by location
Location
No.
Iliac Femoral Popliteal Tibioperoneal Trunk Posterior tibial Peroneal Anterior tibial Total Total
1 86 19 38 7 16 45 106 212
Mean length (cm)
Range
Mean % stenosis
Range % stenosis
12 5.7 ± 0.40 2.40 ± 0.30
1–15 1–6
84 ± 2 86 ± 3
100 60–100 75–100
2.6 ± 0.2 2.6 ± 0.6 2.4 ± 0.3 3.4 ± 0.6 2.9 ± 0.3 4 ± 0.2
1–6 1–5 1–4 1–20 1–20 1–20
85 79 82 82 83 83
± ± ± ± ± ±
70–100 70–90 75–99 60–100 60–100 60–100
rarely (3%), as did distal embolism (two cases; 1.3%), one of which was successfully treated by aspiration). Two instances of no-reflow phenomena were observed and treated. In the immediate post-operative period, there were seven (5%) cases of hemogloburinia and two cases (1.3%) of transitory renal insufficiency. They were resolved within 24 hours without any consequences. Follow-up The mean observation period for this population was 14.4 ± 1 months (range 1–51). One hundred and twenty-five patients were available for = 4-month follow-up evaluation (this cohort did not differ significantly in gender, age, risk factors, or location/type of lesions from the initial population). Of these, 114 patients underwent angiography at 4 months in addition to clinical evaluation and Doppler examination. Of the remaining 44 patients, 4 patients were lost to follow-up, 3 died, and 4 were excluded because they had stent implantation. In these 114 patients, 163 lesions (77% of original treatment group) were re-examined: 123 (76%) were patent with a residual percent stenosis of 17 ± 1.1%, and 40 arteries (24%) showed restenosis (= 50% luminal narrowing) of 82 ± 2.1%, as shown in Table 11.7, the restenosis rate was highest at the femoral level. Restenosis was more frequent for all lesions longer than 7 cm (p < 0.001) (Table 11.8) and at both the femoropopliteal level (55 vs. 19% of < 7 cm; p < 0.03) and the distal segment (80 vs. 18%; p < 0.01).
1 2 2 1 0.7 0.7
stretches the arterial wall. The Rotablator, on the other hand, does not crack the plaque or deform the vessel wall, as is shown by radiological, histological, angioscopic, and ultrasound studies.2–4 Rather, the Rotablator has an abrasive action that removes the obstructing material, preferentially ablating rigid, calcified atherosclerotic tissue while leaving healthy elastic tissue intact.4–5 This differential cutting produces a lumen that is smooth and polished in appearance. Despite the device’s preference for inelastic tissue, however, the endothelium adjacent to a lesion can suffer damage during progression of the burr. The same situation is encountered with a balloon whose length is greater than the stenosis; both may alter the endothelium on either side of a stenosis. As opposed to balloon treatment, however, the Rotablator rarely injures the media,2 an event that has been reported to be the impetus for intimal hyperplasia and restenosis. Whereas it is simple to select a balloon sized to match the lesion and artery, it is not so for rotational atherectomy. Using large-diameter introducers (> 9-French) to accommodate the percutaneous introduction of burrs > 3 mm would significantly increase the rate of access site complications. Dorros et al.,6 for example, used burrs up to 4.5 mm requiring a 14-French introducer for renal arteries. However, their incidence of local and systemic complications were considerable (e.g. 23% hematoma, 5% perforation, 63% hemoglobinuria). From our own experience and these early reports, we now treat only arteries < 6 mm in diameter using up to a 3-mm burr; this gives us residual stenosis of < 50%.
Discussion The mechanism of rotational ablation differs completely from that of balloon dilatation. In the latter, compression of the lesion promotes rupture of the atherosclerotic plaque and Table 11.4
Above knee Below knee Total
Lesion lengths by location < 3 cm
4–6 cm
> 7 cm
45 (42 %) 77 (72 %) 122 (58 %)
30 (28 %) 24 (23 %) 54 (25 %)
31 (30 %) 5 (5 %) 36 (17 %)
Table 11.5
Procedural details
Parameters Approaches: Ipsilateral femoral Contralateral femoral Popliteal Bilateral Atherectomy associated with: Femoral lesion dilatation Popliteal lesion dilatation Distal lesion dilatation
No. of patients 141 5 4 20 14 2 3
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151 patients 1 unsuccessful attempt 150 patients (212 lesions)
86 femoral
Alone 16 (19%)
Figure 11.2
19 popliteal
+PTA 70 (81%)
Alone 9 (47%)
Figure 11.3
Alone 92 (87%)
+PTA 14 (13%)
Treatment with Rotablator alone and with adjunctive balloon dilatation by vessel segment.
This interdiction against rotational ablation in arteries > 6 mm has necessarily limited our experience with the Rotablator at the iliac level. In the one iliac artery we have treated, the vessel was very calcified. Even though a hydrophilic guidewire passed the lesion, the balloon could not be advanced. In this case, we used the 3-mm Rotablator to debulk the lesion, producing a channel to facilitate balloon dilatation. In our experience, adjunctive dilatation is necessary at the femoral level to obtain satisfactory immediate results. This is not the case at the distal segment, where we have usually been able to introduce a burr equal to at least 80% of the arterial diameter. This burr-to-artery diameter ratio may explain our lower restenosis rate at the distal level (21%) compared to the higher rate in the SFA (36%), and in particular, when balloon angioplasty did not follow Rotablator ablation. At present, our series is too limited to offer conclusive proof, but it would seem that the use of adjunctive balloon dilatation might reduce the restenosis rate at the femoral level. Such an observation has been made at the coronary level by Bertrand et al.7 in a collaborative study of 129 patients treated
(a)
+PTA 10 (53%)
106 distal leg arteries
with the Rotablator alone, the rate was 46%, as opposed to only 30% when complementary balloon angioplasty was used. The same effect may occur at the peripheral level, but we have not studied this possibility. Insofar as determining an optimum technique for rotational ablation, we have used three treatment protocols: 1. Beginning the procedure with burrs and increasing the size until an optimal result is reached, with the burr size closely approaching that of the arterial diameter; 2. Initially using a single large burr equal to 75–80% of the arterial diameter; 3. Simply debulking the lesion using a small burr to remove inelastic material, then dilating the vessel at low pressure with a balloon that matches the diameter of the artery. Only for treatment of distal arteries have we developed a preference among these. We believe that it is advisable to use incrementally sized burrs that approach at least 80% of the artery’s diameter. This avoids the need for balloon dilatation and reduces the risk of dissection.
(b) (a) Multiple, severe, anterior tibial, and peroneal stenoses; and (b) the result after Rotablator therapy is excellent.
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(a)
(b)
Figure 11.4 (a) A very tight stenosis exists distal to a femoropopliteal bypass graft; and (b) satisfactory outflow has been re-established with the Rotablator.
The same opinion does not apply, however, to the femoropopliteal arteries or those with diameters > 3 mm. In these larger arteries, it would appear preferable to routinely complete the procedure with balloon dilatation to ensure residual stenosis of no more than 20% in order to limit the incidence of restenosis. Unlike balloon angioplasty, the Rotablator appears to be particularly well suited to deal with calcified and/or eccentric lesions and stenoses at bifurcations or in tortuous arteries. Further, the Rotablator may be useful for the treatment of severe, extensive lesions; by reducing the plaque burden,
(a) Figure 11.5
balloon dilatation may be applied with less risk of dissection. One situation in which the Rotablator must not be used is in the presence of thrombus; chronic thrombus tends to deflect away from the rotating burr, leading to suboptimal results. In terms of outcome, our procedural success with Rotablator therapy in the limb arteries has been high (97%). Other investigators have reported similar results in the 92–95% range.4,6,8,9 However, the published results of a multicenter trial (CRAG) of the Rotablator found only a 77% angiographic success in 107 lesions treated in 72 patients.10 This is not surprising when one considers that only half as
(b) (a) A severe lesion at a bifurcation; (b) results after Rotablator.
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(a)
(b)
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(c)
Figure 11.6 (a) Lesions in the superficial femoral artery and in the popliteal artery; (b) results after Rotablator; and (c) results after balloon angioplasty.
90
87
86
83
80 70 Before
60 50
After Rotablator After Dilatation 44
40
38
30 19
20 10
10
5
3
0 Femoral (n = 86)
Figure 11.7
Popliteal (n = 19)
Distal arteries (n = 106)
Percent stenosis before and after Rotablator and after adjunctive balloon dilatation.
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Table 11.6
Complications according to lesion location (above and below knee)
Ablation site: Spasm Thrombosis Dissection Perforation Distal emboli No reflow Total
Above knee
Below knee
No. cured/ No. total
2 6 1 0 1 2 12
15 6 2 1 1 0 25
16/17 8/12 3/3 0/1 1/2 2/2 30/37
many patients were treated by several physicians in three centers as represented in our single-center study. Clearly, the inevitable learning curve and operator inexperience with the technique probably contributed to these somewhat poorer procedural results. Moreover, their patient population had more advanced disease (56% limb-threatening ischemia vs. 24%), and the lesions treated were twice as long (9 cm average vs. 4 cm). Given that the Rotablator would often be applied in complex lesions unsuitable to other interventions, the complications inherent to the procedure seem acceptable, and most can be easily treated. Overall, in our study, no particular complication was statistically linked to gender, age, or lesion location. However, the frequency of complications at the ablation site seemed to be influenced by the length of the treated lesion (< 6 cm: 15%; > 6 cm: 85%). The most frequent complication we have encountered is arterial spasm (11%), which occurs more often in the distal arteries and for 2 or 3 cm proximal to the treatment site. Of particular note is the fact that the incidence of spasm appears to be related to operator experience. Indeed, spasms occurred at a rate of 14% during our first 50 procedures, decreasing to 8% over the next 50 cases, and finally ending at 2% (p < 0.05). Although some operators have postulated that arterial spasm may be caused by vibrations transmitted to the guidewire during rotation or to the liberation of vasoconstrictive substances contained with the plaque, endothelium, or blood cells, we are of the opinion that is dependent upon technique. In our experience, spasm appears most frequently when too large a burr is used, the rotation sequences are too long, or the rotation speed is too fast or too slow. Also, spasm will occur if the burr becomes entrapped in the wall or the drive
Table 11.7
shaft is deflected by a bent guidewire (the rotation drive shaft irritates the adjacent arterial wall). To prevent spasm, all patients are placed on vasodilators the day before the treatment. During the procedure, we routinely inject molsidomine and nitrates intra-arterially. If a spasm occurs, the same drugs are re-injected. If this medical treatment fails, low-pressure balloon dilatation is performed, which usually relieves the spasm in most arteries. Our acute thrombosis rate has been low (5.6%); almost half that reported in the multicenter trial.10 Moreover, most of these have been successfully treated either by thrombolysis, thromboaspiration, or thromboembolectomy. A number of factors may predispose to thrombosis: a residual stenosis, an intimal flap, elastic recoil, dissection, lengthy lesion, or vasospasm. Once the artery is reopened, low-pressure balloon dilatation may be attempted. The incidence of dissection, perforation, or angiographically visible flaps has been rare (< 2%), and these were encountered at the beginning of our experience. Because these complications are caused by the guidewire or the burr, they can be circumvented by cautious wire manipulation to prevent subintimal incursion and by prudently selecting the burr, avoiding a too-large diameter for the vessel. Although the Rotablator produces fine particles (5–180 µm) that are disseminated in the peripheral circulation,2,5 we have observed only two cases (1.3%) of distal embolism from particulate migration, and thromboaspiration was effective in treating one case. Other authors have experienced this complication at a much higher rate. Ahn et al.,8 for example, encountered emboli in 20% of their cases, but these were coincident to long lesion treatment with large burrs (4.0–4.5 mm). Not surprisingly, the CRAG trial reported a 10% incidence of emboli for the same reasons. Hemolysis, another complication related to rotational atherectomy, appears more or less constant with this technique, due to destruction of the red blood cells by the burr rotation. The intensity of this response is proportional to the ablation time, size of the burr, and length of the treated lesion. According to a study we performed following 54 patients at time intervals up to 24-hours post-atherectomy, we saw an increase in free hemoglobin, a drop in haptoglobin, and a rise in lactic dehydrogenase within the first 5 minutes following the procedure. The phenomenon was transitory, reversible, and usually without attendant complications, but in two of our cases, there was a slight transitory renal failure that resolved within 48 hours. Our 5% rate of hemoglobinuria is again less than half that reported in the CRAG trial (13%).
Number of location of restenosed and patent arteries in follow-up period (n = 163) Patent
Restenosed
No.
Femoral Popliteal Distal All
19 1 20 40
% stenosis 80 90 84 82 ± 2.1
Mean length 6.5 ± 0.8 2 4.9 ± 1.2 5.6 ± 0.7
No.
% stenosis
34 14 75 123
20 18 15 17 ± 1.1
Mean length 4.9 ± 0.5 2.1 ± 0.3 2.4 ± 0.2 3 ± 0.2
% restenosis 36% 7% 21% 24%
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Percutaneous peripheral atherectomy using the Rotablator Table 11.8
Relationship of restenosis to lesion length Femoral and popliteal
Mean length > 7 cm < 7 cm
67
p < 0.001
Distal artery
Restenosed
Patent
Percent
Restenosed
Patent
Percent
11
9 p < 0.03 39
55
4
80
19
16
1 p < 0.01 74
9
One other complication we encountered in two cases was slow flow or no reflow, a phenomenon seen in coronary angioplasty when the contrast agent ceases to flow, although no thrombus, flap, or spasm is visible. Several mechanisms have been proposed for this, from capillary obstruction by atherosclerotic or thrombotic embolism to interstitial edema. In the case of the Rotablator, however, cavitation may produce microbubbles that temporarily block outflow.11 Indeed, in our cases, stagnation of the contrast medium downstream in the popliteal artery followed successful atherectomy in the SFA. The phenomenon disappeared 2–3 minutes after the injection of molsidomine and nitroglycerine. No distal embolism was visible after contrast medium washing. As compared to the CRAG trial, our overall 25% complication rate is half what they observed, and the better part of our complications (46%) were due to spasm, a sequel the CRAG report did not even mention. This difference is particularly noteworthy when one considers that 21 of the 79 atherectomized limbs (27%) in their cohort required urgent or emergent surgical therapy, including two amputations. We have encountered nothing like this in our experience, and it is important to recognize that the CRAG trial was testing the gamut of Rotablator burrs in extremely long lesions (40 cm) requiring up to 35 minutes of rotation time! In these circumstances, neither their results nor their complication rates are surprising. Early in our experience, we recognized that protracted rotational ablation was inadvisable, and we restricted the rotation time whenever possible. Regarding our follow-up results, we have amassed angiographic data on 91% of our patients who were 4-months posttreatment. These data have shown that the restenosis rate is relatively low (24% overall), considering the severity of the initial pathology. This is comparable to the 66% primary patency at 6 months reported by Ahn et al.8 Both the site of the lesion and the length of the segment treated influenced restenosis. For lesions > 7 cm, the rate was very high, and complications were four times as frequent in lesions < 6 cm. This relationship between lesion length and restenosis is, however, not unique to rotational ablation. Other authors have reported a similar correlation for balloon angioplasty.12 Supported by these statistics, we feel that Rotablator therapy should be limited to lesions = 6 cm. If restenosis does occur, repeat treatment should be carried out without hesitation, either with the same procedure or a different technique. In our experience, this produces marked improvement in the secondary patency. This early re-intervention is possible only if regular follow-up is maintained to facilitate early diagnosis, thus avoiding or at least postponing surgery. It is difficult to compare the results of one technique with those of another because the lesions treated are often different.
18
Certainly, in terms of procedural success, the Rotablator is comparable to other atherectomy techniques4,8 and balloon angioplasty.12 However, perhaps the advantage of rotational ablation lies in its ability to enlarge the treatment potential for percutaneous interventions as a whole. Certain lesions cannot be treated by balloon dilatation alone, so the Rotablator is an important auxiliary technique that enhances our interventional capabilities overall. Further, the Rotablator allows percutaneous treatment of other lesions that until now had been impossible to treat non-surgically or posed higher risks with either endovascular or surgical techniques. Moreover, the potential to treat run-off vessels using this method should improve the long-term patency of iliofemoropopliteal bypasses and proximal angioplasties. Other techniques may make such claims as well. Lasers, either excimer or holmium, would also be capable of treating long, eccentric, calcified, ostial or bifurcation lesions.13,14 However, the complication rate appears to be no lower, particularly for spasms in excimer-treated arteries, and the costs of a laser are far greater than an atherectomy device. Moreover, long-term patency rates are disappointing as noted in the LACI trial. The holmium laser can be used in the presence of thrombus, which is an advantage over the Rotablator, but here again the expense of the laser versus the cost of thrombolytic therapy preliminary to Rotablator therapy is unquestionably greater. Directional atherectomy using the Simpson/Silverhauk atherectomy may be preferred to the Rotablator in certain cases of ostial or bifurcation lesions and in short eccentric lesions.16 Its manipulation is more taxing and particularly difficult in tortuous arteries. Moreover, the risks are greater, particularly at the distal level, and the restenosis rate is high.17 The transluminal extraction catheter (TEC) could compete with the Rotablator in certain disease pathologies, most notably for the treatment of focal stenoses and bypass lesions where thromboses are likely to be encountered. However, the device does not perform well in calcified vessels.18 The Rotarex catheter at the femoropopliteal level could also compete with the Rotablator but it is not proved that it is as effective for very calcified lesions.
Conclusion The treatment of long, diffuse, calcified femoropopliteal lesions remain challenging. Debulking with Rotablator could be very useful before angioplasty alone or maybe in the future before placing bare stents or stent grafts.
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The treatment of leg arteries in cases of critical limb ischemia remains a very challenging topic for interventionists. Among the tools available the rotational atherectomy appears to be a useful alternative to other techniques or surgical revascularization especially for the worst cases of infrainguinal occlusive diseases. Dormal et al. recently gave a review of the literature and analysis of their results,19 and underscore on the usefulness of this device for limb-threatening arterial occlusive disease. Also recently, Tamashiro et al. pointed out the role of the Rotablator to treat a patient in critical leg ischemia with long occlusion of the three infrapopliteal vessels.20 The anterior tibial artery was
treated with retrograde Rotablator atherectomy by an open approach though the pedal artery resulting in full patency of the anterior tibial artery and healing of the skin lesions. Our results and these recent data should encourage us to broaden the indications for this technique in leg arteries. The main limitation remains its cost; the catheters are expensive, and when multiple burrs are needed the procedural costs can rise. Without this drawback, it is probable that a far greater number of angioplasties would be preceded by rotational atherectomy. However, this enthusiasm must be tempered by the necessity for sound theoretical and practical knowledge of the device before approaching complex lesions.
REFERENCES 1. Henry M, Amor M, Ethevenot G et al. Percutaneous peripheral rotational ablation using the Rotablator: immediate and mid-term results. Single center experience concerning 146 lesions treated. Int Angiol 1993; 12: 213–44 2. Ahn SS, Auth DC, Marcus DR et al. Removal of focal atheromatous lesions by angioscopically guided high speed rotational atherectomy: preliminary experimental observations. J Vasc Surg 1988; 7: 292–300 3. Ahn SS. Angioscopic controlled atherectomy. In: White GH, White RA, eds. Angioscopy Vascular and Coronary Applications. Chicago: Year Book Medical Publishers, 1988: 114–22 4. Ahn SS, Eton D. The Rotablator high-speed rotary atherectomy: indications, technique, results and complications. In: Ahn SS, Moore WS, eds. Endovascular Surgery, 2nd edition. Philadelphia: WB Saunders, 1992: 295–307 5. McLean GK. Percutaneous peripheral atherectomy. J Vasc Intervent Radiol 1993; 4: 465–80 6. Dorros G, Iyer S, Zaitoun R et al. Acute angiographic and clinical outcome of high-speed percutaneous rotational atherectomy (Rotablator). Cathet Cardiovasc Diagn 1991; 22: 157–66 7. Bertrand ME, Lablanche JM, Leroy F et al. Percutaneous transluminal coronary rotary ablation with Rotablator (European experience). Am J Cardiol 1992; 69: 470–74 8. Ahn SS, Eton D, Yeatman LR et al. Intra-operative peripheral rotary atherectomy: early and late clinical results. Ann Vasc Surg 1992; 6: 272–80 9. White CJ, Ramee SR, Escobar A et al. High speed rotational ablation (Rotablator) for unfavourable lesions in peripheal arteries. Cathet Cardiovasc Diagn 1993; 30: 115–9 10. The Collaborative Rotablator Atherectomy Group (CRAG). Peripheral atherectomy with the Rotablator: a multicenter report. J Vasc Surg 1994; 19: 509–15
11. 12. 13. 14. 15.
16. 17. 18.
19. 20.
Zotz RJ, Erbel R, Philipp A et al. High-speed rotational angioplasty induced echo contrast in vivo and in vitro optical analysis. Cathet Cardiovasc Diagn 1992; 26: 98–109 Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty: factors influencing long-term success. Circulation 1991; 83(suppl I): I70–80 Litvack F, Grundfest WS, Adler L et al. Percutaneous excimer-laser and excimer-laser-assisted angioplasty of the lower extremities: results of initial clinical trial. Radiology 1989; 17: 331–35 McCarthy WJ, Vogelzang RL, Nemcek AA et al. Excimer laserassisted femoral angioplasty: early results. J Vasc Surg 1991; 13: 607–14 Laird JR. Peripheral excimer laser angioplasty (PELA) trial results. Paper presented at the Transcatheter Cardiovascular Therapeutic (TCT) Conference, September 24–28, 2005, Washington DC Gammo R. Plaque excision treatment of infrainguinal PAD. Endovasc Today 2005; 4: 70–4 Hinohara T, Selmon MR, Robertson GC et al. Directional atherectomy: new approaches for treatment of obstructive coronary and peripheral vascular disease. Circulation 1990; 81(suppl III): II79–III91 Wholey MH, Levitt RG, Fein-Millar D. The Transluminal Endarterectomy Catheter: indications, techniques, results and complications. In: Ahn SS, Moore WS, eds. Endovascular Surgery, 2nd edn. Philadelphia: WB Saunders, 1992: 308–15 Dormal PA, Afropoli AM, Dervaux P. Rotablator: a forgotten tool in limb ischemia. Acta Chir Belg 2005; 105: 231–34 Tamashira A, Villegas M, Tamashiro G et al. Retrograde Rotablator in limb salvage: a new technique using an open approach. Cardiovasc Intervent Radiol 2006; 29: 854–6
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A new rotational thrombectomy and atherectomy catheter: the Rotarex system I Henry, M Henry, and M Hugel
Introduction Balloon percutaneous transluminal angioplasty (PTA) has a major role in the treatment of coronary and peripheral significant stenoses and is now the first treatment to be proposed. Nevertheless, this technique alone has some limitations in its application to some specific subgroups of complex lesions, such as calcified, ulcerated, eccentric, long lesions, and thrombotic lesions with the risk of embolization. There is also the problem of restenosis, with a high restenosis rate in some locations (e.g. femoropopliteal arteries, small vessels, ostial lesions, lesions at bifurcations, long lesions, diabetic patients, etc). Several techniques have been proposed to reduce the restenosis rate and to treat some lesions not amenable to balloon angioplasty alone, such as stenting and debulking techniques with atherectomy devices. Atherectomy is defined as excision and removal of obstructive tissue, a concept first introduced by Simpson et al.1–3 The amount of plaque burden in the artery correlates with the restenosis rate. So, by creating a large, smooth lumen and by preventing elastic recoil, rather than increasing luminal diameter by arterial stretching and plaque fracture, as with balloon angioplasty, debulking could yield better clinical outcomes and short- and long-term patency rates. The first directional atherectomy procedure was performed in 1985 by Simpson et al. in a superficial femoral artery using a peripheral atherectomy device. This initial experience demonstrated the safety of directional atherectomy for peripheral vascular disease.4 It was approved by the US Food and Drug Administration (FDA) in 1987. This device was then adapted for coronary procedures and the directional coronary atherectomy (DCA) device was approved by the FDA in 1990 as the first non-balloon percutaneous coronary interventional device. In contrast to DCA, which relies on excision and tissue removal, the transluminal extraction–endarterectomy catheter (TEC) (Interventional Technologies Inc., San Diego, CA) was designed by Stack to cut and aspirate atheroma and debris. In 1989, this device was approved by the FDA for peripheral vascular disease, and in 1992 for revascularization of saphenous vein bypass grafts and native coronary arteries. Other devices have been proposed, for example the Rotablator,5 the Simpson AtherotrackTM,6 the Pullback Atherectomy Catheter,7 and more recently the SilverHawk® atherectomy device.8
A new device has been recently proposed, the Rotarex device (Straub Medical, Wangs, Switzerland), which is a rotational atherectomy catheter now in competition with other atherectomy devices. The device is also a rotational thrombectomy system combining two essential effects: mechanical clot fragmentation and removal of the fragmented material from the vessel under negative pressure, which purports to prevent peripheral embolization. This device is used to treat acute and subacute thrombotic occlusions of native vessels and bypass grafts. It competes with rheolytic thrombectomy catheters (e.g. Hydrolyser, Oasis, Angiojet) which employ a retrograde jet of fluid oriented toward the central lumen of the catheter to destroy clots by the Venturi effect, and with other devices which employ the vortex effect like the Amplatz thrombectomy catheter, the Arrow-Trerotola percutaneous thrombolytic device (PTD) or the Baxter percutaneous mechanical thrombectomy device (PMT) and which pulverizes thrombotic material in contact with the end of the catheter.9–20 We will describe these two applications of this new Rotarex system.
Rotarex system Description: equipment and mechanism of action The system has three components: ● ● ●
the Rotarex catheter; a 40 W D.C. electric motor drive; an electronic control unit.
Inside the whole length of the 8-French polyurethane catheter rotates a coated stainless steel spiral, which glides over a 0.020inch guidewire. The catheter head consists of two cylinders that fit over each other. The outer rotating cylinder is fixed to the spiral; the inner one is attached to the catheter shaft. Each cylinder has two oval slits. The blunt tip of the outer cylinder is perforated for the guidewire. The catheter and motor drive are connected by a magnetic clutch. The motor rotates the spiral at 40,000 rpm, resulting in 80,000 cuts/minute. The high frequency of revolution creates a negative pressure at the catheter head of 5.8 kPa (43.5 mmHg). When the catheter is activated, soft and solid occlusion material is caught in the 69
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Figure 12.1 drive.
The Straub Rotarex catheter attached to the motor
slits, transported by the spiral to the proximal side port and discharged into a plastic bag. No additional suction is required. The transport of the occlusion material is done exclusively by the rotating spiral. The catheter is for one-time use, while the motor drive and the connecting cable to the electronic control unit can be sterilized. Preclinical studies The catheter was tested in an arterial model made of silicon tubing of 4, 6, and 8 mm inner diameter and length 15–30 cm, allowing observation and video documentation of the catheter function. The tubes were bendable to test the behavior of the catheter at various angles. The tubing was filled with occlusion material of different consistencies: (1) bovine blood that was allowed to coagulate for 48 hours or 2 weeks and stored at 4°C; (2) stamp cylinders of “black pudding,” a mixture of thrombus, muscle, fat, and connective tissue, 4, 6, and 8 mm thick, and 15-mm-long, simulating organized thrombus; (3) strips of bovine arteries (3 cm long, 1 mm broad) sutured intraluminally to the vessel wall, imitating intimal flaps. The tubing was clamped at one end and connected to an infusion line on the other, where a mixture of saline and glycerol could be infused under a continuous pressure of 120 mmHg. In this infusion tube an 8-French sheath (Cook, Bjaerverskov, Denmark) was introduced, a 0.020-inch Tefloncoated guidewire threaded through the occlusion material, and the catheter advanced. In a second test series (n = 72), the silicon tubing was replaced by fresh bovine carotid arteries with an average length of 20 cm and a diameter of 6–7 mm. The side branches were ligated and the arteries filled with the above-mentioned occlusion material. During catheter activation, tube and arteries were either kept straight or bent at different angles up
Figure 12.2
Electronic control unit.
Figure 12.3
Schematic draining of the catheter head.
to 50°. Occlusion of the arteries was achieved by tightening a 5-mm-wide rubber band around the vessel, completely interrupting the flow of perfusate. The occlusion was passed with the catheter over the wire. All tests were recorded on video. The time of catheter activation was recorded, the volume of aspirated fluid measured and the fluid passed through different filters for analysis of particle size. The arteries were cut open and examined visually and histologically for remnants of occlusion material and possible intimal damage. Results The catheter removed 48-hour-old thrombi in silicone tubing of 4- and 6-mm diameter completely and regularly; the maximum working diameter was 8 mm. On average, 1 cm of thrombus was aspirated within 2 seconds. Thrombi stored in the refrigerator for 2 weeks often showed adherence to the wall of the tubing, but could also be easily aspirated, leaving occasionally a thin residual layer attached to the inner curvature if the tube was bent. Occlusion material of higher and inhomogeneous consistency, such as muscle, fat and connective tissue, was caught readily in the catheter head and transported to the outside by the spiral. Fluid was aspirated at a rate of 1.5 ml/second. While fresh thrombus was completely homogenized, more solid material was cut into particles of 100–500 µm. Strips of bovine arteries, sutured intraluminally to the vessel wall to imitate intimal flaps, were cut and fragmented, leaving only small stumps at the suture site. Bovine arteries
Figure 12.4 The rotating outer cylinder glides over the inner fixed cylinder with its oval slits. The guidewire runs inside the transport spiral, which is attached to the tip of the perforated head of the outer cylinder.
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A new rotational thrombectomy and atherectomy catheter: the Rotarex system filled with thrombi or “black pudding” could be cleared of the occlusion material without remnants. No intimal damage was noticed on visual examination or after staining. When the arteries were compressed to complete occlusion by a rubber band, the catheter drilled a lumen corresponding to its shaft size. When tubing or arteries were bent, the catheter followed the guidewire smoothly. No perforation was noticed. The catheter needed fluid (blood) for lubrication. Under experimental conditions the temperature of the catheter head rose by 1.5°C after rotating for 4 minutes at 40,000 rpm in a tube of 3-mm diameter perfused with a saline–glycerol solution (80 ml/minutes) at room temperature.
Clinical studies as thrombectomy devices First pilot study Based on the results of the preclinical tests, the Institutional Review Board of the Department of Internal Medicine, University Hospital, Basel, accepted the protocol of a pilot study for the evaluation of the device for the treatment of thrombotic occlusions in femoropopliteal arteries in humans.21 Ten patients (eight women and two men; 58–87 years of age, mean age 70.6 ± 10.1) with acute or subacute occlusion of the femoropopliteal artery with an estimated age < 4 weeks and patent proximal segments of lower leg vessels, were included in the study. All patients were informed in detail about the procedure and gave their written consent. Patients with aneurysms of the popliteal artery, severe coagulation disturbances or a history of adverse reactions to contrast media were excluded. Seven patients suffered from critical ischemia (rest pain) and three from peripheral arterial occlusive disease (PAOD) stage II (intermittent claudication). The estimated age of the lesions was between 2 and 28 days. The mean length of the occluded segments was 5.8 cm (range 2–15 cm). The diagnosis was established by clinical examination, oscillography, Doppler pressure recordings, duplex sonography9 and digital subtraction arteriography. Laboratory examinations included hemoglobin, free plasma arteriography, hematocrit and coagulation parameters, both before, immediately after, and 24 hours after thrombectomy. Non-invasive examinations (oscillography, Doppler pressure recordings, duplex sonography) were performed after 48 hours and after 3 months. Antegrade arteriography was performed via the common femoral artery to determine the length of occlusion and to document the collateral circulation and the peripheral run-off. Using the road-map technique, the occlusion was passed with a Teflon-coated 0.020-inch guidewire and its flexible tip placed in the distal popliteal artery. An 8-French sheath was introduced and 5000 units of heparin injected. The thrombectomy catheter was threaded over the guidewire. One centimeter proximal to the upper end of the occlusion, the catheter was activated by a foot switch and advanced through the occlusion in gentle forward and backward movements under fluoroscopic control. The continuous suction of blood and occlusion material into the reservoir bag was observed. After the catheter had passed the occlusion it was withdrawn in the
71
proximal femoral artery and angiography was repeated via the side port of the sheath. Depending on the result, thrombectomy was either terminated, repeated, or completed by PTA. The number and the duration of catheter passes, and the volume of aspirated fluid, were recorded. Extracted occlusion material was examined histologically. Results Thrombectomy was technically successful in all patients. A mean of 2.4 catheter passes (range 2–3) were required to recanalize the occluded segment, and 2.8 seconds on average were needed to reopen 1 cm of occlusion. Blood and detritus were aspirated at 1.1 ml/second; the total aspirated volume ranger from 20 to 90 ml, depending on the length and consistency of the lesion. In nine patients, an underlying residual stenosis was treated by PTA after the thrombectomy. Fortyeight hours after the reintervention no patient suffered from critical ischemia: eight patients were classified as PAOD stage I, and two patients as stage II. The ankle–brachial index (ABI) improved from 0.41 ± 0.18 (range 0.13–0.65) preinterventionally to 0.88 ± 0.15 (range 0.64–1.11) after the intervention (p < 0.0005). Three months after the intervention the mean ABI was 0.84 ± 0.20 (range 0.52–1.07). All patients received either oral anticoagulation or antiplatelet drugs and were assessed by duplex sonography 48 hours and 3 months after the intervention. The treated arterial segment remained patent in eight patients. Two patients had a reocclusion within 2 weeks after the intervention. In a 60-year-old woman with an occlusion 3 cm long in a smoothly outlined superficial femoral artery of 5 mm diameter and with three patent lower leg vessels, fresh thrombus was removed with the Rotarex catheter in two passes of 7 seconds. Complete vessel patency was restored, no peripheral embolism occurred and additional PTA was not considered to be indicated. As usual, the patient received 5000 units of heparin during the intervention and oral anticoagulation afterwards. After 48 hours duplex sonography revealed a reocclusion. At that time coagulation parameters were not in the therapeutic range, which might have contributed to the rethrombosis. The ABI, which improved from 0.61 to 0.71 after the intervention, remained at this level. The patient was classified as PAOD stage II without the need for a reintervention. The second patient was a 78-year-old diabetic woman with a history of claudication of several years, rest pain for 12 days and a 15-cm-long occlusion of the popliteal artery with poor lower leg outflow. Thrombectomy was primarily successful and complete vessel patency was restored after additional PTA. The ABI rose from 0.65 to 0.95 and duplex sonography showed a residual stenosis of < 50% diameter reduction. One week after hospital discharge the patient complained of recurrence of intermittent claudication and a reocclusion was documented. Since the patient was clinically in PAOD stage II, no further intervention was performed. Reduced outflow due to pre-existing lower leg artery occlusion was considered as a possible cause for rethrombosis. No patient had signs of mechanical damage to red blood cells. There was no increase in free plasma, hemoglobin, nor relevant changes in hemoglobin and hematocrit after thrombectomy. Histological examination of the aspirate showed mostly fresh thrombotic material and small components of fibrotic intima with sclerotic fragments. No serious
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complication occurred. In one patient a small embolus was detected angiographically within the proximal posterior tibial artery and lysed successfully by 100,000 units of urokinase. Other studies Berczi et al. reported a study of 19 limbs of 18 patients treated with the Rotarex device for acute or subacute occlusions of the middle or distal third of the SFA or the popliteal artery.22 Lesion length was 3–20 cm. Thrombectomy was technically successful in 15 of 19 vessels (79%). The primary procedural success including additional procedures such as angioplasty and/or stent graft placement in 17 limbs was 94%. Eight complications were observed (31.5%), two perforations, one arteriovenous fistula and three distal embolizations. Follow-up studies showed three early (4–11 days) and six late (1–6 months) reocclusions. The cumulative primary patency rate was 68% at 3 months, 39% at 6 months, and 12% at 19 months; the secondary patency 68% at 3 months and 53% at 6, 12, and 20 months. The authors concluded that this procedure is quick and effective but should not be used in calcified lesions due to the risk of perforation. Duc et al. published a series of 41 limbs in 38 patients with acute, subacute, or chronic femoropopliteal occlusions of 1–180 days duration (mean 31.6 days) treated with Rotarex. 23 Length of occlusion was 2–35 cm (mean 13.1). After an average of two passages, all but two limbs required PTA for residual stenosis > 25%. Five patients needed additional stenting. As complications, one arteriovenous fistula and ten distal embolizations occurred. Follow-up studies observed two early reocclusions after 1 day and two at 2 weeks. Primary and secondary patency rates were 62/84% at 6 months and 39/68% at 1 year. The amputation-free survival was 100%. The authors concluded that this technique is safe and effective, can be used in short and long occlusions with equal success provided the obstruction is not very calcified. Zeller et al. reported a series of 100 thrombotic lesions in 98 patients, measuring an average of 21 ± 11 cm long (2–40) treated with Rotarex.24 There were 33 acute (< 14 days) occlusions (group I), 58 subacute/chronic (> 14 days) (group II) and 9 acute bypass graft occlusions (group III). There were 4 ± 1.4 passes of the device performed. The amount of aspirated fluid was 240 ± 119 ml. Forty-eight percent of the arteries were stented. Primary success was achieved in 92%, 100% for the ipsilateral approach, and 56% for the crossover approach. Eighteen complications were reported: two amputations after unsuccessful intervention and one death, eight vessel perforations and seven peripheral embolizations. Thirty-day survival and limb salvage was 88% for group I, 100% for group II, 66% for group III. The 3-month restenosis/reocclusion rates were 9% for group I, 3% for group II and 29% for group III. The authors concluded that the technique is easy and useful, but the use of this device is limited by the 8-French diameter of the catheter and the limited capacity for crossover interventions.
Clinical study as atherectomy device: authors’ personal experience A second pilot study for evaluation of the device for the treatment of chronic atherosclerotic stenoses or in-stent restenoses
in femoropopliteal arteries in humans was conducted in our catheterization lab. Population Twenty-one patients (17 men and 4 women; 44–86 years of age, mean age 69.0 ± 11.9) with 26 lesions (tight chronic atherosclerotic stenoses or restenoses) of the femoropopliteal artery or tibioperoneal trunk were included in the study. All patients were informed in detail about the procedure and gave their written consent. Cardiovascular risk factors of these patients were: diabetes 3/21 (14.3%), high blood pressure 19/21 (90.5%), dyslipidemia 15/21 (71.4%), and tobacco 11/21 (52.4%). A history of coronary artery disease was present in 3/21 (14.3%) and previous peripheral transluminal angioplasty in 12/21 (57.1%). None of the patients had a history of femoropopliteal or distal bypass surgery. All the patients suffered from intermittent claudication and were in class IIb of Fontaine’s classification. None of them suffered from critical ischemia (rest pain). The estimated age of claudication varied between 2 months and 1 year. Pre- and post-procedure assessment Diagnosis was established by clinical examination, duplex sonography and digital subtraction arteriography. Duplex sonography was performed before, 24 hours and 6 months after the intervention. An arteriography was performed via the common femoral artery in all patients before the procedure to determine the characteristics of the lesions, to document the collateral circulation, the peripheral run-off and to decide the method of approach. Laboratory examinations included hemoglobin, hematocrit and coagulation parameters, both before and 24 hours after atherectomy. Characteristics of the lesions The characteristics of the lesions are summarized in Table 12.1. The mean arterial diameter of the artery was 5.4 ± 0.8 mm (range 3–6 mm) and the mean preintervention minimal lumen diameter (MLD) was 1.4 ± 0.6 mm (range 0–1.5 mm). The mean percentage diameter of the stenosis was: 83.5 ± 7.9% (range 70–100%) and the mean lesion length 31.1 ± 35.0 mm (range 10–150 mm). The majority of the patients had a good run-off (three distal leg vessel patency, seven patients; two distal leg vessel patency, eleven patients; one distal leg vessel patency, two patients). Technique Adjunctive medical therapy Adjunctive medical therapy for debulking with the Rotarex system is similar to PTA, including preprocedural aspirin (160 mg/day starting at least 1 day prior to the debulking procedure) and intraprocedural heparin (5000 units IV). Molsidomine was administered at the discretion of the operator to minimize vasospasm. The vascular sheath was removed immediately after the procedure. Heparin was given as enoxaperin (40 mg twice daily subcutaneously) for 24–72 hours at the discretion of the operator, depending on the
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Lesion characteristics
Characteristics Location Femoral Femoropopliteal Tibioperoneal trunk Etiology De novo Restenosis
Characteristics Calcifications Eccentricity Collaterals Ulceration
No. patients 19
No. patients Upper part Middle part Low part
4 9 6
Post-PTA In-stent restenosis
2 9
No. patients
6 1 15 11
Expander Palmaz Optimed
7 1 1
12 10 5 1
difficulties and the result of the procedure. All patients received aspirin 160 mg/day continuously after the procedure and clopidogrel 75 mg/day for 1 month. Technique of debulking We used the ipsilateral antegrade approach in most of the cases (19–21) and the contralateral retrograde approach in two cases to treat lesions of the upper part of the superficial femoral artery (SFA). An 8-French sheath was introduced in the femoral artery. In case of a stenosis, it was crossed with a Teflon-coated 0.020-inch guidewire and its flexible tip placed in the distal popliteal artery. In case of an occlusion, the lesion was first recanalized by a 0.035-inch guidewire through a 4-French catheter. The atherectomy catheter was threaded over the guidewire. One centimeter proximal to the upper end of the stenosis or occlusion, the catheter was activated by a foot switch and advanced through the lesion in gently forward and backward movements under fluoroscopic control. The continuous suction of blood and occlusion material into the reservoir bag was observed. After the catheter had passed the lesion it was withdrawn in the proximal femoral artery and angiography was repeated via the side port of the sheath. Depending on the result, atherectomy was either terminated, repeated, or completed by PTA, with or without stent. The number of catheter passes and the volume of aspirated fluid were recorded. Optimal atherectomy The end of the Rotarex procedure was based on angiographic appearance and was at the discretion of the operator. A technical success is defined as a post-procedural residual stenosis < 30% at angiography or a pressure gradient < 5 mmHg. In contrast to PTA, which often leaves moderate residual stenosis (20–50%) that requires stenting to enhance the result, the goal of optimal atherectomy was to create the largest possible lumen without complications, with a final residual stenosis < 30%, to avoid angioplasty and stenting. Optimal atherectomy could be achieved as follows: by debulking alone if the control angiogram demonstrates a residual stenosis < 30%, debulking followed by PTA ± stenting if the angiogram demonstrated a residual stenosis > 30% after
debulking. PTA was performed using a balloon-to-artery ratio of 1:1.2 and inflation pressure of 4–6 atmospheres. The “ideal” residual stenosis is unknown. In our study, we attempted to achieve a residual stenosis of < 30%. Results The immediate angiographic results are given in Figures 12.5–12.7 Technical success Atherectomy was technically successful in all patients and all lesions. One occlusion was first recanalized by a Terumo guidewire before the atherectomy with the Rotarex system. One very tight stenosis needed to perform an angioplasty with a small diameter balloon to enlarge the lumen before the Rotarex system could cross the lesion. A mean of 4.6 catheter passes (range 3–8) were required to enlarge the arterial lumen. Results in terms of MLD and percentage residual diameter stenosis after atherectomy with the Rotarex are shown in Table 12.2. Blood and detritus were aspirated at 1.1 ml/second; the total aspirated volume ranged from 40 to 100 ml, depending on the length and consistency of the lesion. In 19/26 lesions (73.1%), an underlying post-atherectomy significant residual stenosis (> 30%) was present and treated by PTA alone in 15/19 lesions (78.9%) and with PTA + stent in 4/19 lesions (21.1%). The mean residual stenosis after Rotarex was 36.8 ± 15.1% (range 5–55). Six stents were placed for significant residual stenosis (n = 4) or residual dissection (n = 2). The different types were: JoMed (JoMed France SARL, Voisins le Bretonneaux) in one patient; Optimed (Optimed Medizinische Instrumente GmbH, Ettlingen, Germany) in four patients; and Smart (Cordis Corp, Warren NJ) in one patient. The type of stent placed depended on the location, the diameter, and the length of the lesion. Final results after Rotarex and PTA + stent procedure are shown in Table 12.2. Angiographic complications The overall incidence of angiographic complications after the Rotarex procedure was 6/26 (23.1%). Dissection and abrupt closure: A small non-occlusive dissection, not compromising the arterial flow occurred in 15.4% of
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(a) Figure 12.5
(b)
(c)
(d)
(a) SFA calcified stenosis; (b) Rotarex; (c) result after Rotarex; and (d) final result after angioplasty.
cases (4/26 lesions) after the atherectomy procedure. It was treated by PTA (three cases, 75%), and stent (one case, 25%) without further revascularization. No abrupt closure was observed. Distal embolization and no-reflow: Distal embolization causing abrupt cut-off of the target vessel distal to the original target lesion has been seen in one case and treated successfully by thrombosuction. No emergency bypass was needed. This type of macroembolization was probably due to dislodgement of thrombus or friable plaque from the target lesion, or release or incomplete capture of tissue stored in the collection chamber of the device. Perforation: Artery perforation was observed in one case (3.8%) in a tibioperoneal trunk and treated with a covered JoMed stent after unsuccessful prolonged balloon inflations. Vasospasm: No severe vasospasm was observed after Rotarex. Side branch occlusion: No side branch occlusion occurred. Clinical outcomes A clinical success at 24 hours was observed in all patients (100%) with no major clinical complications, no vascular injury requiring blood transfusion or vascular repair. All patients were classified as class I of Fontaine’s classification. The ABI improved from 0.53 ± 0.12 (range 0.13–0.65) preinterventionally to 0.91 ± 0.13 (range 0.64–1.11) postintervention (p < 0.0005). All treated arterial segments remained patent with good results and no significant residual stenosis, except in one patient whose residual stenosis was evaluated to 50% and treated medically. No patient had signs of hemolysis. There were no relevant changes in hemoglobin and hematocrit after thrombectomy. Results are shown in Table 12.3. Follow-up Three months after intervention, the mean ABI was 0.84 ± 0.20 (range 0.52–1.07).
Restenosis and late outcome Three restenoses were observed. Two at 6 months: 2/21 patients, 2/26 lesions (two in-stent restenosis: one Expander and one Optimed). One patient treated by Rotarex and PTA alone for a severe long in-stent restenosis (90% in diameter stenosis, 100 mm in length, Optimed stent), had an occlusion of the left SFA at 4 months treated by femoropopliteal bypass surgery. The other patient was also treated by Rotarex and PTA alone for a severe in-stent restenosis (90% diameter stenosis, 30 mm in length, Expander stent) of the low part of the left SFA, and developed an occlusion at 6 months which was treated medically. The third restenosis occurred at 9 months in a patient who had been treated for a de novo lesion (75% diameter stenosis, 10 cm in length) in the mid part of a small left SFA (maximum lumen diameter 3 mm). This restenosis was treated by femoropopliteal bypass surgery at 9 months. At a mean follow-up of 9.6 ± 2.7 months, all patients were asymptomatic and in class I of Fontaine’s classification.
Discussion In the last decade, great efforts have been made to provide an alternative to time-consuming local fibrinolysis and surgical thrombectomy in the treatment of arterial thrombosis. Percutaneous aspiration thrombectomy through thin-walled, straight catheters is still a common, readily available, simple and cost-effective technique for the removal of fresh thrombi.25 Its restriction to loose – that is, not adherent – thrombi, the necessity of usually several passes, and the risk of plaque avulsion and antegrade dissection have, however, led to the construction of more sophisticated devices.26 Devices to debulk arteries with severe chronic atherosclerotic stenoses prior to angioplasty and stent have been developed. The expectancy was to decrease post-angioplasty residual stenoses and restenosis rates.
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(a)
(b)
(c)
(d)
(e)
(f)
75
Figure 12.6 (a) SFA in-stent restenosis; (b) Rotarex; (c) result after Rotarex; (d) ballon angioplasty; and (e-f) final result after balloon angioplasty.
The experience with the first catheter equipped with a fast-rotating, coaxially driven cam (Trac-Wright, formerly Kensey) was disappointing. The device was, however, the predecessor of several generations of rotational catheters,27,28 which can be roughly classified into two types of devices: ●
●
those using recirculation, e.g. pulverization of thrombi by a hydrodynamic vortex created either by a high-speed impeller1,29–31 or the Venturi effect;12,17,32 non-circulation catheters with concomitant suction, using either a rotating recessed propeller33,34 or rotating cutting blades35,36 and aspiration via a roller pump or any other suction modality.37
These devices are effective in clearing fresh thrombi, especially in arterial and hemodialysis grafts; however, their effectiveness decreases with the age of thrombi and their adherence to the vessel wall. Since many occlusions are “acute or chronic” thromboses, a thrombectomy device should have the potential to remove not only fresh but also underlying organized thrombi. Furthermore, it should track over a guidewire in order to prevent vessel perforation. Finally, it should transport the occlusion material to the outside without the risk of peripheral embolization. The new Rotarex catheter described here meets many of these requirements: its construction is relatively simple, using only one lumen for the spiral and coaxial guidewire. No extra channels for suction, lubrication, or cooling are needed.
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(a)
(b)
(c)
(d)
(e)
(f)
Figure 12.7 (a) SFA in-stent restenosis; (b) Rotarex; (c) result after Rotarex; (d) balloon angioplasty; and (e–f) final result after balloon angioplasty.
The transport of the occlusion material is done exclusively by the spiral. Some devices are easily obstructed by sticky occlusion material, especially by fibrin, which has to be transported through a narrow catheter over a distance of 80 to 100 cm. In the new catheter, this drawback was eliminated by a special coating of the spiral and by adjusting the rotational speed
Table 12.2
to 40,000 rpm. As with all rotating devices, heat caused by friction can be a problem.14 The new device needs blood for lubrication. Therefore, it should not be advanced continuously in an occlusion, but in gentle forward and backward movements, allowing the uninterrupted aspiration of blood and avoidance of running dry. Provided these precautions were observed, no
Angiographic results
Before atherectomy After atherectomy After procedure (PTA + stent)
Mean arterial diameter (mm)
Minimal lumen diameter (mm)
Mean stenosis (%)
5.4 ± 0.8 5.3 ± 0.9 5.4 ± 0.7
1.4 ± 0.6 3.2 ± 0.4 5.2 ± 0.8
83.5 ± 7.9 36.8 ± 15.1 2 ± 3.5
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A new rotational thrombectomy and atherectomy catheter: the Rotarex system Table 12.3 Hematocrit percentage and hemoglobin percentage before and after
Before After
Hematocrit (%)
Hemoglobin (g/dl)
40.0 ± 4.1 38.0 ± 4.3
13.5 ± 1.4 12.7 ± 1.5
undue warning of the catheter was noted. The average time for thrombectomy or atherectomy in these two pilot studies was short and did not exceed 90 seconds for occlusions up to 15 cm in length or long severe stenoses. Blood loss during thrombectomy or atherectomy is generally low, amounting to 80–90 ml/minute, depending on the composition of the occlusion material that has to be transported and the blood available in the artery. A useful parameter for the assessment of the efficacy of a thrombectomy catheter is the radial force coefficient; that is, the ratio of the lumen recanalized by thrombectomy to the catheter diameter. For this new catheter, the coefficient is 2 in vitro, meaning that the catheter with a diameter of approximately 3 mm clears a thrombus of 6 mm. In vivo the radial expansion coefficient depends on the composition of the occlusion material. It is about 2 in fresh thrombi but drops to 1 in solid material, which means that the reopened or debulked lumen corresponds to the diameter of the catheter head. Experimental data suggest use of the catheter for the treatment of obstructed vessels with a diameter up to 8 mm. These studies showed its feasibility and efficacy in superficial femoral or popliteal arteries of 5–7 mm diameter. Its applicability in larger vessels, such as pelvic arteries, vena cava, or pulmonary arteries, needs to be validated in further trials. Zeller et al.24 treated 16 iliac artery occlusions but was not able to remove all thrombi from the vessel. A disadvantage of the Rotarex catheter must be pointed out. It seems not well suited for lengthy occlusions bypass beginning near the origin of the SFA or femoropopliteal bypass grafts in the crossover technique. The catheter is too short, so the occlusion cannot be traversed throughout in its entire length. Furthermore, with an acutely angled aortic bifurcation the rotating spiral can be distorted so that it blocks up or breaks.2,4 Nevertheless, the Rotarex can be used in obtuse bifurcation angle as we showed in our series. Compared with other thrombectomy or atherectomy devices, the potential of the Rotarex catheter to remove not only fresh loose thrombus but also solid, organized occlusion material must be considered as an advantage. With fresh thrombi we may expect to remove all the material, but with organized occlusion it remains, in most cases, a residual stenosis, so we have to treat either by PTA alone or PTA plus stent. The catheter can also treat calcified plaques but seems less efficient than the Rotablation atherectomy catheter (Rotablator), in particular in small distal peripheral arteries.5 The risk of perforation is high in calcified arteries. Therefore, adjunctive PTA after atherectomy or atherectomy is often necessary to eliminate residual stenosis. We expect that debulking prior to angioplasty can avoid stenting in peripheral arteries and decrease the restenosis rate at follow-up, but we have no proof and further large-scale
77
randomized studies are needed. Debulking could be useful to treat long lesions of the SFA before angioplasty and before placing long covered stents, to have a good expansion of this stent. As shown in arterial models, the wire-guided catheter removes thrombus or atherosclerotic material without intimal abrasion, severe arterial dissection or perforation if the original caliber of the artery is larger than the catheter head. Consequently, the catheter in the 8-French version is not suitable for thrombectomy or atherectomy in vessels distal to the popliteal artery. For use in small vessels, a 5-French version is needed. Hemolysis occurs in recirculation catheters without aspiration, but its clinical effect seems minimal. In these small studies no change in hemoglobin or hematocrit was noticed after thrombectomy or atherectomy. Except for a small embolus on a posterior tibial artery after thrombectomy, which was removed by focal fibrinolysis, and one in a distal leg artery after atherectomy, treated successfully by thrombosuction, no relevant complications occurred. It can be assumed that the negative pressure built up by the catheter system is sufficient to avoid peripheral embolization. Nevertheless in other publications some embolizations were reported.22–24 As expected from the preclinical tests, the catheter was easy to handle and helped to save considerable time by shortening thrombectomy to a few minutes, thereby avoiding lengthy procedures such as local fibrinolysis or surgical intervention. The potential benefit of debulking could be to reduce the restenosis rate (we observed only three cases of restenosis in the 26 lesions treated, 11.5%) and treatment of some difficult lesions not well treated by PTA alone. Indications for treatment with the Rotarex system could be: ● ● ●
● ● ●
● ●
as a thrombectomy device; thrombotic lesions; acute and subacute occlusions and particularly femoropopliteal lesions; as an atherectomy device; in-stent restenosis; ulcerated, embolic, eccentric, ostial, and long lesions (either stenosis or occlusion); as we have seen, debulking long lesions could be useful before placing long stent; bifurcated lesions; calcified lesions (but the Rotablator, whose safety and efficacy has been well documented, could be better for this type of lesion, and particularly in small vessels). The risk of perforation seems higher in calcified lesions.
Due to the efficacy and safety, the potential benefit of such a debulking device for the treatment of peripheral stenoses or occlusions has to be well evaluated. The immediate, mid- and long-term results of this technique compared with those obtained with conventional therapy (PTA plus stent) in larger multicenter randomized series, show that use of this device greatly increases the duration and cost-effectiveness of the procedure. Theoretical advantages of debulking techniques are tissue removal, the stepwise controlled approach and reduced mechanical trauma to the vessel wall (less “overstretching”). Its limitations
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are specific complications (possibility of stent damage, perforation, dissection), duration of the procedure, and costs.
Conclusion The Rotarex system is a thrombectomy and atherectomy catheter, which is easy to handle. Its feasibility and efficacy has already been published for the treatment of acute and subacute occlusions avoiding or reducing lytic substances. Few publications were done on the treatment of chronic arterial occlusive disease using the Rotarex system. It appears feasible and safe in
arteries > 4–5 mm in diameter. The main limitation is the difficulty to treat long lesions beginning at the SFA origin, this device is not well suited for the crossover technique. Immediate and mid-term results are promising with a low restenosis rate. Indications for this device have to be determined but is seems that long lesions and in-stent restenosis could be better treated with this device than with PTA alone. Larger randomized studies (atherectomy vs. conventional angioplasty) are needed to evaluate if atherectomy before angioplasty could avoid stenting in arteries < 6 mm in diameter, reduce the restenosis rate, and improve the clinical outcome.
REFERENCES 1.
2. 3. 4. 5.
6. 7. 8. 9. 10. 11.
12. 13. 14. 15.
16. 17. 18.
19.
Simpson JB, Johnson DE, Thapliyal HV et al. Transluminal atherectomy: a new approach to the treatment of atherosclerotic vascular disease. Circulation 1985; 72(suppl III): III-I I I-III-146 (abstract) Simpson JB, Robertson GC, Selmin MR. Percutaneous coronary atherectomy. J Am Coll Cardiol 1988; 11(suppl A): 100A (abstract) Simpson JB. Future interventional techniques. In: Califf RM, Mark DB, Wagner GS, eds. Acute Coronary Care in the Thrombolytic Era. Chicago: Year Book Medical, 1988: 392–404 Simpson JB, Selmon MR, Robertson GC et al. Transluminal atherectomy for occlusive peripheral vascular disease. Am J Cardiol 1988; 61: 96G–101G Henry M, Amor M, Ethevenot G et al. Percutaneous peripheral rotational ablation using the Rotablator: immediate and mid-term results. Single center experience concerning 146 lesions treated. Int Angiol 1993; 12: 231–44 Hoshino S, Midorikawa H. Clinical results of directional peripheral atherectomy. Nippon Geka Gakkai Zasshi 1996; 97: 568–73 White CJ. Peripheral atherectomy with the Pullback atherectomy catheter: procedural safety and efficacy in a multicenter trial. PAC investigators. J Endovasc Surg 1998; 5: 9–17 Gammo R. Plaque excision treatment of infrainguinal PAD. Endovascular Today 2005; 4: 70–4 Soulen MC; Zaetta JM, Amygdalos MA et al. Mechanical declotting of thrombosed dialysis grafts: experience in 86 cases. J Vasc Interv Radiol. 1997; 8: 563–7 Bildsoe MC, Moradian GP, Hunter DW et al. Mechanical clot dissolution: new concept. Radiology 1989; 171: 231–3 Schmitz-Rode TH, Adam G, Kilbinger M et al. Fragmentation of pulmonary emboli: in vivo experimental evaluation of two highspeed rotating catheters. Cardiovasc Intervent Radiol 1996; 19: 165–9 Bucker A, Schmitz-Rode T, Vorwerk D et al. Comparative in vitro study of two percutaneous hydrodynamic thrombectomy systems. J Vasc Interv Radiol. 1996; 7: 445–9 Reekers JA, Kromhout JG, Van Der Waal K. Catheter for percutaneous throombectomy: first clinical experience. Radiology 1993; 188: 871–874 Nazarian GK, Qian ZQ, Coleman CC et al. Hemolytic effect of the Amplatz thrombectomy device. J Vasc Interv Radiol 1994; 5: 155–160 Beyer Enke SA, Deichen J, Zeitler E. The long-term results after Hydrolyser-supported angioplasty – a prospective study (in German). Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr. 1999; 171: 126–9 Rousseau H, Sapoval M, Ballini P et al. Percutaneous recanalization of acutely thrombosed vessels by hydrodynamic thrombectomy (Hydrolyser). Eur Radiol. 1997; 7: 935–41 Henry M, Amor M, Henry I et al. Thrombectomy with the hydrolysing catheter. A propos de 50 cas (in French). Arch Mal Cœur Vaiss 1997; 90: 797–804 Pitton MB, Neufang A, Duber C. Therapy of thromboembolic blockages in the crural arteries: clinical experience with the Angiojet thrombectomy catheter (in German). Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr. 1999; 171: 380–5 Starck EE, Wagner HJ. Rotation aspiration thromboembolectomy (in German). Deutsch Med Wochen schr. 1991; 161: 1–6
20. 21. 22. 23.
24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35.
36.
37.
Höpfner W, Vicol C, Bohndorf K et al. Percutaneous transluminal hydrodynamic thrombectomy – the initial results (in German). Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr. 1996; 164: 141–5 Schmitt HE, Jäger KA, Jacob AL et al. A new rotational thrombectomy catheter: system design and first clinical experiences. Cardiovasc Intervent Radiol 1999; 22: 504–9 Berczi V, Deutschmann HA, Schedlbauer P et al. Early experience and mid-term follow-up results with a new rotation thrombectomy catheter. Duc SR, Schoch E, Pfyffer M et al. Recanalization of acute and subacute femoropopliteal artery occlusions with the Rotarex catheter: one-year follow-up, single center experience. Cardiovasc Interv Radiol 2005; 28: 603–10 Zeller T, Frank U, Burgelin K et al. Early experience with a rotational thrombectomy device for treatment of acute and subacute infra aortic arterial occlusions. J Endovasc Ther 2003; 10: 322–31 Brossmann J, Muller Hulsbeck S, Heler M. Perkutane thrombektomie und mechanische Thrombolyse. Fortschr Rontgenstr 1998; 169: 344–54 Kensey KR, Nash JE, Abrahams C et al. Recanalization of obstructed arteries with a flexible, rotating tip catheter. Radiology 1987; 165: 387–9 Triller J, Do DD, Maddern G et al. Femoropopliteal artery occlusion: clinical experience with the Kensey catheter. Radiology 1992; 182: 257–61 Bildsoe MC, Moradian GP, Hunter DW et al. Mechanical clot dissolution: a new concept. Radiology 1989; 171: 231–3 Pozza CH, Gomes MR, Qian Z et al. Evaluation of the newly developed Amplatz maceration and aspiration thrombectomy device using in vitro and in vivo models. AJR 1994; 162: 139 Uflacker R. Mechanical thrombectomy in acute and subacute thrombosis with the use of the Amplatz device: arterial and venous application. J Vasc Intervent Radiol 1997; 8: 923–32 Rilinger N, Görich J, Scharrer-Pamler R et al. Short-term results with the use of the Amplatz thrombectomy deice in the treatment of acute lower limb occlusions. J Vasc Intervent Radiol 1997; 8: 343–8 Guenther RW, Vorwerk D. A new aspiration thrombectomy catheter with propeller tipped rotating wire: in vitro study. J Intervent Radiol 1990; 1: 17–20 Guenther RW, Vorweck D. Aspiration catheter for percutaneous thrombectomy: clinical results. Radiology 1990; 175: 271–273 Yedlicka JW, Carlson JE, Hunter DW et al. Thrombectomy with the transluminal endarterectomy catheter (TEC) system. J Vasc Intervent Radiol 1991; 2: 343–7 Rillinger N, Görich J, Scharrer-Palmer R et al. Percutaneous transluminal rotational atherectomy in the treatment of peripheral vascular disease using transluminal endarterectomy catheter (TEC): initial results and angiographic follow-up. Cardiovasc Intervent Radiol 1997; 263: 267 Müller-Hülsbeck S, Schwarzenberg H, Bangard C et al. Saugpumpenunterstützte Aspirationthrombektomie: in vitro Vergleich mit einem. Thrombusfragmentierungsverfahren Fortschr Rontgenstr 1998; 162: 191–4 Gehani AA, Rees MR. Can rotational atherectomy cause thermal tissue damage? A study of the potential heating and thermal tissue effects of a rotational atherectomy device. Cardiovasc Intervent Radiol 1998; 21: 481–6
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Orbital atherectomy system: a novel means of peripheral vascular rotational atherectomy DT Cragen and RR Heuser
Introduction Balloon angioplasty and stenting in the peripheral vasculature is an immensely valuable tool that remains limited by the fact that the occlusive plaque is simply displaced and not removed. Long peripheral lesions or calcified lesions can present a significant challenge to the interventionist as they may not be easily displaced. Furthermore, restenosis rates continue to limit the success of percutaneous peripheral interventions and debulking the plaque with minimal injury to the vessel wall remains an elusive goal. The Orbital atherectomy system (OAS) (Cardiovascular Systems, Inc., St. Paul, MN) is a novel device utilizing a diamond-embedded, eccentrically mounted crown spinning at high rotational speeds to “sand” and debulk the lesion and provide safe, effective, and efficient atherectomy. Previous use of rotational atherectomy in the peripheral vasculature using a centrally mounted burr was limited by heat generated by the device, large access sheath sizes required to deliver large burrs, and inadequate atherectomy in many cases due to unavailability of burr sizes to match the lumens of larger vessels. The use of rotational atherectomy in the coronary bed with the currently available device, the Rotablator (Boston Scientific, Natick, MA), has also been limited by the heat generated by the rotating burr and by the occlusive burr which prevents antegrade flow while engaged with the lesion.
Device description The OAS uses an eccentrically mounted crown embedded with diamonds about its midsection to ablate tissue endovascularly (Figure 13.1). The OAS is advanced over a 0.014-inch guidewire to just outside the sheath. The OAS crown and sheath are then connected to a 0.9% saline bag and the nitrogen gas-based controller console. The sheath is flushed with the saline and the device is staged outside the body to deliver the desired level of revolutions per minute (rpm). Once appropriately staged, the device is then introduced through the sheath (all current crowns can be advanced through a 6-French sheath) and advanced to the site of stenosis. At the site of stenosis, the crown is activated. Multiple passes can be made through the lesion during each 30-second run. The crown is advanced and withdrawn using the drive shaft and handle with a maximum 7 cm excursion on each pass.
The eccentric position of the crown’s center of mass results in an orbital motion about the center of the wire and results in an achieved lumen that is significantly larger than the crown size itself (Table 13.1). Because the abrasive diamond particles are situated on the widest point of the device at its midsection, it can safely ablate tissue both on forward and backward motion of the device within the area of stenosis. At the end of each run, angiography determines whether further passes are necessary. As the device is operated and plaque is removed, the force exerted on the plaque decreases gradually as the radius of orbit increases. If a larger lumen is desired with the current crown, the rpm can be increased successively to 140,000 and maximally to 200,000. Each increase in driving speed results in an increased orbit of the device and an increased achieved lumen diameter. Increasing the speed of the device, also augments the force exerted on the atheroma, in addition to increasing the achieved lumen size. The crown can then be removed and exchanged for a larger crown if further atherectomy is required. Alternatively, angioplasty and stenting can proceed as indicated. The eccentric, semi-elliptical shape of the crown was designed in part to allow blood and saline infusions to pass while ablation is proceeding. This reduces heat build-up within the lesion, which has been shown to stimulate restenosis in coronary trials of the Rotablator device. The OAS drive shaft is powered by a compressed gas turbine (usually containing nitrogen). The speed of the drive shaft is regulated by a pressure valve located on the front panel of the OAS controller console (Figure 13.1). The pressure valve is adjusted with each crown before the device is introduced into the sheath to calibrate for the desired rpm. It can then be recalibrated in the body to adjust the speed as necessary. An electrical footswitch is used to control the flow of saline through the device’s sheath used for cooling and lubrication. The footswitch also activates and deactivates the gas turbine that drives the device.
Preclinical testing Significant preclinical testing was performed on the OAS in vitro, ex vivo, and in animals to document safety and efficacy.1 In vitro studies included characterization of the 79
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(a)
(b)
(c) Figure 13.1 OAS components: (a) single-use disposable catheter/crown device with controller console; (b) Orbital atherectomy device with handle and diamond-embedded crown tip; and (c) close-up of Orbital atherectomy sheath and crown showing the eccentric crown with a mid-crown band of abrasive diamond coating.
behavior of the different crown sizes at various speeds and determined the maximum orbits (Table 13.1). When large amounts of atheroma are removed and released into the bloodstream, distal microvasculature plugging can occur and lead to the no-reflow phenomenon (absence of flow with a patent vessel). Extensive testing of the OAS device was performed in ex vivo studies to quantify downstream particle size. Using explanted, artificially perfused porcine coronary arteries as the model, the downstream particles were collected and analyzed. A mean
particle size, regardless of the crown size used, of 1.7–3.1 µm was observed. Nearly 99% of the particles collected were < 5 µm and 99.7% were < 20 µm. Therefore, approximately 99% of all particles liberated during atherectomy with OAS are smaller than a red blood cell and should pass through the capillaries and be removed by the reticuloendothelial system. During animal studies, OAS was used on porcine peripheral arteries 1 month after injury by balloon angioplasty. There were no significant complications observed during treatment (i.e. no
Table 13.1 The three currently available crown sizes and their achieved maximal lumen diameters at the three recommended rotational speeds are shown. Note that all three crowns can be introduced through a 6-French sheath Crown size (mm) 1.2 1.7 1.9
Rotational speed (rpm) 80,000 140,000 200,000 80,000 140,000 200,000 80,000 140,000 200,000
Maximum lumen diameter (mm) 1.7 2.0 2.4 2.7 3.3 3.6 3.5 3.8 4.5
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(c) Figure 13.2 CaptionCase study: (a) Baseline angiography shows 8–9 cm total occlusion of the mid-distal right superficial femoral artery with extensive collateral vessel recruitment and flow; (b) the 1.9 mm crown is being passed through the lesion increasing the rotational speed with each pass; and (c) final results after atherectomy with resolution of the chronic total occlusion and much less prominent collateral vessels.
perforations, dissections, reflow, or significant distal embolization) and all debulking efforts were successful. Histopathologic examination of the explanted vessed showed no evidence of device-related vascular wall injury in the majority of treated arteries. The most severe injury observed was limited to the internal elastic lamina and did not extend to the adventitial layer.
Clinical studies In the US, a single-arm, prospective, multicenter trial is underway in patients with at least one treatable de novo stenosis < 10 cm in
length in an infrainguinal peripheral artery. The study is designed to establish both the safety and efficacy of the device and has nearly completed enrollment. The primary efficacy endpoint is the mean decrease in percentage diameter stenosis of the target lesions. The primary safety endpoint is the occurrence of severe adverse events at 30 days. Secondary endpoints include procedural success as quantified by angiography; overall clinical status of the patient at 1 and 6 months of follow-up; incidence of adverse events and 1 and 6 months; incidence of symptomdriven target lesion revascularization at 6 months; change in ankle–brachial index (ABI); and the degree of clinical improvement using Rutherford and Becker’s scale at 1 and 6 months.
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Currently, the OAS is only available in the US as an investigational tool within this ongoing study.
Case study A 75-year-old woman with a long history of tobacco use, hypertension, and hyperlipidemia and known to have peripheral vascular disease presented with rest ischemia of the right foot. An ABI of 0.1 was obtained in the right foot and 0.5 in the left foot. She was referred for angiography and endovascular intervention. Vascular access was obtained via a contralateral femoral approach and a 6-French access sheath was advanced across the aortic bifurcation to the right common femoral artery. An 0.035” Glidewire was then advanced across the chronic total occlusion and a 4-French GlideCath was advanced over the Glidewire to the popliteal artery. The Glidewire was then removed and replaced with a 0.009-inch atherectomy guidewire through the GlideCath which was then removed. A 1.7-mm OAS crown was then used to make three passes through the area of occlusion at 80,000, 140,000, and finally 200,000 rpm. Angiography still confirmed significant stenotic disease and we exchanged the crown for a 1.9-mm OAS crown and repeated three passes through the stenosis at the recommended three speed settings. Angiography then confirmed excellent antegrade flow with markedly fewer recruited collateral vessels. No further treatment was provided at the site of occlusion. The total OAS operation time was < 150 seconds. The patient had no significant complications and was discharged home the following day on aspirin and clopidogrel. The patient had immediate relief of her rest foot pain and her ABI improved significantly from 0.1 to 0.45. In this case, use of the OAS resulted in recanalization of a chronic total
REFERENCES 1.
Heuser RR, Safian R, Bosiers M, et al. Orbital Atherectomy. Endovasc Today 2006; (5)9: 20–6
occlusion with < 30% residual stenosis and relief of critical limb ischemia. There was no need for further angioplasty or stenting at the treated site.
Discussion Peripheral arterial disease is a serious, debilitating disease affecting millions of people worldwide. The OAS is a novel means of performing fast, efficient, safe, and efficacious debulking of the occlusive atheroma in the peripheral vasculature. Theoretically, its biggest advantages over currently available techniques include efficient removal of plaque, minimal injury of the vessel wall, and the ability to easily adjust the crown size and/or the rotational speed to obtain a larger vessel diameter. Previous attempts at rotational atherectomy in the peripheral arteries have been limited by inability to upsize the burr without upsizing the delivery sheath to match the burr size. The eccentric design of the OAS crown allows the operator to obtain lumens up to 4.5 mm through a 6-French sheath system and thereby minimize access-site complications. Furthermore, heat build-up at the site of ablation (which is associated with vascular restenosis) is decreased with the eccentric crown, which allows blood and saline to flow through the vessel while ablation is proceeding. The OAS is currently undergoing a clinical trial in the US to determine its safety and efficacy in the peripheral arterial system. In addition, the FDA has been petitioned to allow investigational use of the OAS system within the coronary arteries. Initial clinical results with the OAS in infrainguinal lesions have been promising and we eagerly await further safety and efficacy results from the ongoing trial.
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Subintimal angioplasty G Markose and A Bolia
Background It has been almost 20 years since subintimal angioplasty (SIA) was first described. This technique has now enjoyed broad clinical acceptance as well as a resurgence of interest and application. Originally used in the femoropopliteal segment, its role has been extended to the treatment of infrapopliteal lesions, including the recanalization of the trifurcation and long tibial occlusions, as well as in the iliac segment and occasionally in the subclavian artery. Experienced centers have repeatedly reported primary success rates of around 90% in the infrainguinal vessels, as well as 1-year limb salvage rates as high as 85–90%, and 5-year primary assisted patency rates of 64% while not interfering with subsequent vascular surgery. Indeed subintimal angioplasty has proved to be very effective in lower-limb ischemia management, both for intermittent claudication and critical ischemia. Currently the “gold standard” of management of peripheral arterial stenosis and occlusion is by restoration of the arterial flow by direct arterial revascularization using autogenous reversed saphenous vein grafts. However many patients with peripheral vascular disease usually have several other co-morbidities, such as heart disease, diabetes, and renal failure, that would put them at higher surgical and anesthetic risk. Surgery has been shown to be associated with increased mortality (30-day survival of 96 vs. 100% for angioplasty) and morbitidy.1 Vein harvest site and graft infections can be devastating when they occur. In addition, some patients may not have an adequate amount of saphenous vein to harvest to allow for autologous saphenous vein grafting, and alternative conduits are required. This, in turn, decreases graft patency and limb salvage rates, with 3-year limb salvage rates decreasing to 95% using arm vein and 75% using prosthetic materials for superficial femoral artery arterial disease.2 The techniques of Dotter3 and Gruntzig4 revolutionized the treatment of peripheral vascular disease, heralding the arrival of endovascular treatment techniques such as percutaneous transluminal angioplasty (PTA). PTA is now an established technique for the treatment of peripheral vascular disease, widely used in the treatment of stenotic and occlusive lesions in the lower-limb arteries. Unfortunately the primary success rates and long-term outcomes of PTA in the recanalization of long occlusions have been unsatisfactory. Subintimal angioplasty, sometimes described as percutaneous intentional extraluminal recanalization (PIER) was first introduced in 1987 to treat femoropopliteal occlusive disease in intermittent claudication.5 Since that time, this technique’s
success has seen its use extended to treatment of stenotic and occlusive lesions in the iliac and popliteal arteries, trifurcation, and crural vessels where it has found an important role in the management of critical limb ischemia. Recent studies have shown that SIA can produce good results not only in chronic critical limb ischemia but also in intermittent claudication. SIA can now help to extend the scope of endovascular therapy to include a large number of previously untreatable femoropopliteal and tibial occlusions and helps by increasing the long-term patency in these vessels. SIA can be attempted on those patients deemed poor candidates for surgery due to the anesthetic risks or because they have insufficient vein to allow bypass grafting, and also in patients with flush occlusions of the SFA. In addition SIA can be used to re-open occluded native vessels following graft occlusion.6,7 The technique is simple, inexpensive, has low complication rates, good primary success rates, and good long-term outcomes.
Indications SIA dramatically increases the limits of endovascular treatment compared to conventional PTA. These include: 1. Chronic occlusions that have hardened with time, and where an intraluminal approach would fail. A subintimal dissection plane in these circumstances is relatively easily made. 2. Long occlusions where an intraluminal position of the guidewire would be hard to maintain. 3. Previously failed PTA. 4. Flush SFA occlusions (with a very small stump or no stump at all). Conventional PTA is very difficult or impossible in these situations. 5. Long length stenoses that normally have poor outcome with PTA. 6. Heavily calcified vessels. Often these are difficult to treat by PTA, but can be more easily managed by SIA as the wire follows the path of least resistance along the subintimal plane. 7. Diffusely diseased vessels that frequently have occlusions that are not treatable intraluminally. 8. Occluded native artery in situations where the bypass graft has failed. 9. Popliteal occlusions that extend into the trifurcation vessels, allowing reconstitution of some or all of the run-off vessels. 83
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A = Atheroma L = True vessel lumen S = Subintimal channel
A
L
(e) Cross Sectional Representation of Artery
Pre angioplasty
L
(a)
(b)
(c)
A
Post angioplasty
S
A
(d )
Figure 14.1 Diagrammatic representation of subintimal dissection: (a) The guiding catheter is brought up to the occlusion and directed towards the vessel wall; (b) the guidewire and catheter are introduced into the subintimal space; (c) a loop is formed with the proximal end of the guidewire and advanced to dissect through the subintimal space; (d) the loop is then used to break back into the true lumen; and (e) the atheroma and other occluding material is displaced laterally following angioplasty creating a newly opened subintimal channel.
10. When an arterial perforation occurs during an attempt at PTA, a subintimal dissection channel can be used to exclude the perforation site.
Technique Technique for femoropopliteal lesions The aim of SIA is to intentionally dissect into the subintimal space, below the intima but above the media within the vessel wall, past any intraluminally sited occluding material, re-enter the vessel lumen distally, and dilate the whole length of the dissection with a balloon.5,8–10 In the treatment of SFA disease, usually an ipsilateral antegrade puncture is made in the common femoral artery for occlusions that begin close to the origin of the SFA. (A contralateral retrograde puncture can be used with an “up and over” technique across the aortic bifurcation, particularly in obese patients, but this allows less control.) Using SIA, only a very small stump (5 mm or less) of proximal vessel (e.g. SFA) is required to start the dissection plane. When a reasonable length of proximal SFA is available, then the puncture can be made selectively into the SFA itself. Catheters with an angled tip, such as a 4-French Bolia minicatheter (Terumo, Japan) or a 5-French Cobra-type catheter (Cook, UK) are useful to help direct the end of the guidewire towards the vessel wall to break into the subintimal space for proximal SFA lesions. Alternatively a 5-French Van Andel-type predilating catheter (Cook, UK)11 can be used. The catheter is antegradely introduced up to the origin of the occlusion. Heparin (3000–5000 units) is injected intra-arterially prior to
crossing the lesion. Tolazoline (5 mg), a vasodilator that helps to dilate the distal vessels and decreases the possibility of spasm during the procedure, can also be given intra-arterially. The catheter tip is brought up to the level of the occlusion (Figure 14.1a), and a curved tipped hydrophilic guidewire (Terumo, Japan) is used to enter the occlusion and then subsequently traverse the length of the occlusion (Figure 14.1b). The guidewire tip should be directed towards the vessel wall and away from any important collateral vessels that may be present. The guidewire, with the support of the catheter, is then advanced into the junction between the occluding material and vessel wall. In the majority of cases the guidewire advances into a dissection channel in the subintimal space, this being the path of least resistance. Entry into the subintimal space can be confirmed by injecting a small volume of dilute contrast medium. If a Bolia mini-catheter is used, once the initial dissection has been made, this can be exchanged for 5-French balloon catheter (usually 5–6 mm in diameter and 4 cm long). When it is in the subintimal space, the guidewire usually moves relatively freely with little resistance. Increased resistance is found in previously angioplastied vessels and sometimes in heavily calcified vessels. The guidewire is then manipulated to a form a U-shaped loop of ideally 3–5 cm in length (Figure 14.1c). The leading edge of the loop is then used to advance the dissection distally. The catheter provides support while it and the guidewire are advanced distally along the length of the occlusion. The guidewire is advanced first, followed by the catheter. If the guidewire fails to advance further, due to resistance, the catheter should then be advanced to provide support to one arm of the loop. This allows the dissection to be continued until the distal end of the occlusion is reached. Once this point has been reached, it is recommended
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(a)
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(d)
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Figure 14.2 (a–c) This patient has a moderate length occlusion of the SFA in the mid thigh with good distal run-off; (d, e) successful recanalization of the occluded segment was achieved subintimally.
to shorten the loop length to 2–3 cm. Further advancement of the guidewire can then result in the guidewire loop reentering the true lumen (Figure 14.1d). Adjunctive procedures such as a slight twisting or screwing action can help to re-enter the true lumen. Re-entry is marked by a sudden decrease in the resistance to forward pressure on the guidewire, and can be confirmed by advancing the catheter into the distal artery and injecting a small volume of contrast medium. A relatively disease-free vessel distal to the stenosis or occlusion is favorable to achieving re-entry. Occasionally the dissection channel has to be extended beyond the occlusion to obtain re-entry, usually as a result of diffuse vessel wall disease being present distal to the occlusion. Generally, extension of the dissection channel more distally is not significant, unless a major collateral becomes compromised and vessel lumen re-entry is not obtained. Because of this, it is advisable not to breach any major distal artery collaterals in the learning phase of this technique. In cases where luminal re-entry is problematic, IVUSguided (Pioneer, Medtronic, USA) and fluoroscopically guided (Outback, Cordis Corporation, USA) re-entry catheters are now available which are reported to have good success.12 If not already exchanged for a balloon catheter, once the lesion is crossed the guiding catheter is exchanged for a 5- or 6-mm-diameter 5-French balloon catheter. The entire length of the subintimal channel is then dilated, in a distal-to-proximal direction using short (5–10 seconds) inflations of approximately 10–12 atmospheres (Figures 14.2–14.4). Flow is assessed by the injection of small volumes of contrast medium, and flow impairment can be treated with repeated balloon inflation. Any residual stenosis of greater than 30% is repeatedly balloon dilated, including the use of higher inflation pressures. Refractory stenoses may require placement of a stent in the affected region.
Following successful recanalization, aspirin, if not contraindicated, is advised, usually 150 mg daily for at least 3 months. Oral anticoagulants such as warfarin or other antiplatelet agents do not have to be routinely given, unless already used for other clinical indications. Technique for tibial lesions SIA is useful in long (greater than 3 cm) occlusions of the tibial vessels. The technique is similar to that used for femoropopliteal lesions, with several modifications. A balloon catheter (usually with a 3-mm-diameter, 2-cm-long balloon on a 120-cm-long 5-French shaft) is used to primarily cross and dilate the lesion rather than using a guiding catheter. Of note, in treating tibial stenotic and occlusive disease, it is important to use a 0.035 guidewire system and catheters with a 5-French shaft. The resistance encountered when crossing a long tibial vessel occlusion (greater than 20 cm) can be substantial and this larger system has enough strength to allow the combination of catheter and guidewire to progress along the entire length of the occlusion. Again, a U-shaped loop is formed in the hydrophilic guidewire. The loop length is kept shorter (2–3 cm), so that only the soft part of the guidewire makes the leading edge of the loop. This decreases the likelihood of perforation in these smaller and more delicate vessels. The loop is used to achieve the dissection throughout the length of the tibial vessel and also to obtain distal true lumen re-entry. If resistance prevents passage of the guidewire/catheter system distally through the subintimal space, the system can be strengthened by the use of a half-stiff or stiff hydrophilic guidewire (Terumo, Japan). In the more distal arterial tree, the intima becomes thinner, and thus it is usually not difficult to enter the true lumen in
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(a)
(b)
(c)
(d)
Figure 14.3 (a, b) This patient has a full-length flush occlusion of the SFA in the thigh; (c, d) successful recanalization of the entire length of the SFA was achieved with subintimal angioplasty.
the distal tibial vessels. Once the lesion has been crossed, balloon dilatation is then performed similar to that in the femoropopliteal segment (Figures 14.5 and 14.6). Technique for iliac vessels SIA can be used for total occlusions of the iliac vessels. Ideally this should be done in a craniocaudal direction to prevent continuing the dissection plane into the aorta. This therefore requires either a contralateral (“up and over”) femoral approach, or a combined ipsilateral and contralateral femoral approach, or a combined approach via the brachial or axillary artery and the ipsilateral femoral artery. The latter allows the treatment of bilateral iliac artery occlusions. Using the contralateral femoral approach, either a SosOmni (Angiodynamics, USA), Simmons 1 or 2, or Renal (Cordis Corporation, USA) catheters can be used (depending on the angle of the aortic bifurcation) to cannulate the diseased (ipsilateral) iliac vessel and to then abut the occlusion. A loop is formed with a hydrophilic guidewire just proximal to the lesion and a subintimal dissection is performed, as described earlier, with the loop as the leading edge in a cranialto-caudal direction, followed by the catheter. As the end of the lesion is approached, the loop is shortened to allow easier reentry into the true lumen. True lumen re-entry is confirmed with a small test injection of contrast medium. If not already
done so, the catheter is exchanged for an appropriately sized balloon angioplasty catheter, and angioplasty performed. The presence of residual stenosis can be assessed by further injections of contrast medium. Any residual stenosis can then be re-dilated. Occasionally a resistant stenosis may require the insertion of a stent, which is placed in a similar way to conventional intraluminal stenting. Longer lesions may require a combined contralateral and ipsilateral approach.13 In addition to cannulating the diseased iliac vessel from the contralateral side and commencing a craniocaudal dissection, as described above, a caudocranial dissection is commenced from the ipsilateral side. The dissection channels then meet up, and one of the guidewires can then be passed through the whole length of the lesion. Sometimes a snare is required to capture the guidewire and pull it through the lesion from one side to another. Angioplasty is performed as described earlier, and occasionally stenting is required for refractory stenosis. Similarly, bilateral iliac vessel and distal aorto-iliac occlusions can be treated by commencing a craniocaudally directed subintimal dissection via a puncture in the left brachial or axillary artery, and retrograde caudocranial-directed subintimal dissections via the femoral arteries. The craniocaudal dissection requires placement of a sheath in the left axillary or brachial artery. A guiding catheter, such as a 5-French vertebral or Van Andel catheter, is then advanced over the wire to just cranial to the vessel occlusion. A loop is then formed with
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(e)
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Figure 14.4 (a–c) Further example of a full-length flush occlusion of the SFA with good distal run-off; (d–f) treated successfully with subintimal angioplasty. Note the relative smoothness of the subintimal channel unaffected by intraluminal debris.
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Textbook of peripheral vascular interventions Retroperitoneal hemorrhage The treatment of flush occlusions of the SFA by SIA sometimes requires a high antegrade puncture of the common femoral artery. This puncture needs to be high enough to allow catheter and guidewire manipulation into the occluded SFA, but not so high as to risk retroperitoneal hemorrhage. In these high puncture situations, the medical and nursing carers must be informed so as to be extra vigilant due to the higher risk of retroperitoneal hemorrhage. The risks of retroperitoneal hemorrhage are further increased in patients taking warfarin, heparin, multiple antiplatelet agents and in hypertensive patients. Vascular closure devices are being increasingly used in these circumstances to help reduce the risk of retroperitoneal hemorrhage.
Left
(a)
(b)
Figure 14.5 (a) An example of subintimal angioplasty in the tibial vessels. Note the occlusion of the popliteal artery, proximal occlusion of the anterior tibial artery and occlusion of the other tibial vessels; (b) successful subintimal angioplasty of the proximal anterior tibial artery allowing “straight line” arterial flow to the foot.
a hydrophilic wire proximal to the occlusion and a craniocaudally directed dissection is commenced, led by the loop of the wire closely followed by the catheter. The craniocaudal guidewire can then be fed, or pulled after being snared, through the lesion and out of the femoral sheath. This process is then repeated for the occlusion on the other side, so that a guidewire is passing through both of the occlusions simultaneously. These guidewires are then replaced with exchange wires and angioplasty of the occluded vessels can be performed, using a “kissing balloons” technique (Figure 14.7). The angioplasty balloons should ideally be delivered via the femoral route, thereby minimizing the size of sheath required in the left axillary or brachial artery. As before, refractory stenoses can then be re-angioplastied or stented. A similar anticoagulation protocol is used as for femoropopliteal lesions.
Complications The complications of SIA are similar to those of conventional PTA. Of these the four most significant complications are: retroperitoneal hemorrhage following a high puncture, peripheral embolism, vessel perforation, and elastic recoil.
Peripheral embolism There is a 5 to 8% risk of embolic complications following femoropopliteal SIA. In the majority of cases percutaneous aspiration thrombectomy can remove the majority of emboli, usually using large 5-French to 8-French non-tapered embolectomy catheters and a large (50 ml) suction syringe with adequate suction. If this fails, then another strategy would be the “push and park” concept.14 Here, the embolus is pushed using either the embolectomy or balloon catheter distally into one of the run-off vessels. Usually the embolus advances in a straight line into the common peroneal artery. This allows blood flow to the foot via the other tibial vessels. However, this technique is reliant on at least two run-off vessels being available. Rarely, surgical embolectomy is required to remove the occluding material following SIA. Vessel perforation Vessel perforation during SIA can occur either during the subintimal dissection or during the balloon inflation of the subintimal tract with an incidence of 5–8%. This approximates to be at least twice as common compared with conventional PTA. However the development of a perforation will not necessarily terminate the procedure, and over half of patients who develop an intra-procedural perforation can continue to have a successful SIA.15 In fact SIA can be used to treat vessel perforation as a result of conventional PTA. The associated risk factors for intra-procedural vessel perforation include increasing patient age, diabetes, and smoking. If a vessel perforation occurs, then the extent of injury should be evaluated. This will have to be done on radiological assessment, as it is not possible to directly measure the quantity of blood leaking through the perforation. Often (during the subintimal dissection) the perforation will seal by itself and no further action is required. If treatment is required, the perforation can be excluded by creating a new, alternative dissection channel on the contralateral vessel wall, starting proximal and extending distal to the site of perforation. This diverts the blood away from the perforation and further distally into the leg (following the path of least resistance), while at the same time shifting the atheroma to the damaged side of the vessel and compressing on the perforation site. If this treatment fails, or there is a large perforation as noted by large amounts of contrast medium extravasating into the surrounding tissues, then an embolization coil (usually of
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(b)
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Figure 14.6 (a, b) Extensive tibial vessel disease with only the anterior tibial artery patent proximally and just above the ankle joint; (c, d) the intervening anterior tibial artery is occluded. The entire length of the anterior tibial artery is recannulated following subintimal angioplasty.
3 mm diameter) can be placed in the subintimal tract immediately proximal to the site of perforation, to occlude the tract and stop the blood flow to the perforation. Many of these patients can then be recalled several weeks later for a repeat attempt. A new subintimal tract can then be created, bypassing the embolization coil. Vessel perforation as a result of balloon inflation tends to produce a large defect, which is usually difficult to treat by subintimal bypass. In this circumstance, balloon tamponade
(a)
(b)
(c)
Figure 14.7 (a) Aorto-iliac arterial disease with occlusion of the distal aorta; and (b) bilateral proximal common iliac arteries; (c) subintimal dissection allows reconstitution of the aortic bifurcation and common iliac arteries.
at the site of the perforation is attempted, using low balloon pressure (2–4 atmospheres) for 2–3-minute periods repeated up to four times if necessary. If this fails to close the defect, then either a covered stent may be used to seal the defect or embolization coils can be deployed proximal to the perforation to occlude the subintimal channel and the flow of blood to the perforation. In patients with deranged clotting or abnormality of platelet function, treatment of these large defects may require correction of their clotting abnormality or the use of adjunctive blood products (such as fresh frozen plasma or platelets) in addition to coil embolization of the dissection tract. Elastic recoil This complication is rare, occurring in less than 1% of cases. It is however very unpredictable. If the recanalized segment fails to remain open due to elastic recoil, an emergency situation can arise as a result of blood stasis and then thrombosis of blood within the segment as well as proximal or distal to the recanalized segment. This can be treated initially with repeated balloon inflations, administration of Tolazoline (5 mg) or glyceryl trinitrate (GTN) (50–250 µg) locally intraarterially. In refractory cases deploying long self-expanding stents at the site of the occlusion may be of help. However evidence suggests that the long-term patency of subintimally placed stents is poor.16 Surgical bypass is then sometimes required.
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Results and long-term outcomes Numerous publications over recent years have outlined the efficacy, safety, and cost-effectiveness of SIA. Unfortunately there has to date been no randomized control trial directly comparing bypass surgery with SIA, and many centers apply differing treatment choices. One thing that is certain is that SIA has a learning curve, and those centers with the most experienced practitioners have the best results, with initial technical success rates rising from 83 to 100% with increasing experience of the procedure.17 Once the procedure has been mastered, many centers have reported generally favorable results for both intermittent claudication and critical ischemia, with very low rates of surgical intervention, procedural complication, and mortality. Most importantly it is recognized that SIA does not compromise future surgical bypass. A recent study provides good long-term evidence for the efficacy of SIA in intermittent claudication with technical success in 87% of patients. Primary assisted patency rates on an intention to treat basis at 5 years was 54%, rising to 64% in successfully recanalized patients.18 This study also identified length of occlusion, male sex, and age as independent risk factors for re-occlusion. It also highlighted the usefulness of a duplex surveillance program, as all patients who underwent a successful procedure were placed on surveillance, so that restenoses were diagnosed and treated early. Evidence for the efficacy of SIA in critical ischemia, can be drawn from the results of Lipsitz et al. who looked at a group with severe lower limb ischemia treated with SIA.19 Of the 39 patients in the group, 25 had gangrene and 5 had rest pain. Whilst they had technical success rate of 87%, more significantly 84% of the patients with gangrene healed with SIA alone, and 100% had complete pain resolution. The cumulative 1-year patency rate following successful SIA was 74%. Surgery in technical failure group was not affected by the attempt at SIA. These are very respectable results for such a minimally invasive technique in a group of patients with very severe vascular disease. Treiman et al. reported that 92% of a group of high-risk patients with critical ischemia with no other treatment options available experienced clinical symptomatic improvement at 1 year following SIA.20 This outlines the benefit of SIA, particularly in this group of patients, with significant medical co-morbidities who would pose a significant anesthetic and surgical risk. There appear to be several factors that contribute to longterm patency. These include smoking, occlusion length, and the number of calf run-off vessels.21 The relationship of longterm patency with the number of calf run-off vessels was also identified in the group of patients studied by Laxdal et al.,22 and those studied by Lazaris et al.23 who also confirmed the
relationship between the length of occlusion and long-term patency with a hazard of reocclusion of 1.02 for every centimeter of occlusion. Therefore it is best to try to improve the run-off into at least one good caliber run-off calf vessel, and preferably into at least two run-off calf vessels to help maintain long-term patency. SIA in the infrapopliteal segment is currently only offered in a few centers, though it has been shown to be of benefit particularly in limb salvage. The most recent evidence reports technical success rate of infrapopliteal SIA of 86%, with a 3-year limb salvage rate of 94%, and with an 84% freedom from the symptoms of critical limb ischemia at 3 years.24 Vraux et al. reported an 81% limb salvage rate at 6 months in a group of patients who were all considered unsuitable for surgery either due to poor medical condition, extensive ulceration, swelling, or lack of sufficient vein for autologous bypass. A significant proportion, 68%, had occlusions greater than 10 cm long, which may help to explain the technical success rate of 78%.25
Conclusion SIA is a safe adjunct in the treatment of lower-limb occlusive disease. Most studies agree that it does not compromise further surgical management, and has decreased morbidity and mortality compared with surgical bypass. This is important in patients with vascular disease, since many of these patients have significant medical co-morbidities and reduced life expectancy. SIA, by extending the therapeutic range of conventional PTA, increases the treatment options in this group of patients, and can either delay or obviate the need for surgery. A learning curve does exist when performing SIA, and this most likely explains the better results from more experienced centers. The technique is however easy to learn, and does not require any extra equipment than used for conventional PTA. The development of a surveillance program, coupled with timely treatment of restenosis has been shown to be of significant benefit in maintaining long-term patency, and decreasing the need for surgery. Studies so far suggest better results for SIA in intermittent claudication compared to critical limb ischemia. This may in part be related to the absence of good calf run-off vessels in critical limb ischemia. However, there is good evidence that SIA can help prevent limb loss and allow ulcer/gangrene healing in critical limb ischemia. This may be as a result of SIA “buying time” for the development of collateral vessels. Given that this group of patients are usually very debilitated and can be very poor candidates for surgical bypass, attempting SIA could prove of dramatic benefit if successful, while generally not affecting future surgical management.
REFERENCES 1.
2.
Hynes N, Akhtar Y, Manning B et al. Subintimal angioplasty as a primary modality in the management of critical limb ischaemia: comparison to bypass grafting for aortoiliac and femoropopliteal occlusive disease. J Endovasc Ther 2004; 11: 460–71 Faries PL, LoGerfo FW, Arora S et al. A comparative study of alternative conduits for lower extremity revascularization: all
3.
autogenous conduit versus prosthetic grafts. J Vasc Surg 2000; 32: 1080–90 Dotter CT, Judkins MP. Transluminal treatment of arteriosclerotic obstruction: Description of a new technique and a preliminary report of its application. Circulation 1964; 30: 654–70
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Subintimal angioplasty 4.
5. 6. 7. 8. 9. 10. 11. 12.
13. 14.
Gruntzig A, Hopff H. [Percutaneous recanalization after chronic arterial occlusion with a new dilator-catheter (modification of the Dotter technique)] Dtsch Med Wochenschr 1974; 99: 2502–10, 2511. In German Bolia A, Brennan J, Bell PR. Recanalisation of femoropopliteal occlusions: improving success rate by subintimal recanalisation. Clin Radiol 1989; 40: 325 Nasim A, Sayers RD, Bell PRF, Bell A. Recanalisation of the native artery following failure of a bypass graft. Eur J Vasc Endovasc Surg 1995; 10: 125–7 Walker PR, Papavassiliou VG, Bolia A, London N. Subintimal angioplasty of native vessels in the management of occluded vascular grafts. Eur J Vasc Endovasc Surg 2001; 22: 41–3 Bolia A, Miles KA, Brennan J, Bell PRF. Percutaneous transluminal angioplasty of occlusions of the SFA by subintimal dissection. Cardiovasc Intervent Radiol 1990; 13: 357–63 Reekers JA, Bolia A. Percutaneous intentional extraluminal (subintimal) recanalisation: how to do it yourself. Eur J Radiol 1998; 28: 192–8 Reekers JA, Kromhout JG, Jacobs MJ. Percutaneous intentional extraluminal recanalisation of the femoropoliteal artery. Eur J Vasc Surg 1994; 8: 723–8 Bolia A. Subintimal angioplasty in lower limb ischaemia. J Cardiovasc Surg 2005; 46: 385–94 Jacobs DL, Motaganahalli RL, Cox DE, Wittgen CM, Peterson GJ. True lumen re-entry devices facilitate subintimal angioplasty and stenting of total chronic occlusions: Initial report. J Vasc Surg 2006; 43: 1291–6 Bolia A, Fishwick G. Recanalization of iliac artery occlusion by subintimal dissection using the ipsilateral and the contralateral approach. Clin Radiol 1997; 52: 684–87 Higginson A, Aleaddin F, Fishwick G, Bolia A. “Push and Park” an altenative strategy for management of embolic complication during balloon angioplasty. Eur J Vasc Endovasc Surg 2001; 21: 279–82
15.
16. 17. 18. 19. 20.
21. 22. 23.
24. 25.
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Hayes PD, Chokkalingham A, Jones R et al. Arterial perforation during infrainguinal lower limb angioplasty does not worsen outcome: results from 1409 patients. J Endovasc Ther 2002; 9: 422–27 Treiman GS, Treiman RL, Whiting JH. Results of percutaneous subintimal angioplasty using routine stenting. J Vasc Surg 2006; 43: 513–9 Yilmaz S, Sindel T, Yegin A, Luleci E. Subintimal angioplasty of long SFA occlusions. J Vasc Interv Radiol 2003; 14: 997–1010 Florenes T, Bay D, Sandbaek G et al. Subintimal angioplasty in the treatment of patients with intermittent claudication: long term results. Eur J Vasc Endovasc Surg 2004; 28: 645–50 Lipsitz EC, Ohki T, Veith FJ et al. Does subintimal angioplasty have a role in the treatment of severe lower extremity ischaemia? J Vasc Surg 2003; 37: 386–91 Treiman GS, Whitting JH, Treiman RL, McNamara RM, Ashrafi A. Treatment of limb-threatening ischaemia with percutaneous intentional extraluminal recanalisation: a preliminary investigation. J Vasc Surg 2003; 38: 29–35 London NJM, Srinivasan R, Sayers RD et al. Subintimal angioplasty of femoropopliteal occlusions: the long term results. Eur J Vasc Surg 1994; 8: 148–55 Laxdal E, Jenssen GL, Pederson G, Aune S. Subintimal angioplasty as a treatment for femoropopliteal occlusions. Eur J Vasc Endovasc Surg 2003; 25: 578–82 Lazaris AM, Salas C, Tsiamis AC et al. Factors affecting patency of subintimal infrainguinal angioplasty in patients with critical lower limb ischaemia. Eur J Vasc Endovasc Surg 2006; Sep 9; [Epub ahead of print] Ingle H, Nasim A, Bolia A et al. Subintimal angioplasty of isolated infragenicular vessels in lower limb ischaemia: long term results. J Endovasc Ther 2002; 9: 414–6 Vraux H, Hammer F, Verhelst R. Subintimal angioplasty of tibial vessel occlusions in the treatment of critical limb ischaemia: midterm results. Eur J Vasc Endovasc Surg 2000; 20: 441–6
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) G Baweja and RR Heuser
Introduction Chronic total occlusion (CTO) of peripheral arteries can cause disabling claudication or critical limb ischemia. In contrast to other vascular beds, occlusions are at least three times more common in the femoropopliteal arteries. For the patient with critical limb ischemia, multilevel disease with occlusion of some or all of the tibial arteries is typical. Patients with long infrainguinal occlusions generally tend to be sicker and bypass grafting in this population is often associated with a considerable procedure-related morbidity and mortality. Surgical intervention is usually reserved for patients with critical limb ischemia and consequently many patients with long, chronic superficial femoral artery (SFA) occlusions remain untreated, leaving them in pain and discomfort. While treatment of short CTO lesions of the iliac and femoropopliteal vessels with endovascular techniques has become the standard approach, longer complex lesion intervention can be extremely challenging and time-consuming. Iliac and femoropopliteal CTOs traditionally had high failure rate in the range 5–35%1,2 and 15–25%,3 respectively. Fortunately, with increasing complexity of the arterial occlusions, technical skills, and devices needed to successfully cross and treat the occlusion also continue to improve significantly. Nowadays, an initial endovascular approach can achieve limb salvage rates equivalent to surgical bypass.3,4
Pathology of total occlusion CTOs consist of various degrees of fibro-atheromatous plaque and thrombus depending on the mechanism of occlusion and its duration. A tough fibrous cap is often present at the proximal and distal margins of the CTO, with softer material in between. When the fibrous occlusion is long, densely organized, and homogenous, guidewire passage intraluminally is very difficult and subintimal approach in this type of lesion is likely to be more successful.
Patient selection Revascularization procedures are indicated for patients with disabling claudication, ischemic rest pain, or impending 92
limb loss. At the present time, for infrainguinal occlusions, the patency rates for long, complex disease are lower than the patency rates for open bypass.5 The rapid advances in interventional devices have inspired interest in tackling these long occlusions with an endovascular approach with the option of open surgery still remaining if the intervention later fails. Recently published guidelines state that the effectiveness of the use of stents, atherectomy, cutting balloons, thermal devices, and lasers for the treatment of infrainguinal lesions (other than to salvage a suboptimal result from balloon dilation) is not well established, and primary stent placement is not recommended in these arteries. In these guidelines, stent implantation is categorized under one broad definition and includes self-expandable, balloon-expandable, spiral-shaped, and covered stents.6 Lesion assessment Initial imaging of patients with iliac and femoral occlusions can be done with computed tomography angiography (CTA) or magnetic resonance angiography (MRA). This allows for excellent definition of the aortic, iliac, and femoral occlusions and the status of the femoral artery for access in case of iliac occlusions and helps in deciding on an antegrade versus retrograde contralateral femoral access for infrainguinal lesions. A limitation to percutaneous treatment is occlusive disease of the common femoral artery at the site of access. In this situation, open femoral access can be used when treating iliac or femoral–popliteal disease with endovascular techniques. In the catheterization laboratory, lesions should first be assessed with appropriate angiographic views, for example a 35∞ ipsilateral lateral angiogram. Most long SFA occlusions begin with a proximal stump followed by distal vessel reconstitution by collaterals from the profunda femoris artery. Special attention must be paid to the length of the proximal stump and the location of the distal reconstitution as it clearly influences device selection. A flush occlusion at the SFA origin or an extension of an occlusion to the popliteal trifurcation is not suitable for endovascular treatment, especially with antegrade approach.7 Diffuse, irregular, eccentric, calcified occlusions are much more difficult to recanalize and have less long-term success.8 Lesion length is an important factor when determining long-term success though it probably
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) plays lesser role in deciding between endovascular and surgical approach.
Crossing total occlusions Femoropopliteal CTOs are effectively treated with up-andover techniques, whereas iliac lesions are often best approached via ipsilateral retrograde femoral access. In order to provide the support needed to cross long infrainguinal lesions, a long 6- or 7-French sheath like Ansel or Raabe (Cook Inc., Bloomington, IN) is placed over the iliac bifurcation with the tip into the superficial femoral artery. Once the access is obtained, the patient is anticoagulated with either heparin or bivalirudin. We often use a combination of a hydrophilic guidewire such as a 0.035-inch Glidewire (Terumo, Somerset, NJ), and a support catheter such as the 4–5-French angled Glidecath as initial approach for crossing a CTO. The procedure from this point on requires road-map imaging to visualize the distal vessel as angiographic imaging through the support catheter is largely unhelpful. It is important that the hydrophilic guidewire enters the occlusion with the tip straight without any spiraling as this allows for the proper tip engagement into the lesion. At this point one can either attempt crossing intraluminally or looping the wire purposely to enter subintimal space. Despite the counterintuitive nature of starting a subintimal plane intentionally, the technique is relatively simple and usually more successful (70–90% of cases) than intentional true lumen passage for long-segment CTOs.9 Some interventionalists prefer retrograde approach over antegrade puncture for infrainguinal angioplasty. In a randomized study of 100 consecutive patients, retrograde puncture was found to be technically easier with a tendency to fewer complications like hematoma, but resulted in a higher radiation dose.10
Subintimal angioplasty Once wire enters the occlusion, it often loops back on itself for several centimeters with the 180∞ turn. One should try to maintain the width of the distal wire loop to remain smaller than or equal to the width of the native vessel as widening of the loop tip signifies more subintimal vessel dissection. This can limit successful re-entry of wire into the distal vessel true lumen. To avoid widening of the wire loop, one can push the support catheter to catch up over the proximal unlooped part of the Glidewire and then pull the wire back into the catheter to straighten the tip. After straightening the wire, it is readvanced with a small width loop as described previously.11 If the support catheter gets trapped in the subintimal space and does not follow the Glidewire, a smaller-diameter 0.035inch compatible catheter, such as the Quickcross catheter (Spectranetics Corporation, Colorado Springs, CO) may be used. Finally, the wire is re-entered into the distal true lumen under direct visualization. The support catheter is then advanced into the distal segment, beyond the occlusion, and confirmation of true lumen is done with contrast injection through this catheter. If there is difficulty in re-entering the true lumen, re-entry devices like the Outback or Pioneer
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catheters are used as described below. Alternatively, lowerprofile 0.014-inch torqueable stiff wires (e.g. confianza wire) with or without over-the-wire angioplasty balloon can sometimes be used successfully to achieve true lumen entry. It is preferable to try re-entry devices over vigorous attempts to reenter lumen with wire alone as this may lead to worsening of subintimal dissection and progression of dissection plane below the knee compromising distal collaterals. Primary patency rates of subintimal angioplasty range from 60 to 80% at 6 months and 60 to 70% at 12 months.12 In critical limb ischemia, limb salvage is achieved in approximately 80–90% of patients. Secondary interventions are usually quick and simple and approach does not interrupt subsequent bypass options.
Re-entry devices The key factor to subintimal success is having a relatively healthy, non-calcified target for re-entry in the distal vessel. Lesions with dense calcification, diffuse disease of the distal target, and small-caliber lumens often prove difficult to gain successful re-entry. In addition, in some cases re-entry is not achieved until subintimal passage to a site significantly remote from the level of patent vessel lumen. This causes subintimal angioplasty or stenting of an unintended target beyond the diseased segment and may jeopardize important collaterals. In these cases, re-entry tools such as the Pioneer catheter (Medtronic Vascular) or the Outback (Cordis, Miami, FL) can be used.13 It is important to remember that a 7-French sheath is necessary for these devices. Pioneer catheter The Pioneer catheter is a 7-French phased-array 20 MHz intravascular ultrasound (IVUS) catheter and is connected to a Volcano (Volcano Corporation, Rancho Cordova, CA) IVUS console. The catheter has two monorail 0.014-inch compatible wire ports, one with a curved retractable 24-gauge nitinol needle distally. The catheter is gently maneuvered under ultrasound guidance until the tip of the nitinol needle is oriented toward the true lumen and is lined up at the 12 o’clock position on the ultrasound image. The needle tip is then carefully advanced and deployed. A floppy-tip extra-support 0.014-inch guidewire is then passed through the needle into the distal vessel and is confirmed with angiography. The needle is then retracted, and the Pioneer catheter is removed, leaving the wire behind with distal end in the true lumen. At this point, secondary interventions are performed with standard techniques (Figure 15.1). Outback catheter The Outback catheter (Lumend Inc) is a 5-French multipurpose type catheter with 22-gauge nitinol canula that can be advanced or retracted from the end of the catheter to penetrate from the dissection plane to the true lumen. With the help of two orthogonal fluoroscopic views, the angle of the catheter is adjusted to point the end toward the true lumen. The proprietary locate, tune, and deploy technique is used to deploy the needle through the intima to the true lumen. A 0.014-inch wire is then advanced into the true lumen and the
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Figure 15.2
(a) A
B
C
D
(b) Figure 15.1 (a) Pioneer catheter with integrated 20 MHz phase array transducer and 24-gauge nitinol curved needle; (b) the Pioneer facilitating the true lumen re-entry: A. wire trapped in a subintimal location; B. Pioneer catheter is advanced to the target segment, where the needle is deployed under ultrasound guidance; C. guidewire is then passed through the needle into true distal lumen and the Pioneer is removed; D. lesion is treated successfully with an angioplasty device advanced over the wire.
Outback catheter is then removed. Secondary interventions are then performed either on this wire or after exchanging it with a 0.35-inch wire system (Figure 15.2).
Angioplasty and stenting Common iliac artery occlusions are routinely stented with balloon-expandable stents because of their high radial force and precise placement. In the external iliac, one can use either the balloon-expandable or self-expanding stents depending upon the lesion characteristics and location. Femoral or popliteal occlusions are treated with primary angioplasty with long balloons at nominal or greater pressures and longer inflations up to 2–3 minutes. If there is a presence of a flowlimiting dissection, then self-expanding bare nitinol stents should be deployed. Some interventionalists have also used laser, thermal, or atherectomy devices in this setting to treat residual lesions after angioplasty.
Outback catheter from Lumend.
needle deployments, but these devices are often used in complex difficult-to-cross lesions that have an increased risk of rupture with angioplasty. It is imperative that covered stents be available in the catheterization laboratory at the time of CTO intervention. The other important complication of intervening total occlusions is thromboembolism that can occur in 1–4% of cases. Adequate anticoagulation is therefore necessary during the procedure.
Chronic total occlusion devices Because of often complex and long occlusions, more than 80% of patients usually need a more specialized crossing technique over the standard technique. Recently, several devices have entered the market that may enable treatment of these difficult lesions. These devices cross the calcified plaque using different physical principles, such as blunt microdissection, optical coherence reflectometry, or laser. Some of the devices like magnum wires, rotational atherectomy, Kensey catheter, and Rotacs are already of historical significance only and will not be described any further in this chapter. Excimer laser The photoablative effect of an excimer laser can be used to recanalize total occlusions by debulking atherosclerotic and thrombotic material. In addition, it can facilitate subsequent balloon dilation at lower pressure to prevent dissection and reduce the risk of thromboembolic events. An excimer laser produces photons of ultraviolet light at a unique wavelength of 308 nm that is readily absorbed in human tissues, including atherosclerotic material and clots (Figure 15.3).
Complications The major complication related to the treatment of chronic total occlusion is vessel rupture secondary to catheter manipulation or angioplasty. Long or calcified occlusions are often more prone to such complications. The true lumen re-entry devices itself may not result in perforation related to the
Figure 15.3 (a) The Spectranetics CVX-300 excimer laser system and (b) TURBO elite laser ablation catheter (FDAapproved October 2006). (See Color plates.)
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) The activated laser catheter must be advanced very slowly, not exceeding 1 mm/sec. Fluoroscopic road mapping is used throughout to verify alignment of guidewires and catheters to the vessel lumen. Improvements in saline-infusion techniques with lasers have resulted in lower incidence of dissection. Thorough flushing of the vessel with saline effectively facilitates transmission of the laser light to the atherosclerotic tissue. In addition, effective removal of the contrast medium prevents formation of shockwaves that can result in dissections of the vessel wall. There also appears to be direct platelet aggregation inhibition with the use of excimer lasers, making it an attractive tool for treating chronic thrombotic lesions.14 The mid-term outcomes of patients with long chronic iliac artery occlusions after excimer-laser-assisted interventional recanalization were recently reported in 43 patients after 4year follow up. The primary technical success rate was 95.3%, with a major complication rate of 6.9% and clinical improvement in 97.6% of cases. The overall primary and secondary patency rate as determined by ankle–brachial index and duplex ultrasound was 86.1 and 95.4 % respectively.15 This is similar to the patency rates of short stenoses. In a study of laser-assisted recanalization of chronic SFA occlusions in 318 consecutive patients over 1 year, the primary and secondary patency rate was 83.2 and 90.5% respectively.16 There is data supporting use of lasers in the tibioperoneal region as well. In the LACI (Laser Angioplasty in Chronic Ischemia) prospective, multicenter, clinical registry patients with poor surgical risk with critical limb ischemia were treated with excimer laser in the SFA, popliteal and/or infrapopliteal arteries with adjunctive PTA, and optional stenting. Patency with distal flow to the foot was achieved in 89% of patients and the rate of limb salvage was 93% at 6 months.17 Blunt microdissection New catheter technology has recently been developed to recanalize CTOs through a process of blunt microdissection. The Frontrunner X39 CTO Catheter (LuMend Inc., Redwood City, CA) is a single-use catheter consists of an articulating, distal tip assembly. This tip features a crossing profile of 0.039 inches with actuating jaws that open to 2.3 mm and is remotely actuated by a manual rocker handle to facilitate blunt microdissection of the plaque (Figure 15.4). The Frontrunner catheter is commonly used in combination with the 4.5-French Frontrunner Micro Guide Catheter that provides additional support and acts as a conduit for a more
Figure 15.4
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rapid wire exchange once the frontrunner crosses the CTO. The microdissection can be performed in various planes to separate tissue in the target vessel segment. Though originally designed for coronary intervention, the Frontrunner CTO Catheter has now been used extensively to facilitate guidewire placement across peripheral CTOs. In a prospective study of 36 patients with 44 symptomatic CTOs (2 terminal aortic, 24 iliac, 16 femoral, and 2 popliteal), blunt microdissection was carried out with this type of catheter. Procedural success, evaluated angiographically, was achieved in 91% with no complications related to blunt microdissection itself.18
Vibration angioplasty Vibrational angioplasty is based on the concept of using highfrequency mechanical vibrational energy to help recanalize chronic total occlusions. The Crosser system consists of a generator, a transducer, and the single-use CROSSER catheter (Figure 15.5). The generator converts AC power into highfrequency current. This high-frequency current is then converted into vibartional energy by piezoelectric crystals contained within the transducer. The Crosser catheter is a nitinol-core standard 0.014-inch and 0.018-inch guidewires monorail catheter system with a stainless steel tip. Mechanical vibrations are transmitted to this stainless steel tip at approximately 20 kHz or 20,000 cycles per second. This vibrational energy provides mechanical impact at a stroke depth of approximately 20 µm and pulverizes the solid CTO tissue. In addition, high-frequency vibration creates vapor-filled micro-bubbles in the blood. These micro-bubbles expand and implode producing liquid jets that can break the molecular bonds and cause erosion of the CTO tissue helping recanalization of an occluded artery. This system has already been used safely and effectively in coronary artery total occlusions.19,20 Recently, the PATRIOT (Peripheral Approach To Recanalization In Occluded Totals) data on 40 patients was presented at the TCT 2006 meeting.21 The average CTO length was 10.6 cm with half of the attempted occlusions in the SFA and the remainder in the popliteal artery or below. CROSSER activation time averaged 2.5 min. Procedure time (PT) and fluoroscopy time were 2 h and 39 min respectively. There were no procedural complications and no clinical perforations. Technical success (successful passage of a guidewire into the true distal lumen) was achieved in 78% of the occlusions attempted. Improvement in
Schematic of blunt microdissection with Frontrunner device.
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Figure 15.5 (a) The Crosser system generator – high frequency current is converted into vibrational energy; (b) Crosser catheter – mechanical vibration at 20,000 cycles/second.
ABI (> 0.10) was achieved in 85% of patients with successful recanalization. (a) Optic coherence reflectometry with radio-frequency ablation All the new technologies described above are unable to see the true lumen of the vessel. Optical coherent reflectometry with radio-frequency ablative energy (Safe-Cross wire, Intraluminal Therapeutics, CA) is a forward-looking system that has been utilized to treat CTO.22 Using near infrared light, this guidewire system can distinguish calcified from noncalcified plaque and atherosclerotic lesions from arterial wall and display the signals on a monitor in real time. The green bar indicates lumen and radiofrequency ablative energy is enabled. The red bar means wire is against the vessel wall and radio-frequency energy is disabled (Figure 15.6). There are some technical limitations with the current system. The wire tip cannot be manually shaped or bent without risking the fracture of optical fibers inside the wire. The wire itself is not easily steerable, though this problem has been significantly improved in the latest generation of SafeCross wire. The GRIP registry study is one of the first peripheraldevice studies to focus on total occlusion recanalization with the Safe-Cross system.23 The device success rate, defined as the achievement of distal lumen position, was 76%, For the 56 lesions that were recanalized, the mean preprocedural ABI was 0.59; the mean post-procedural ABI was 0.86. In another study, Dippel et al. demonstrated a 72.7% success rate in recanalizing CTO in the peripheral vasculature following failure of conventional techniques.24
(b) Figure 15.6 (a) Safe-Cross system; (b) optical coherence reflectometry guided radio-frequency ablation-waveform display.
was undetermined in the majority of patients, 17 patients had arterial occlusions older than 2 years and half the patients had intermittent claudication from 8 months to 10 years. Surprisingly, 80% of CTOs including iliac and infrainguinal occlusions responded favorably to thrombolysis. Most arterial occlusions (more than a few centimeters in length) are associated with some degree of arterial thrombosis, and thus may be amenable to thrombolysis. Advances in the availability of smaller catheters (3 and 4 French) and development of an open-end injectable guidewire have increased the rate of success due to both a better delivery system and fewer complications. In the absence of bleeding complications, lytic therapy can be continued as low-dose prolonged infusion until complete clot lysis is achieved.
Thrombolytic therapy While thrombolytic therapy is still the treatment of choice in acute and subacute arterial occlusions and graft thrombosis, there are a few reports regarding thrombolytic therapy in chronic arterial occlusions.25–27 In a series reported by Motarjeme, 276 arterial occlusions (lesion length 3–66 cm) were treated in 268 patients with thrombolytic therapy. Though the duration of the occlusion based on angiography
Medical management Though the detailed medical management is beyond the scope of this chapter, the role of medical therapy in patients with advanced PVD should not be underestimated. Even in patients requiring invasive intervention, medical management has been proven to improve outcome, prolong the success of
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) the intervention, improve functional capacity, and prolong life. One must address all modifiable risk factors including smoking, hypertension, dyslipidemia, obesity, physical inactivity, and diabetes. In addition, the appropriate use of beta-blockers, antiplatelet therapy, angiotensin-converting enzyme (ACE) inhibitors, and statins are recommended for patients with peripheral vascular disease.
Future technologies There are many new innovative technologies on the horizon to treat chronic vessel occlusions. Omniwave technology using acoustic energy, Cronus stereotaxis wire for magnetic navigation28 and collagenase infusion29,30 are few of such novelties under investigation. Recent advances in rapid imaging, along with the development of special catheter devices visible under MRI, have made real-time MRI (rtMRI) guided therapeutic interventions feasible.31 Recently Raval et al. demonstrated successful real-time MRI-guided recanalization of a long peripheral artery CTO in a swine model.32 This technology
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may offer advantages in future human peripheral artery visualization during CTO traversal, while avoiding x-ray radiation and nephrotoxic contrast agents.
Conclusion At present, endovascular intervention is generally well accepted as an effective treatment modality in the majority of occlusive iliac artery lesions, but its role in the femoropopliteal region is still debatable. A successful intervention of chronic total occlusions depends a lot on operator’s patience, technique, and experience. New technologies, including the Frontrunner catheter, Safe-Cross system and re-entry catheters, have significantly improved our success of crossing long total occlusions. These innovations, along with ever-increasing operator experience, have considerably enhanced long-term patency in even the most complex chronic occlusions. In the future, more patients will have the opportunity for a less invasive treatment for their arterial disease.
REFERENCES 1. 2.
3.
4.
5. 6.
7. 8. 9. 10. 11. 12. 13.
14.
Uher P, Nyman U, Lindh M, Lindblad B, Ivancev K. Long-term results of stenting for chronic iliac artery occlusion. J Endovasc Ther 2002; 9(1): 67–75. Carnevale FC, De Blas M, Merino S, Egana JM, Caldas JG. Percutaneous endovascular treatment of chronic iliac artery occlusion. Cardiovasc Intervent Radiol 2004; 27(5): 447–52 Lofberg AM, Karacagil S, Ljungman C et al. Percutaneous transluminal angioplasty of the femoropopliteal arteries in limbs with chronic critical lower limb ischemia. J Vasc Surg 2001; 34(1): 114–21 Leville CD, Kashyap VS, Clair DG et al. Endovascular management of iliac artery occlusions: extending treatment to TransAtlantic Inter-Society Consensus class C and D patients. J Vasc Surg 2006; 43(1): 32–9 Yilmaz S, Sindel T, Yegin A, Luleci E. Subintimal angioplasty of long superficial femoral artery occlusions. J Vasc Interv Radiol 2003; 14(8): 997–1010 Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic). J Am Coll Cardiol 2006; 47(6): 1239–312 Saha S, Gibson M, Magee TR et al. Early results of retrograde transpopliteal angioplasty of iliofemoral lesions. Cardiovasc Intervent Radiol 2001; 24(6): 378–82 McLafferty RB. Patient selection: lesion characteristics and predictors of outcome. Perspect Vasc Surg Endovasc Ther 2006; 18(1): 25–9 Bolia A, Brennan J, Bell PR. Recanalization of femoro-popliteal occlusions: improving success rate by subintimal recanalisation. Clin Radiol 1989; 40: 325 Nice C, Timmons G, Bartholemew P, Uberoi R. Retrograde vs. antegrade puncture for infra-inguinal angioplasty. Cardiovasc Intervent Radiol 2003; 26(4): 370–4 Nadal LL, Cynamon J, Lipsitz EC et al. Subintimal angioplasty for chronic arterial occlusions. Tech Vasc Interv Radiol. 2004; 7: 16–22 Ingle H, Nasim A, Bolia A et al. Subintimal angioplasty of isolated infragenicular vessels in lower limb ischemia: long-term results. J Endovasc Ther 2002; 9: 411–16 Jacobs DL, Motaganahalli RL, Cox DE et al. True lumen reentry devices facilitate subintimal angioplasty and stenting of total chronic occlusions: Initial report. J Vasc Surg 2006; 43(6): 1291–6 Topaz O, Minisi AJ, Bernardo NL et al. Excimer laser effect on platelet aggregation. Am J Cardiol 2001; 87: 849–55
15. 16. 17. 18.
19. 20. 21. 22. 23.
24.
25. 26. 27. 28. 29.
Balzer JO, Gastinger V, Thalhammer A et al. Percutaneous laserassisted recanalization of long chronic iliac artery occlusions: primary and mid-term results. Eur Radiol 2006; 16(2): 381–90 Scheinert D, Laird JR, Schroder M et al. Excimer laser-assisted recanalization of long, chronic superficial femoral artery occlusions. J Endovasc Ther 2001; 8: 156–66 Laird JR. Late breaking clinical trials. LACI (laser angioplasty in chronic ischemia) trial. TCT Annual Meeting, September, 2002, Washington DC. Mossop PJ, Amukotuwa SA, Whitbourn RJ. Controlled blunt microdissection for percutaneous recanalization of lower limb arterial chronic total occlusions: a single center experience. Catheter Cardiovasc Interv 2006; 68(2): 304–10 Melzi G, Cosgrave J, Biondi-Zoccai GL et al. A novel approach to chronic total occlusions: the crosser system. Catheter Cardiovasc Interv 2006; 68(1): 29–35 Grube E et al. High frequency mechanical vibration to recanalize chronic total occlusions after failure to cross with conventional guidewires. J Invasive Cardiol 2006; 18: 85–91 Laird J. Recanalization of peripheral artery CTOs using the CROSSER catheter system: The PATRIOT feasibility study results. TCT Annual Meeting, September, 2006, Washington DC. Morales PA, Heuser RR. Chronic total occlusions: experience with fiber-optic guidance technology – optical coherence reflectometry. J Interv Cardiol 2001; 14: 611–6 Kirvaitis RJ, Heuser RR, Das TS et al. Usefulness of optical coherent reflectometry with guided radiofrequency energy to treat chronic total occlusions in peripheral arteries (the GRIP trial). Am J Cardiol 2004; 94(8): 1081–4 Dippel EJ, Shammas NW, Takes VS, Youngblut MM. Single center experience with the novel intra-luminal Safe-Cross wire for percutaneous treatment of peripheral vascular chronic occlusions. TCT-185. September 15–17. Am J Cardiol 2003: 82L Wholey MH, Maynor MA, Wholey MH et al. Comparison of thrombolytic therapy of lower extremity acute, subacute and chronic arterial occlusions. Cathet Cardiovasc Diagn 1998; 44: 159–69 Motarjeme A. Thrombolysis and angioplasty of chronic iliac artery occlusions. J Vasc Interv Radiol 1995; 6: 665–725 Motarjeme A. Thrombolytic therapy in arterial occlusion and graft thrombosis. Semin Vasc Surg 1989; 2: 155–78 Atmakuri SR, Lev EI, Alviar C et al. Initial experience with a magnetic navigation system for percutaneous coronary intervention in complex coronary artery lesions. J Am Coll Cardiol 2006; 47(3): 515–21 Strauss BH, Goldman L, Qiang B et al. Collagenase plaque digestion for facilitating guide wire crossing in chronic total occlusions. Circulation 2003; 108(10): 1259–62
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32.
Raval AN, Karmarkar PV, Guttman MA et al. Real-time magnetic resonance imaging-guided endovascular recanalization of chronic total arterial occlusion in a swine model. Circulation 2006; 113(8): 1101–7
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Catheter-directed intra-arterial thrombolytic therapy NN Khanna and RR Kasliwal
Introduction
In chronic limb ischemia:
Up until now, surgery was the only means of treating limb ischemia because of thrombosis in the peripheral arterial system. Acute lower limb ischemia (ALLI) is a surgical emergency and is associated with significant mortality and high rates of limb loss if there is delay in the treatment.1,2 Until now, surgical embolectomy had been the only approach but it is still associated with 10–18%3,4 amputation rate and 5–18% mortality.5,6 This is because surgical balloon thromboembolectomy (Fogarty embolectomy) causes endothelial damage and cannot de-clot small arteries of the leg and foot. Moreover, surgery carries a risk of infection and anesthesia. Catheter-directed intra-arterial thrombolytic therapy (CDTT) has been developed and perfected to treat thrombotic occlusion of the peripheral arteries. CDTT consists of direct intra-arterial infusion of a concentrated dose of fibrinolytic agents into the thrombus to restore blood flow to the ischemic limb. This uncovers underlying stenotic lesions which are then treated by an endovascular or surgical approach. Because the lytic agent is infused locally, the risk of bleeding is drastically reduced and the systemic affects of the drug are also reduced. In 1963, McNicol et al. and Verstraete et al. were the first to report their experience of local intra-arterial thrombolysis for peripheral arterial occlusions using intra-arterial streptokinase infusion. The father of interventional radiology, Charles Dotter9 proposed the basic presets of catheter-directed local delivery of thrombolytic agents directly at the sight of thrombosis. Dotter’s coaxial system led to larger arteriotomy size and resulted in a higher incidence of hemorrhagic complications. Subsequent refinement of the catheter design by Porstman10 and Gruntzig11 in 1970s and 1980s lead to a resurgence of peripheral intra-arterial thrombolysis in 1990s.
●
General goals of catheter-directed intra-arterial thrombolysis
●
●
to recanalize a chronic total occlusion; to soften the old clot which may then be treated by endovascular technique; to restore proximal vessel patency to facilitate distal bypass.
In this chapter, we will discuss the current status of catheterdirected intra-arterial thrombolytic therapy, including its indications, techniques, hardware, and results.
Thrombolytic agents The following thrombolytic agents are in general practice: ● ● ● ● ●
streptokinase (STK) urokinase recombinant tissue plasminogen activator (rtPA) anistreplase (APSAC) reteplase.
Urokinase and rtPA are commonly used in clinical practice. Although urokinase is very effective, its use has been banned in the US. rtPA is the only agent which is being used in that country. The pharmacokinetics, advantages and disadvantages of streptokinase, urokinase, and rtPA are given in the Table 16.1. Several new thrombolytic agents are under clinical trial. Recently, clinical studies in peripheral arterial occlusion have been published for recombinant urokinase,7 recombinant glycosylated pro-urokinase,8 and recombinant staphylokinase.9 Recombinant glycosylated pro-urokinase and recombinant staphylokinase have been shown to be effective without inducing fibrinogen depletion. Fibrin specificity of these agents appears to be an important advancement in CDTT because fibrinogen depletion is significantly (p < 0.01) related to hemorrhagic complications of urokinase and rtPA.10
In acute limb ischemia: ● ● ●
● ●
to restore antegrade flow by thrombolysis; to lyse thrombus in distal run-off vessels; to convert urgent surgical revascularization to elective surgical/endovascular revascularization; to limit the extent of surgical revascularization; to minimize the level of amputation when limb salvage fails.
Streptokinase (STK) In the early days of intra-arterial thrombolysis, STK was the most widely used agent. Hess et al.11 in 1982 originally proposed repeated intrathombus injection of 1000–3000 IU of STK with step-by-step advancement of catheter between two injections (stepwise infusion). However, this regimen was soon replaced by low-dose continuous infusion with the aid of 99
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Textbook of peripheral vascular interventions Table 16.1
Thrombolytic agents for CDTT
Dose:bolus Infusion Half-life Fibrin specificity Rate of lysis Hemorrhage Clinical success Immunogenic Platelet activation
rtPA
Urokinase
Streptokinase
— 0.5–2.0 mg/h < 5 min High Rapid 10% 90% No No
250,000 U 50,000–100,000 units/h 15 min Intermediate Slow 10% 75–90% Yes No
Empirical Empirical 23 min Low Slow 20% 60–70% Yes Yes
an arterial infusion pump at a rate of 5000 IU/hour following excellent results reported by Katzen in 1981.12 However, his results were not reproduced by MacNamara and other groups13 and in recent years, and rtPA has largely superceded and replaced streptokinase as the preferred agent in clinical use. Urokinase The dosage schemes varied initially, but now the low-dose concept is being gradually replaced with high-dose regimen. The most popular protocol was introduced by MacNamara13 and consists of initial infusion of 4000 IU/minute for 2 hours or until restoration of antegrade flow followed by 2000 IU/minute for the next 2 hours and 1000 IU/hour for the next 4–24 hours or until the lysis is completed. Systemic heparin infusion is continued during CDTT and is continued until definite endovascular or surgical treatment of underlying lesion is completed. MacNamara reported complete lysis in 75% cases.13 The average time for initial re-establishment of antegrade flow was 3.3 hours and for complete clot lysis was 13 hours. Significant bleeding complications were seen in only 4% of cases. Further analysis resulted in the following useful precepts: 1. Easy traversibility of the clot with non-hydrophilic guidewire (0.035-inch outside diameter) indicated that the thrombus was still not organized and predicted 100% success of thrombolysis (the wire traversal test) (Figure 16.1). 2. Significant lysis within the first 2 hours also predicted 100% likelihood of achieving complete clot lysis with continued infusion of urokinase. 3. Heparin infusion (maintaining APTT from 80 to 120 seconds) prevented pericatheter thrombus, distal embolization and was not associated with increased incidence of bleeding. 4. The final 10–20% of the clot is slow to lyse and can be often mistaken for an atherosclerotic plaque. PTA at this stage may lead to fragmentation and distal embolization of the thrombus resulting in acute ischemic insult of the leg and foot. 5. Underlying flow limiting lesion is present in 70% of the cases and surgery or PTA can be performed immediately after thrombolysis with no additional risk of bleeding.
Phase 1 of the Thrombolysis or Peripheral Arterial Surgery (TOPAS) trial compared the safety and efficacy of three dosage schemes of recombinant urokinase with the operative interventions in 213 patients with acute lower extremity ischemia. It concluded that 240,000 IU/hour for 4 hours and then 120,000 IU/hour to a maximum of 48 hours was the most appropriate regimen with a lytic efficacy of 71% and a bleeding risk of just 2%.14 Recombinant tissue plasminogen activator (rtPA) The range of usual dosage schemes for catheter-directed thrombolytic therapy has been 0.05–0.1 mg/kg/hour or 0.25–1.0 mg/hour. Usually either 0.05 mg/kg/hour or 1 mg/hour infusion is used. There are few prospective randomized trials comparing different thrombolytic agents. One open-ended trial compared intra-arterial STK with intra-arterial and intravenous tPA in 60 patients with recent onset or deterioration of pre-existing limb ischemia.15 Initial angiographic success
Figure 16.1
Wire traversal test.
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Catheter-directed intra-arterial thrombolytic therapy was 100% with intra-arterial tPA, 80% (p < 0.04) with intra-arterial STK, 45% (p < 0.01) with intravenous tPA. The 30-day limb salvage rates were 80, 60, and 45% respectively. In the Surgery versus Thrombolysis for Ischemia of the Lower Extremity (STILE) study, there was no difference in efficacy or bleeding complications in patients receiving tPA or urokinase.16
Dosage Table 16.2 summarizes the recommended doses of various thrombolytic agents for catheter-directed peripheral intra-arterial thrombolysis.
Delivery catheter systems Several catheters have been specifically designed for infusion of thrombolytic agents. Most of them are = 5 French in caliber and may have an end-hole or side-holes over different infusing lengths (5, 10, 15, 20 cm). They may or may not require an end-hole occluding wire. Recent designs incorporate a oneway valve at the distal end so that the tip-occluding wire is not needed during pulse spray infusion. Some people have also used a two-catheter system coaxially (e.g. 5-French outer with a 3-French inner) to bathe long segments evenly and to change the infusion length as the thrombolysis progresses. Some of the commercially available drug delivery catheters are: ● ● ● ●
Angiodynamic drug delivery catheter McNamara coaxial catheter Mewissen multi-side-hole catheter (Figure 16.2) Katzen infusion wire
Table 16.2
● ● ●
SOS infusion wire Cragg Convertible wire Dispatch catheter
However, till now there is no evidence that a particular infusion catheter or technique is superior to the other. Infusion methods Stepwise infusion This consists of stepwise advancement of the tip of infusion catheter as the thrombus dissolves. It is labor-intensive and requires the patient to remain in the angiographic suite. Graded infusion This refers to the protocol of periodic tapering of infusion rate. McNamara13 was the first to demonstrate the shortening of the duration and reducing the dose of lytic therapy by using this technique. Continuous infusion This is the most common method of catheter-directed thrombolysis. This may or may not be preceded by intrathrombus lacing. Pulse spray technique This refers to the technique of forcibly injecting thrombolytic agent into the thrombus to fragment it so as to increase the surface area available for the action of thrombolytic agents. It was originally developed for the potential of accelerating lysis.
Adjunctive technique Catheter suction thromboembolectomy (thromboaspiration), and mechanical thrombectomy by Possis Angiojet or
Recommended doses of various thrombolytic agents for CDTT
Agent
Infusion technique
Dose
Urokinase
Continuous infusion Graded infusion
120,000–240,000 IU/h McNamara protocol 4000 IU/min for 2 hours or up to restoration of antegrade flow followed by 2000 IU/min for 12–24 h or until complete lysis 60,000 IU followed by McNamara protocol 250,000 IU followed by 50,000 IU/h 5000 IU every 30 s for 20 min 2000 IU/cm occlusion length 1000–2000 IU/min in distal thrombus
Intrathrombus lacing Pulse spray
rtPA
Streptokinase Topas trial
Intraoperative thrombolysis Continuous infusion Pulse spray Intraoperative thrombolysis Continuous infusion Intraoperative thrombolysis
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0.05–0.1 mg/kg/h 3 × 5 mg (0.33 mg/ml) at 5–10 min interval) followed by 0.05 mg/kg/h infusion 0.1 mg every 30 s for 20 min 3 × 5 mg bolus over 30 min 3000–4000 every 3–5 5000–150,000 IU slow bolus or within 30 min 240,000 IU/h × 4 h 120,000 IU/h for up to maximum of 48 h
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(a)
(b)
(d)
(e)
(c)
Figure 16.2 (a) Acute thrombosis of right superficial femoral artery and popliteal artery; (b) result after 24 hours of thrombolysis; (c) mechanical thrombectomy with Oasis thrombectomy catheter; (d) final result after sequential thrombolysis with urokinase. Complete resolution of thrombus in right superficial femoral artery; and (e) final result: complete resolution of thrombus in popliteal artery.
(a)
(b)
(c)
Figure 16.3 (a) Acute thrombosis of left axillary artery; (b) catheter-directed intra-arterial thrombolysis (CDTT) using a multiple-hole Meweissen catheter placed in the entire length of thrombus; (c) final result after 18 hours of CDTT.
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Catheter-directed intra-arterial thrombolytic therapy Hydrolyser are adjunctive techniques to remove arterial clots. They may be used in conjunction with peripheral intra-arterial thrombolysis. Peri-procedural anticoagulation (heparin) is recommended until the underlying cause has been corrected. Aspirin therapy is also recommended.
Clinical indications The potential benefit of thrombolytic intervention with respect to alternative treatment modalities should be balanced against the potential risks of intra-arterial thrombolysis. The following are the indications of catheter directed intra-arterial thrombolytic therapy. Acute arterial occlusion Acute limb ischemia is a clinical challenge to clinicians. The problem presented by acute ischemia is compounded by the problems following revascularization due to reperfusion injury. In spite of several advancements in the management (both surgical and endovascular) acute limb ischemia continues to be associated with significant mortality and limb loss. Except in cases of profoundly ischemic limb where unacceptable delay in effective reperfusion is anticipated with thrombolysis, or in patients of irreversible limb ischemia, intra-arterial thrombolysis is the treatment of choice. If started early, it offers the greatest potential for saving lives and limbs. Therapeutic anticoagulation and correction of underlying lesion is also a part of overall management strategy in these patients. Surgical/Fogarty embolectomy has been associated with 10–30% mortality and limb loss. Intra-arterial thrombolysis followed by endovascular correction of the underlying lesion, on the contrary, is associated with just 1.6% 30-day mortality and 8% amputation rate.17 An interesting cost-effectiveness study by Kolassa et al. reported that CDTT is 47% more costeffective than immediate surgical intervention (based on the cost per life saved).18 Chronic arterial occlusion CDTT for chronic arterial occlusions is successful in 80% of the cases. However, it requires prolonged infusion. Chronic occlusions and chronic critical limb ischemia is often associated with extensively diseased vascular bed, advanced age, and coronary artery disease. The pioneering work of Amir Motarjeme19 revealed that even if one segment is recanalized the improvement in blood flow is sufficient to treat rest pain or ulcers. If the revascularized segment remains patent for 3 months, the non-healing ulcer will heal and interestingly the recurrence of this occlusion is not necessarily followed by the recurrences of the ulcer. However, for the treatment of gangrene, pulsatile blood flow to the foot is essential. Therefore, complete revascularization is advised. In a study of 238 patients, Mortarjeme reported 78% 5-year limb salvage rate and 60% 4-year primary patency rates with intra-arterial thrombolysis.20 Reocclusions are usually late and most of the time are associated with a benign course and less marked
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symptoms. They occur primarily in infrainguinal locations and can be prevented by regular duplex surveillance and timely treatment of restenosis (Figures 16. 4 and 16.5). Occluded bypass grafts Although open surgical procedure has been the traditional approach for bypass graft occlusion, intra-arterial thrombolysis has been advocated as an alternative means for restoring arterial patency. It is quite simple and effective, and successful CDTT unmasks the cause of bypass graft failure in the majority of cases thereby facilitating further treatment strategy. It also cleans clots in the distal outflow thereby reducing the chances of rethrombosis. Graft patency after successful CDTT and endovascular correction of the underlying stenosis is 89% at 1 year and 79% at the end of second year. Secondary patency is better for aortobifemoral bypass and venous grafts as compared to prosthetic grafts (24–69% vs. 29%) and below knee-vein grafts with thrombosis of small outflow vessels. Patients with graft occlusion of less than 2 weeks duration should be offered thrombolytic therapy as primary treatment modality. Thromboembolism Clinical diagnosis of arterial embolism in the leg is suggested on the basis of a sudden onset of clinical symptoms, the presence of an embolic source, and the absence of preceding claudication. Thrombolysis as well as thromboaspiration are the preferred lines of treatment as Fogarty’s thromboembolectomy is incomplete in 30% of cases. Full dose of intravenous heparin should be used in conjunction with intra-arterial thrombolysis. Thrombolysis is particularly useful in the setting of a fragmented thrombus which occludes many branches, and where it is complicated by a propagated thrombus (Figure 16.6). Peroperative thrombolysis Peroperative thrombolysis is used for residual thromboembolic material following mechanical thromboembolectomy or for thrombotic occlusion of small arteries in patients already undergoing an open surgical procedure. Thrombolytics are given as bolus or slow infusion as close as possible to the clot or within the thrombus itself. Acute occlusion following PTA Two to three percent of patients undergoing PTA have acute thrombotic occlusion. It is successfully managed by intra-arterial urokinase or rtPA infusion. Distal emboli can also be treated successfully by catheter-directed thrombolytic therapy. Thrombosed popliteal aneurysm These occur in association with an aortic aneurysm and usually present with acute ischemia. The aim of intra-arterial thrombolysis in these patients is only to restore patency of the thrombosed distal run-off vessels. The aneurysm itself is treated surgically.
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(a)
(b)
(d)
(e)
(c)
Figure 16.4 (a, b) Chronic thrombosis of left axillary artery, brachial artery, radial, and ulnar arteries; (c–e) complete resolution of thrombus in axillary artery, brachial artery, radial, and ulnar arteries and palmer arch arteries after 108 hours of CDTT.
Trash foot/blue toe syndrome Classically this was thought to be caused by cholesterol embolism from ulcerated plaque but is now thought to be due to thromboemboli. Intra-arterial thrombolysis is very effective in these groups of patients and usually changes the prognosis from amputation to no tissue loss. Heparin-induced thrombotic thrombocytopenia (HITT) Heparin induced thrombotic thrombocytopenia (HITT) was until now considered as absolute contraindication for intraarterial thrombolysis for the risk of bleeding complications. However, it is the only treatment available and represents an important breakthrough in the treatment of this condition as surgery is not possible because of the inability to use heparin. CDTT is not associated with unusual bleeding despite the thrombocytopenia. Acute ischemic stroke Intracranial microcatheter-directed thrombolysis by urokinase or rtPA has yielded 80% success in thrombus clearance
within 1 to 2 hours of infusion.21 Reports have suggested that the incidence of intra-cerebral hemorrhage is not significantly increased by intracranial thrombolysis. Thrombosed dialysis access grafts These are readily treated by thrombolysis and adjuvant PTA with 90% initial success. Secondary patency rates at 6 months and 1 year are 75 and 25%.22 The procedure is very fast and hemodialysis can be resumed within 2 hours. Therefore, these patients can remain on their hemodialysis schedule without the need for placing a temporary hemodialysis catheter and a surgical revision can be avoided for a long time. Bookstein’s strategy of pulse spray delivery of urokinase to declot the dialysis graft is very popular at the present time. Massive pulmonary embolism Massive pulmonary embolism (Figure 16.7) is a cardiac emergency and is best treated by CDTT using urokinase or TPA delivered directly into the clot in a pulmonary artery.
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(a)
(b)
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(c)
(d) Figure 16.5 (a) Chronic popliteal thrombosis (duration 3 months); (b) CDTT using multiple side-hole 4-French multipurpose catheter placed in the entire length of popliteal and proximal part of anterior tibial artery; (c, d) complete lysis after 76 hours of thrombolysis showing totally recanalized popliteal artery and anterior tibial artery.
Its results are better than that of IV heparin alone and thrombolysis is achieved much faster than with IV heparin. It is often accompanied by intrapulmonary artery hydrolytic thrombectomy by Angiojet or plain and simple thrombosuction.
●
● ● ● ●
Contraindications
● ●
Absolute ● established cerebrovascular accident (including TIAs within the last 2 months); ● intracranial trauma within the last 3 months; ● neurosurgery (intracranial, spinal) within the last 3 months; ● active bleeding diathesis; ● recent gastrointestinal bleeding (< 10 days). Relative cardiopulmonary resuscitation within the last 10 days; ● major non-vascular surgery or trauma within the last 10 days; ●
uncontrolled hypertension: > 180 mmHg systolic or > 110 mmHg diastolic; puncture of non-compressible vessel; intracranial tumor; hepatic failure, particularly those with coagulopathy; bacterial endocarditis; pregnancy; diabetic hemorrhagic retinopathy.
Complications Hemorrhage is the most common complication of CDTT. It may occur because of lysis of pre-existing hemostatic plug or loss of vascular integrity. Berridge et al.23 did a meta-analysis of ten prospective series of patients undergoing peripheral intra-arterial thrombolysis to determine the incidence of hemorrhagic complications. The overall risk of hemorrhagic stroke was 1% (14 out of 1401 patients). Major and minor bleeding occurred in 5.1 and 14.8% of patients. Recently Dawson et al.24 reported on the series of patients of the British Thrombolysis Study Group and found the incidence of
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(a)
(b)
(d)
(e)
(c)
Figure 16.6 (a, b) Massive thromboembolism in a patient of dilated cardio myopathy and atrial fibrillation resulting in saddle embolism of aortic bifurcation, total occlusion of left common iliac artery and left common femoral artery, partial occlusion of right common femoral artery, and saddle embolism at right common femoral bifurcation; (c) CDTT using 4-French pigtail catheter via left radial route placed at aortic bifurcation; and (d, e) complete resolution of thrombus after 12 hours of CDTT.
hemorrhagic stroke to be 2.3% (27 of 1157 patients) (half of which occurred during thrombolysis). STILE and TOPAS investigators (comparing surgery vs. thrombolysis) reported incidence of intracranial bleeding to be 1.2 and 2.1% respectively.7 Bleeding into the retroperitoneal space from the inadvertent posterior wall puncture may go undetected until hypotension develops or the patient presents with unexpected abdominal symptoms or back pain or sudden development of anemia without obvious blood loss. In cases of major hemorrhage, CDTT is discontinued and any coagulation defect if present is corrected. Irrespective of the site of major bleeding, management follows a standard pattern of discontinuation of CDTT and anticoagulation, replenishment of coagulation factors and blood, surgical evacuation of hematoma (if necessary), and rapid reversal of fibrinolytic state by tranexemic acid or epsilon aminocaproic acid (in cases of life-threatening hemorrhage). Distal embolization of a partially lysed clot is also a potential risk. Small emboli are clinically silent but large fragments that occlude distal tibial or foot arteries are potentially more harmful and may lead to clear clinical deterioration. However,
CDTT should be continued in this case. Additional measures to be considered are the repositioning of the infusion catheter more distally, increasing the dose or new boluses of thrombolytics, thromboaspiration, and angiojet. Allergic reactions can occur with STK and usually present with flushing, vasodilation, rash, hypotension, or anaphylaxis. Late reactions include serum-like illness and presents with joint pain, fever, and microscopic hematurea, usually 10–21 days after the thrombolysis. It has a benign outcome although permanent renal impairment has been reported.
Technique of catheter directed intra-arterial thrombolytic therapy (CDTT) Patient selection Patient selection is aimed at re-establishing blood flow. Best results are seen in thrombus which is less than 2 weeks old. However, lysis has been successful up to 90 days
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(f)
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Figure 16.7 (a) Massive pulmonary embolism leading to saddle embolism in main pulmonary artery and massive occlusive thrombus in bilateral pulmonary arteries; (b–e) Possis Angiojet thrombectomy of main pulmonary artery and right and left upper and lower lobe pulmonary arteries; and (f–h) excellent thrombolysis and recanalization of bilateral pulmonary arteries.
(although it takes longer time to lyse and the rate of success is low). The predictors of success are: ●
●
guidewire traversal test (if the guidewire traverses the clot, the chances of success are 100%); age of thrombus < 14 days (almost 100% success);
● ● ●
length of thrombus < 5 cm; good distal run-off; evidence of clot resolution within 2 hours (almost 100% success).
Patient selection is also aimed at minimizing the risk of bleeding or in other words excluding patients who are at a
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high risk of bleeding and ischemic complications and reperfusion injury. These contraindications are: ● ● ● ●
● ● ● ● ● ● ●
recent internal bleeding = 10 days; cerebrovascular accident < 6 months; transient ischemic attack < 2 months; history of gastrointestinal bleeding, cardiopulmonary resuscitation, major trauma, pregnancy < 6 months; systolic BP > 180 mmHg and diastolic BP > 110 mmHg; recent major surgery < 2 weeks; infective endocarditis; hepatic and renal failure; patients with intracardiac thrombus; established compartment syndrome or evidence of myolysis; patients with electrolyte imbalance, systemic acidosis, or left ventricular dysfunction.
Patient preparation Informed consent should be taken before the procedure and the risk and benefits of the procedure should be explained. Consent should also be taken for additional surgical or interventional procedure which may be required when underlying stenotic lesion is uncovered. Laboratory work should include complete blood counts, electrolytes, urea and creatinine, myoglobin, CPK, bleeding and coagulation time, blood grouping and cross-matching, prothrombin time, partial thromboplastin time, and activated clotting time (for monitoring heparin therapy). Some centers also assess parameters which reflect systemic lytic state (e.g. fibrinogen, fibrin degradation product (FDP), plasminogen levels). Very low levels of fibrinogen (< 10%) predicts bleeding complications. Technique The first step is to do an initial baseline angiography to map out the location and size of thrombus, the feeding collaterals and distal run-off vessels. Arterial access is then gained through antegrade ipsilateral approach or contralateral retrograde crossover approach. A 5-French or 6-French arterial sheath is placed. Then a guidewire transversal test is done to characterize the thrombus. Failure to cross the thrombus predicts a lower success rate and prolonged infusion time. In this situation the catheter is left proximal to the clot. In many cases the thrombus subsequently softens and can be crossed easily. After crossing the thrombus the infusion catheter is placed in the thrombus and the lytic agent is infused. Any of the previously described infusion methods can be adapted.
Monitoring the therapy Patients of catheter-directed intra-arterial thrombolytic therapy are kept under close observation in the intensive care unit. The ACT is kept between 200 and 250 seconds and the PTTK is kept between 2 and 2.5 times control. Continuous intra-arterial heparin is given through the side part of the arterial sheath to prevent clot formation around the catheter. Continuous hemodynamic and hematocrit monitoring is done for assessment of any
possibility of internal bleeding. The access site is closely observed and urine output is closely monitored. After completion of lysis the infusion catheter and the arterial sheath are removed and systemic anticoagulation is started after 4 hours. Angiographies are done frequently to assess the progress of thrombolysis and many the infusion catheter are advanced or readjusted regularly. After completion of thrombolysis underlying lesions are treated by PTA or stenting.
Experience at the Polyclinique Essey-Les-Nancy, France Our data for catheter-directed intra-arterial thrombolysis in 113 consecutive patients is reported below. Material and methods Eighty-three patients received intra-arterial thrombolysis between January 1999 and December 2005. The mean age of these patients was 60.6 ± 8.5 years (46–89 years). The majority of them were males and had thrombosis of the native arteries of the lower extremity. Thirty-nine had thrombosis of aortobifemoral or femoropopliteal bypass grafts. Eight-two of these 113 patients were referred to us within 15–90 days of the onset of thrombosis. The thrombolysis was done with intra-arterial infusion of urokinase according to McNamara’s protocol (4000 IU/minute for 2 hours followed by 2000 IU/minute for the next 2 hours and 1000–2000 IU/min until lysis completion. All patients received adjuvant aspirin and heparin infusion. Urokinase was delivered by Mewissen or thrombolysis catheter (Medicorp S.A., Villers-les-Nancy, France). The infusion catheter was positioned within the thrombus and advanced forwards as the fibrinolysis progressed. The patients were shifted to the CCU and brought back to the catheterization lab every 2–4 hours for angiographic reassessment of the progress of fibrinolysis, until the lysis was complete or there was no improvement. In most of the cases underlying stenosis was present and was treated. Patients with failure of lysis were either subjected to clot removal by thromboaspiration or were sent for surgery. All patients were followed up by angiography at 6 hours and by duplex scan at 1 day, 1 month and 6 months. Results One-hundred and thirteen consecutive patients with mean age of 60.6 ± 8.5 years underwent CDTT. Thrombosis was present in native arteries in 74 patients and in the bypass grafts in 39 patients. The duration of thrombosis was 1–4 days in 26 patients, 15–90 days in 82 patients and more than 90 days in 5 patients (Box 16.1) Complete clot lysis was seen in 80% of the patients (92/113). The mean duration of fibrinolysis was 18 hours. Incomplete lysis was seen in 19% of the patients (21/113). In the patients who failed to achieve significant clot lysis the majority had a more than 30-day-old thrombus. In seven of these patients the lysis was significant but still incomplete and
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Catheter-directed intra-arterial thrombolytic therapy Box 16.1 ● ●
No. of patients: Age
●
Male / Female
●
Bypass Grafts: Duration of thrombosis 䊊 1–14 days 䊊 15–90 days 䊊 ≥ 91 days Duratioin of fibrinolysis
●
●
Box 16.3 113 60.6 ± 8.5 (46–89) Aorticilicac : 30 Femoropopliteal: 41 Tibioperoneal : 3
25 82 5 18 hours
the residual clot was removed by thromboaspiration. The remaining 14 patients were sent for surgery. Significant underlying stenosis was present in 70 patients. Twenty-seven of them were treated with angioplasty alone while 43 patients received stent implantation. The success of CDTT was greater in patients of thrombosis of bypass graft (88%) (Box 16.2). Nineteen patients had minor complications in the form of local hematoma at the puncture site. Four patients had a major hematoma requiring surgery or blood transfusion. Distal embolism was seen in five patients and was successfully managed by increasing the infusion rate of urokinase and advancement of the infusion catheter near the emboli or by thromboaspiration. One patient died because of severe renal and cardiac failure. This patient had advanced chronic renal failure and severe coronary artery disease. None of our 113 patients had systemic or intracranial bleeding.
Discussion At six months, 63 of these 79 patients were followed up. Fifty-three had patent-treated arteries and grafts while restenosis
Complications
• Hematoma 䊊 Major: 4 䊊 Minor: 19 • Embolism: 5 • Death: 1 (Due to severe renal and cardiac failure) • Intracranial/systemic bleeding 0
was seen in ten patients. They were managed by repeat PTA in nine cases. One patient went for surgery because of personal preference. CDTT is very effective and saves the patients from limb loss or dying. It is better than surgery in most of the situations as surgery carries higher risk of complications. Ouriel reported lower in-hospital complications and mortality rates with fibrinolysis as compared to surgery (22 vs. 80%, p < 0.05).24? In the STILE trial at 6-months follow-up, patients who received PIAT had lower amputation rate (16 vs. 30%, p < 0.02) in comparison to those who went for surgery. The Rochester trial reported the results of a 12-month follow-up. The mortality rates in the thrombolysis group were 16 versus 58% in surgery group (p < 0.01). Conclusion PIAT is a safe, effective and alternative treatment modality for the treatment of thrombosis of native arteries and bypass grafts. The initial results are very encouraging and reports from various trials (STILE, TOPAS, ROCHESTER)4,5,6 suggest that it is perhaps better than surgery in terms of saving lives and limbs and is perhaps more cost-effective. Many advances have occurred in the CDTT technique and the experience is now growing in the interventional arena. The technique is now being picked up by cardiologist, radiologists, and vascular surgeons.
Box 16.2 Thrombolysis experience at the Polyclinique, Essey-les-Nancy, France Immediate results • Complete lysis: • Incomplete lysis: 䊊 Thromboaspiration: 䊊 Surgery: • Significant underlying stenosis:
Box 16.4 92 (81%) 21 (19%) 7 14 70
79% 88% 81%
Thrombolysis follow-up
113 Patients Day 1 Day 30
92 Patients F/U = 82 Patients 79 Patients
6 months
F/U = 63 53 patients
PTA (43 stents) • Success in 䊊 Native arteries: 䊊 Bypass grafts: 䊊 Occlusions 1–14 days: 䊊 Occlusions 15–90 days:
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21 incomplete lysis Lost to F/U: 10 3 occluded 2 surgery 1 PTA Lost to F/U: 16 10 Restenosis 1 surgery 9 PTA
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REFERENCES 1. Baxter-Smith D, Ashton F, Slaney G. Peripheral arterial embolism: a 20 year review. J. Cardiovasc Surg 1988; 29: 453 2. Linton RR. Peripheral arterial embolism: a discussion of the postembolic vascular changes and their relation to the restoration of circulation in peripheral embolism. N Eng J Med 1941; 224: 189 3. McPhail NV, Frastesi SJ, Barber GG et al. Management of acute thromboembolic limb ischemia. Surgery 1983; 93: 381–5 4. The STILE investigators. Results of a prospective randomized trials evaluating surgery versus thrombolysis for ischemia of the lower extremities. Ann Surg 1994; 220: 251–68 5. Macky WC. Peripheral embolization and thrombosis. In: Strandness DE Jr, van Berda A, eds. Vascular Disease: Surgical and Interventional Therapy. New York: Churchill Livingstone, 1994: 341–54 6. Ouriel K, Shortell CK, De Weese JA et al. A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg 1994; 19: 1021–30 7. For the TOPAS Investigators, Ouriel K, Veith FJ, Sasahara AA. Thrombolysis or peripheral arterial surgery (TOPAS): Phase 1 results. J Vasc Surg 1996; 23: 64–75 8. Hartmann JR, Enger EL, Villiard EM et al. Dose ranging trial of intra arterial r-prourokinase (A 74187) for thrombolysis of total peripheral arterial occlusions (abstr). J Am Coll Cardiol 1994; 23: Suppl: 95A 9. Collen D, Moreau H, Stockx L et al. Recombinant staphylokinase variants with altered reactivity. IV. Identification of variants with reduced antibody induction but intact potency. Circulation 1997; 95: 463–72 10. The STILE Investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity: The STILE trial. Ann Surg 1994; 220: 51–68 11. Sullivan KL, Gardiner GA, Shapiro MJ et al. Acceleration of thrombolysis with a high dose transthrombus bolus technique. Radiology 1989; 173: 805–8 12. Katzen BT, Van Breda A. Low-dose streptokinase in the treatment of arterial occlusion. Am J Roentgenol 1981; 136: 1171–8
13. McNamara TO. Overview of thrombolysis for interventionalist. Ninth ETC Peripheral Course Book. Poieters: Europa, 1998, 105–21 14. Ouriel K, Shortell CK, De Weese JA et al. A comparison of thrombolytic therapy with acute peripheral arterial ischemia. J Vasc Surg 1994; 19: 1021–70 15. Berridge DC, Gregson RHS, Hopkinson BR et al. Randomized trial of intra arterial recombinant tissue plasminogen activator, intravenous plasminogen activator and intra-arterial streptokinase in peripheral arterial thrombolysis. Br Surg 1991; 78: 988–95 16. Allermand H, Wetergard-Nielsen J, Nielsen O. Lower limb embolectomy in old age. J Cardiovasc Surg 1986; 27: 440–2 17. Blaisdell FW, Steel M, Allen RE. Management of acute lower extremity ischemia due to embolism and thrombosis. Surgery 1978; 84: 822–34 18. Jivegard L, Holm J, Shresten T. The outcome in arterial thrombosis misdiagnosed as arterial embolism. Acta Chir Scand 1986; 152: 251–6 19. Motarjeme A. Thrombolytic therapy in arterial occlusion and graft thrombosis. Semin Vasc Surg 1989; 2: 155–78 20. Motarjeme A. Initial and long term results of thrombolysoangioplasty for limb salvage. American Roentgen Ray Society, New Orleans, Louisiana, April 1990, 4: 469–72 21. Mori E, Tabuchi M, Yoshida T, et al. Intracarotid urokinase with thromboembolic occlusion of the middle cerebral artery stroke. 1988; 19: 802–2 22. Kumpe DA, Cohen MAH. Angioplasty/thrombolytic treatment of falling and failed hemodialysis access sites: Comparison with surgical treatment. Prog Cardiovasc Dis 1992; 34: 263–79 23. Berridge DC, Niakin GS, Hopkinsom BR. Local l low dose intra arterial thrombolytic therapy, the risk of major stroke and haemorrhage. Br J Surg 1989; 76: 1230–2 24. Dawson K, Armon A, Braithwaite B et al. Stroke during intra arterial thrombolysis: a survey of experience in the UK (abstr). Br J Surg 1996; 83: 568
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Thromboaspiration and thrombectomy in peripheral vessels NN Khanna
Introduction Acute and subacute thromboembolic and local thrombotic lesions of the limbs are the most common cause of amputation. The standard surgical treatment of thrombotic occlusion below the inguinal ligament is the Fogarty embolectomy. However, multiple technical problems are associated with this procedure because of atherosclerotic blockages; for example, an inability to pass the obstruction, dissection, arteriospasm, and embolization of the thrombus distally in the vascular bed.1–3 Catheter-directed thrombolytic therapy (CDTT) is time consuming and expensive (requiring intensive care and repeated check angiograms) and is associated with a high risk of embolism and hemorrhage. In addition, local stenosis carries the risk of re-occlusion.4–13 The more recent catheter-directed techniques of removing a large chunk of thrombus in the peripheral arteries are: ● ●
thromboaspiration; catheter-based thrombectomy devices.
While thromboaspiration can only be used to aspirate fresh thrombi, thrombectomy devices can actually remove large chunks of fresh as well as 1- or 2-week-old thrombus. The first directional atherectomy procedure was performed in 1985 by Simpson et al. in a superficial femoral artery using a peripheral atherectomy device.14 This initial experience demonstrated the safety of directional atherectomy for peripheral vascular disease. It was approved by the US Food and Drug Administration (FDA) in 1987. In contrast to Directional Coronary Atherectomy (DCA), which relies on excision and tissue removal, the transluminal extraction–endarterectomy catheter (TEC) (Interventional Technologies Inc., San Diego, CA) was designed by Stack to cut and aspirate atheroma and debris. In 1989, this device was approved by the FDA for peripheral vascular disease. Soon, these atherectomy devices were being used as thrombectomy devices for removing large chunks of thrombus from peripheral arteries (Figure 17.1a–c). Thrombectomy devices work on the following three principles (Table 17.1): ●
●
Vortex principle. This fragments the thrombus without removing it: 䊊 Amplatz thrombectomy catheter (ATD, Microvena); 䊊 Arrow–Trerotola Thrombolysis System (Arrow). Bernouli/Venturi principle (rheolytic thrombectomy): 䊊 Hydrolyser (Cordis);
AngioJet (Possis Medical); Oasis (Boston Scientific). Mechanical clot fragmentation plus clot removal (a combination of the above two principles). 䊊 䊊
●
Straub-Rotarex (Straub Medical) This combines two essential effects: the mechanical clot fragmentation and removal of the fragmented material from the vessel under negative pressure with the theoretical effect of preventing distal embolization of thrombus. Initial model experiments,15 a single-center experience,16 and a multicenter study17 gave promising results. The Straub-Rotarex thrombectomy system This consists of three components: a 40-W electric motor connected to an 8-French/6-French, polyurethane thrombectomy catheter via an electromagnetic clutch. Within the catheter a coated steel spiral rotates at a speed of 40,000 rpm and produces a continuous vacuum (up to 5.8 kPa = 43 mmHg). The catheter tip consists of two superimposed cylinders, each having two lateral openings with the outer cylinder connected to the rotating spiral and the inner cylinder to the catheter shaft. The thrombus is first crossed with 0.035-inch Terumo wire and then a 4-French Multipurpose Terumo glide catheter (Terumo Corp., Leuven, Belgium) is used to exchange the Terumo guidewire with a 0.014-inch/0.018-inch guidewire. The device is advanced over the guidewire to remove the thrombus. Multiple passes are made until all thrombotic material is removed. The device removes approximately 10 cm of thrombus per minute. In a single-center series,18 technical success was 84% (defined as a remaining residual stenosis of < 50%). A residual stenosis of < 30% was achieved in 32% of these. This group reported a primary success rate after additional Percutenous Transluminal Angioplasty (PTA) to be 92%. The success rate in ipsilateral approach was 100% and in contralateral crossover approach 56%. The low success rate in contralateral approach is explained by the short length of the catheter (80 cm), which was not sufficient for complete recanalization of the superficial femoral artery. The complication rate with this device was 18%, of which only 8% were device-specific complications. The device-specific complications were perforation (which was sealed by PTA in three cases and covered in five cases) and retroperitoneal hemorrhage. 111
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(a)
(b)
(c) Figure 17.1 (a) Acute thrombosis of aorto renal graft; (b) DCA of thrombosed graft; and (c) final result: total recanalization.
Amputation-free survival without recurrence of critical limb ischemia after 1 year was better than in the TOPAS5 and STILE studies6 comparing surgery with local lysis, especially in native arteries. In the TOPAS trial, amputation-free survival was 65 and 69.9% for the urokinase group and the surgery
Table 17.1 Thrombolysis experience Polyclinique, Essay-les-Nancy, France No. of patients Male/female Vessels Bypass grafts Native vessels Iliac Femoral Popliteal Tibioperoneal trunk Ant. tibial Peroneal Occlusive thrombus
at
group, respectively. However, it was 95% in this cohort with comparable baseline characteristics. The main limitation of the Rotarex device is an inability to completely recanalize long lesions through a contralateral approach because of the short length of the catheter, an inability to completely remove thrombus from vessels of large diameter (e.g. iliac arteries), and a higher incidence of perforations.
the
85 47/29 85 11 74 14 38 14 6 1 1 33
The Hydrolyser This works using the Venturi effect and is a 6-French/7-French triple lumen catheter with a small injection lumen, a larger exhaust lumen, and a 0.020-inch guidewire lumen. The device is available in different lengths and is activated with a standard pressure injector filled with saline.19 For infrainguinal occlusion, the success rate is approximately 82% with positive clinical outcomes in 73% of native vessels and 53% of grafts. In about 50% of the successful interventions, additional local lysis is required to restore the distal outflow. Distal embolization of clot particles is seen in 15%. The catheter uses a high-velocity saline stream to microfragment and remove thrombus. It is available in 6, 8,
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and 10 French for use in hemodialysis access grafts and large vessels.
and results in less vessel injuries and a lower rate of distal embolization (Figure 17.3a–g).
Oasis (Boston Scientific Inc.) This is a 6-French thrombectomy system, very similar to the Hydrolyser device. It works on the Venturi principle and has just two lumens (Figure 17.2a–c).
The Amplatz Clot Buster (ATD) This is a 7-French 100-cm-long catheter based system that induces fragmentation of thrombus without removing it.21 The device leads to time-dependent transient hemolysis. The main disadvantage of this device is the fact that it cannot be guided over a wire. There is also a potential risk of vessel wall injury.
The Possis AngioJet The Possis AngioJet catheter tip consists of multiple holes that direct high-pressure water jets into the catheter lumen to remove fragmented thrombus by means of the Venturi effect. A special pump is necessary to provide a pressure of 70,000–105,000 kPa to the catheter. In a multi-center trial in infrainguinal application,20 success rate was 90%. Technical success was improved by adjunctive fibrinolysis in 30% and thromboaspiration in 18%. There was a 2% distal embolization rate and 4% rate of dissection. The advantage of this device is that it can also be used in calf arteries (also through a contralateral approach because of the longer catheter length)
(a)
The Trerotola device This is a low-speed, rotational device (5 French) primarily designed for venous thrombolysis in dialysis fistulae.22 A stainless-steel cable is connected to a self-expanding fragmentation basket made of nitinol. After passing the occlusion in a closed position, the basket is opened, activated, and slowly withdrawn through the clot leading to a fragmentation of the clot without removing it. The advantage of this device is low profile and simple handling. The main disadvantage of this device
(b)
(c) Figure 17.2 (a) Thrombosis of right SFA; (b) oasis thrombectomy; and (c) final result.
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(a)
(b)
(c)
(d)
Figure 17.3 (a) Massive pulmonary embolism; (b–e) extensive Possis AngioJet thrombectomy in each branch of the pulmonary artery and main pulmonary artery; (f) and (g) final result: significant thrombus removal.
is the limited length and potential risk of peripheral emboli with clot particles up to 3 mm in diameter. It can also potentially injure the walls of the blood vessels.
Thromboaspiration Over the last few years, this technique has become very popular among global interventionalists and cardiologists. It is a very simple technique of directly aspirating the clot with the help of a guiding catheter or sheath. It competes with Fogarty’s embolectomy. It is often better than Fogarty embolectomy because it is done under fluoroscopic guidance and can completely remove the clot, unlike the Fogarty method, which is successful in only 70% of the cases. Moreover, Fogarty is a blind procedure and is more traumatic. Thromboaspiration is an adjunctive technique to CDTT
when clot lysis is either incomplete or is complicated by distal embolism leading to deterioration of the limb ischemia. It is also an accepted technique for removing emboli in patients with mitral stenosis and atrial fibrillation.
Technique This consists of advancement of a 6-French/7-French (wide-lumen) guiding catheter or sheath under fluoroscopic guidance up to the level of the thrombus/emboli. The guidewire is then removed and the guiding catheter/sheath is attached to a 50-ml syringe. The thrombus/emboli is then aspirated manually and the guiding catheter/sheath is withdrawn under negative suction. The procedure is repeated several times until the thrombus is completely removed. Repeated angiograms are done to confirm the clot removal (Figure 17.4a–c).
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(e)
(f)
(g) Figure 17.3, cont’d.
(a)
(b)
Figure 17.4 (a) Acute arterial embolization of brachial artery; (b) final result after thromboaspiration.
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Experience at the Polyclinique Essey-les-Nancy, France (Tables 17.1 and 17.2) Eighty-five patients underwent thromboaspiration for clot removal at the Polyclinique Essey-les-Nancy between January 1997 and December 1998. Fifty-six were males and 29 were females. Seven patients had chronic atrial fibrillation. Thrombosis was present in 72 arteries/grafts while embolism was present in 13. Seventy-four patients had thrombosis in native arteries (14 in iliac arteries, 37 in femorals, 14 in popliteal, 6 in tibioperoneal trunk, 1 in anterior tibial and 1 in peroneal artery). Nineteen patients had residual thrombus after CDTT. Occlusive thrombus was present in 33 patients (Figure 17.5a and 17.5b). The procedure was successful in completely removing the clot in 78 patients (92%) and failed in 7 (8%) cases. The failure was due to distal embolization in the foot in four patients. In the majority of the cases underlying stenosis was present (52/85) and was treated with PTA in 12 patients, PTA plus stent in 33, Rotablator in 3, Laser in 4, Hydrolyser in 3, and
Table 17.2
Thromboaspiration results
Concomitant procedures Fibrinolysis Hydrolyser Possis AngioJet Laser Rotablation Stents (PTA + stent) PTA Success Failure
19 3 1 4 3 33 12 78 (92%) 7 (8%)
AngioJet in 1. There were no complications except a dissection in one case which was successfully treated with a stent.
Discussion Thromboaspiration is a safe, cost-effective, simple, and quick method of aspirating thrombi from native arteries/bypass grafts.
(a)
(b)
Figure 17.5 (a) Thrombus aspiration in occlusion of right SFA; (b) thrombus aspiration for acute occlusion of right popliteal artery.
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Thromboaspiration and thrombectomy in peripheral vessels It is particularly useful in cases of arterial embolism and residual clots after thrombolysis. In many cases it can also be used as a first line of management in acute limb ischemia (where urgent revascularization is warranted). It is better than Fogarty embolectomy as it is done percutaneously under fluoroscopic control and angiographic guidance. Fogarty on the other hand leaves behind
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residual clots in 30% of cases. We were successful in 92% of our cases with this technique and had no major complications. Anecdotal experiences are available in literature from various groups, but large-scale trials are awaited to clarify the exact place of thromboaspiration for successful clot removal from peripheral arteries.
REFERENCES 1. 2. 3. 4.
5.
6.
7. 8.
9.
10. 11.
Blaisdell FW, Stelle M, Allen RE. Management of acute lower extremity ischemia due to embolism and thrombosis. Surgery 1978; 84: 822–34 Gordon RD, Fogarty TJ. Peripheral arterial embolism. In: Rutherford RB, ed. Vascular Surgery, second ed. Philadelphia: WB Saunders, 1984: 451 Pemberton M, Varty K, Mydahl S, Bell PRF. The surgical management of acute limb ischaemia due to native vessel occlusion. Eur J Vasc Endovasc Surg 1999; 17: 72–6 Palfreyman SJ, Michaels JA. Vascular surgical society of Great Britain and Ireland: Systematic review of intra-arterial thrombolytic therapy for peripheral vascular occlusions. Br J Surg 1999; 86: 704 Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinant urokinase with vascular surgery as initial treatment for acute arterial occlusion of the legs. Thrombolysis or Peripheral Arterial Surgery (TOPAS) Investigators. N Engl J Med 1998; 338 (16): 1105–11 Weaver FA, Comerota AJ, Youngblood M et al. Surgical revascularization versus thrombolysis for nonembolic lower extremity native artery occlusion: results of a prospective randomized trial. The STILE Investigators. Surgery versus Thrombolysis for Ischemia of the Lower Extremity. J Vasc Surg 1996; 24(4): 513–23 Lammer J, Pilger E, Neumayer K, Schreyer H. Intraarterial fibribolysis: long term results, Radiology 1986; 161: 159–63 Diffin DC, Kandarpa K. Assessment of peripheral intraarterial thrombolysis versus surgical revascularization in acute lower-limb ischemia: a review of limb-salvage and mortality statistics. JVIR 1996; 7: 57–63 Hess H, Mietaschke A, von Bilderling P, Neller P. Peripheral arterial occlusion: Local low-dose thrombolytic therapy with recombinant tissue-type plasminogen activator (rt-Pa). Eur J Vasc Endovasc Surg 1996; 12: 97–104 Tepe G, Lutz O, Hahn U, Pereira P et al. Gepulste Spraylyse mit Reteplase bei peripheren arteriellen Verschlussen – Technik aund erste Ergebnisse. Fortschr Rontgenstr 2000; 172: 780–84 Zahringer M, Heidel W, Gawenda M, Brochhagen HG, Landwehrr P. Akuter thrombembolischer Verschlub der A. Poplitea und
12. 13.
14. 15. 16. 17. 18. 19. 20. 21. 22.
Trifurkation aus einer als Anlageanomalie erhaltenen A, ischiadica. Fortschr Rontgenstr 1999; 171: 79–81 McNamara TO, Bomberger RA, Merchant RF. Intra arterial urokinase as the initial therapy for acutely ischemic lower limbs. Circulation 1991; 83(suppl 1): I–106, I–119 Meyerovitz MF, Goldhaber SZ, Reagan K et al. Recombinant tissue-type plasminogen activator versus urokinase in peripheral arterial and graft occlusions: a randomized trial. Radiology 1990; 175: 75–8 Simpson JB, Selmon MR, Robertson GC et al. Transluminal atherectomy for occlusive peripheral vascular disease. Am J Cardiol 1988; 61: 96G–101G Schmitt HE, Jager KA, Jacob Al et al. A new rotational thrombectomy catheter: system design and first clinical experiences. Cardiovasc Intervent Radiol 1999; 22: 504–9 Zeller T, Muller C, Frank U et al. Das Straub-Rotarex – thrombektomie-System: Erste Erfahrungen. Fortschr Rontgenstr 2001; 173: 626–31 Jager KA, Schmitt EM, Schmitt HE, Labs KH. Peripheral thrombectomy with the new Straub-Rotarex Catheter: A multicenter study. Intern Angiol 1999; (suppl. 1): 17A Zeller T. Recanalisation of thrombotic arterial and bypass occlusions using a mechanical thrombectomy device. The Paris Course on Revascularization 2003; 511: 522 Bucker A, Schmitz-Rode TH, Vorwerk D, Gunther RW. Comparative in vitro study of two percutaneous hydrodynamic thrombectomy systems. JVIR 1996; 7: 451–4 Trerotola SO, Lunc GB, Scheel PJ et al. Thrombosed dialysis access grafts: Percutaneous mechanical declotting without urokinase. Radiology 1994; 191: 721–6 Bildsoe MMC, Moradian GP, Hunter DW, Castaneda-Zuniga WR, Amplatz K. Mechanical clot dissolution: new concept. Radiology 1989; 171: 231–3 Tretola SO, Johnson MS, Schauwerker DS et al. Pulmonary emboli from pulsed-spray and mechanical thrombolysis: Evaluation with an animal dialysis-graft model. Radiology 1996; 200: 169–76
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The future of thrombolysis T McNamara
Increasing applications Stroke 1. The increasing age of the world’s population will increase the number of patients with stroke. 2. The triage will improve to bring patients in earlier. 3. Existing techniques will improve as follows: a. Combining ultrasound delivered through the tip of a catheter increases the effectiveness of lysis resulting in shorter times to re-establishment of flow without increasing the risk of bleeding. b. Giving a concurrent infusion of microbubbles (IV) should also shorten the time to achieve flow. c. Clinical trials of both of these additions to lysis are being conducted. d. Theoretically, combining these modalities would be additive (or synergistic) to clearing clot. This is not presently being trialed.
Myocardial infarction The above may also be applied to acute coronary occlusions to bring about faster lysis with a fraction of the dose of lytic now utilized. The result could be expected to achieve more complete lysis with less of the negative reflow phenomenon seen with balloon angioplasty alone; but without increasing the risk of bleeding. Venous occlusions At this time leg DVT is handled with systemic heparinization followed by 6–12 months of coumadin. This yields a high percentage of valvular insufficiency, and the sequelae of postthrombotic syndrome is in the region of 80%. The above techniques plus the pharmacomechanical combination obtained with the Trellis device, Rotarex, and the AngioJet could restore flow in a single setting with the ability of the patient to be quickly discharged (perhaps even on the same day), with valve function preserved. Pulmonary embolism Anecdotal reports of markedly improving the clearing of hemodynamically significant pulmonary embolism with both
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power pulse spray, and combination of ultrasound and lysis have been reported. At this time the applications are in patients who are having hemodynamic problems and whose clots have been resistant to systemic lysis and anticoagulation. A formal study to confirm the efficacy could result in a major change in the practice of medicine for this group of patients, resulting in a shorter ICU time, less morbidity, and some decrease in mortality.
Improved methods Pharmacomechanical The Trellis device combines trapping of the clot and lytic between two balloons, maceration of the clot by a rotating sinusoidal guidewire, and aspiration of clot fragments. The Rotarex utilizes a similar method with more emphasis on aspiration, while the AngioJet utilizes the Venturi effect to primarily aspirate, but has now been combined with an initial jet infusion of lytic into the clot followed by a dwell time of 20 minutes which has been associated with more rapid and complete clearing of clot. The EKOS system combines multiple ultrasound transducers within an infusion catheter. The ultrasound loosens the matrix of the cross-linked fibrin strands enabling easier and faster permeation of the clot by the lytic; resulting in faster lysis. Microbubbles In vitro and in vivo work has demonstrated faster lysis with the IV administration of microbubbles plus IV adminstration of lytic and then external ultrasound at the site of the clot. This can be expected to be true in humans, and to be augmented by the delivery of each modality directly into the clot.
Improved drugs Plasmin Instead of using the plasminogen activators to convert plasminogen to plasmin, the infusion of plasmin could result in faster lysis, and with the plasmin that escapes the region of the clot being quickly inactivated. This is theoretically attractive, and trials are now beginning.
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis PE Thorpe and FJ Osse
Introduction: treating acute deep vein thrombosis Deep vein thrombosis (DVT) is a medical condition which occurs with predictable consistency within the population despite innovations in therapy. Many cases of DVT are not diagnosed, since the signs and symptoms are either transient or vague. They are often misconstrued as muscle ache. Ultrasound has improved diagnostic capability, but only if the suspicion of thrombosis is perceived in the clinical presentation. The incidence of DVT appears to be increasing with an aging population. Statistics from the American Heart Association say up to two million Americans are affected annually by DVT and 200,000 die each year from the complication of pulmonary embolism.l As clinicians, we inconsistently utilize prophylaxis in high-risk patients whom we place
in high-risk circumstances.2 Furthermore, physicians are often slow to recognize early signs or symptoms of both extremity thrombosis and pulmonary embolus. The diagnosis is often made in the midst of a clinical crisis after both patients and doctors miss or ignore subtle clues that were present for days or weeks. Symptomatic DVT results from the presence of a critical mass of thrombus that supersedes collateral capacity and autolysis (Figures 19.1 and 19.2). The swelling and pain secondary to venous hypertension from the obstructed venous flow bring the patient to clinical attention. Whether in the emergency room, the physician’s office or in the hospital, clinical suspicion of DVT should prompt anticoagulation and investigation.3 More commonly, a patient with newly diagnosed DVT, other than phlegmasia, is treated as an outpatient. Upon duplex confirmation of thrombus in the deep venous system, the patient is treated with low molecular weight
Figure 19.1 Clinical appearance of a 22 year-old man one month after undergoing right hip-spur surgery. The patient had been a varsity football player in college and was very healthy otherwise. He was subsequently diagnosed with heterozygous Factor V Leiden mutation. The thrombus, most likely related to immobilization plus hypercoagulability, was approximately 3 weeks old when the patient was treated with mechanical thrombectomy, for debulking (Oasis by Cordis), and catheter-directed tPA for 48 hours. The initial right femoral venogram is seen on the right.
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Figure 19.2 Two images of the right femoral vein (prone) showing before and after catheter-directed tPA therapy. The 48 hour infusion was performed with 1mg/100 cc normal saline/hour. No angioplasty or stent was indicated.
heparin and sent home. We know that many do well. Others, despite adequate anticoagulation, progress to a symptomatic post-thrombotic syndrome. Ideally, symptomatic patients with occlusive or partially occlusive multi-segmental thrombus would be evaluated for the risks and benefits of actually eliminating the “clot burden” in addition to anticoagulation. The persistent presence of thrombus in the deep venous system can result in suboptimal venous flow and damage to the valves. The body attempts to resolve venous obstruction with a combination of autolysis and redirection of venous flow through collateral channels. If the extent of thrombus exceeds the compensatory effects of recanalization and collateralization, venous hypertension results and causes edema and/or discomfort. Chronic venous hypertension is associated with multiple symptoms (pain, cramping, limb heaviness, pruritis, parasthesias) and signs (edema, induration, venous ectasia, redness and calf tenderness, and stasis ulcers). A wide range of disability, clinical morbidity and deterioration of limb function can occur. The focus of this chapter is the spectrum of endovascular interventions available for thrombus removal in the clinical setting of acute DVT. In other words, we will discuss the interventional approach for treatment of acute thrombus in order to (1) re-establish deep venous flow to thereby reduce pain and edema; (2) preserve valve integrity; (3) remove thrombus that could embolize; and (4) prevent continued obstruction and valve damage that leads to post-thrombotic syndrome. An appreciation of the long-term sequella of persistent thrombosis, for example valve damage, venous hypertension, and post-thrombotic syndrome, hopefully prompts a clinician to consider the options of intervention with thrombolytic therapy, mechanical thrombectomy, and endovenous reconstruction. The long-term results of such interventions are limited to several series of 3–5 year follow-ups.4,5 In our follow-up of 1–10 years, patients treated with urokinase plus anticoagulation reported less pain and swelling compared to patients
treated with anticoagulation alone.6 Therefore, if endovascular intervention is a clinical consideration, we offer the following discussion about the techniques and available devices. It is a rapidly expanding area of innovation and industry focus with the frequent appearance of new tools which are intended to increase efficiency without sacrificing safety.
Diagnostic workup Patients referred with symptomatic acute DVT undergo a diagnostic workup including a history, hypercoagulability screening, physical exam, and baseline duplex exam. Attention to the difference of segmental flow velocities, as well as the waveforms, can provide clues to proximal venous obstruction. Common iliac occlusion and distal IVC obstruction are suggested by loss of phasicity and relatively low velocity at the femoral level. However, flow velocity may be deceptive if there are large collaterals or a prominent internal iliac system, but the waveform will still show little or no phasicity. An ascending phlebogram is obtained by manual injection of lowosmolar, non-ionic contrast through the pedal IV. A 22 g Jelco is placed in a dorsal pedal vein and secured with extension tubing and a distal-end 3-way stopcock. Using 60 cm3 syringes, contrast is pushed into the vein, observing for extravasation. This can be difficult and slow at the initial exam. It becomes easier as the venous resistance decreases. We advocate the phlebogram as a valuable baseline “road-map” of the state of venous flow in the extremity. Although some interventionalists avoid this study, due to the difficulty of placing an IV in an edematous foot, we find it valuable in several ways. First, it provides an access for infusion of thrombolytic drugs as well as contrast. Second, it is important to determine the flow status in the upper calf and popliteal region since these veins must be open for the calf-pump to function properly. Without continuity of flow from the calf into the deep system
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis of the thigh and pelvis, endovascular therapy rarely succeeds long-term. All patients referred for suspicion of DVT undergo duplex ultrasound. The standard examination does not include evaluation of valves. It also does not include iliac veins unless specifically requested. We find that iliac occlusions can remain undiagnosed for years, since duplex imaging of the common femoral vein shows flow. The loss of phasic flow, indicating a proximal obstruction, is often not recognized in an exam performed to rule out lower extremity thrombosis. Three-dimensional CT reconstructions and magnetic resonance venography (MRV) can provide information about pelvic vein and iliac compression. MRV has been compared with contrast venography and ultrasound in detection of DVT. All thrombi detected by contrast phlebograms were also detected with duplex and MRV. There was 98% correspondence in diagnosis of DVT with these modalities.7
Endovenous therapy Thrombolysis, balloon dilatation, and stent placement comprise the main elements of endovenous therapy for revascularization. Thrombectomy devices, useful in clearing dialysis fistulae, have not exclusively supplanted lytic therapy in the treatment of acute DVT. This is due in part to the limited size of the debulking channel, the fact that chronic thrombus often underlies acute obstruction, and that the devices work best with soft thrombus. Anticoagulation is required to prevent immediate rethrombosis. Duration of anticoagulation after the initial re-endothelialization phase may vary. Selected patients, without DVT, who are stented for iliac compression, may do well without warfarin.8 Our approach to endovascular therapy for thrombotic occlusion, for both acute and chronic occlusion, advocates the following philosophy. If one considers a limb as an “organ system,” in the sense that venous segments exist in continuity with smaller veins below and larger veins above, one can see that, ideally, they should not be treated in isolation. The run-off exam or knowledge of outflow is important in arterial disease. Similarly, continuity of venous flow is important for success in endovascular venous procedures. For example, flow in a stented iliac segment depends on flow from the femoral, popliteal, and infrapopliteal segments. If there is subacute and chronic DVT in the calf and thigh, treating only the superficial femoral vein without addressing the occlusive thrombus in distal veins, will result is suboptimal restoration of deep venous flow. If tibial flow is occluded, blood preferentially goes to the superficial veins. This pathway will persist even when the SFV is reopened because blood is being shunted to the saphenous system in the lower calf. The reopened SFV will not be the path of least resistance, due to persistent occlusion more distally. The limb will have diminished flow in the deep system, despite perforators, since the saphenous vein remains the path of least resistance. Ignoring strategic distal thrombus can cause early technical failure. A newly reopened femoral system is at greater risk for rethrombosis if there is little deep venous flow channeled into this segment. It is similar to placement of an arterial bypass graft above poor run-off. Patency will be less than in a limb with good run-off. In addition, residual distal thrombus can limit clinical improvement due to persistent hypertension in the calf. In both venous and arterial reconstruction,
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interaction among all segments must be taken into account to achieve optimal results. We have found a combination of catheter- and flow-directed therapy is most beneficial for treating multi-segmental thrombosis. Improving flow in the whole limb may be essential for good long-term clinical results in patients with thrombus located at every level.
Mechanical thrombectomy Thrombectomy refers to physical removal of soft, fresh thrombus. The idea of doing this is with a small, percutaneously inserted device that atraumatically “vacuums” the thrombus out of the vessel. Such a device would offer the speed of surgical intervention with the advantage of minimally invasive therapy. The Fogarty balloon, a standard tool for rapid thrombus debulking, requires a surgical incision. A number of new devices have emerged, and their design benefits and limitations are discussed in several review articles.9–12 The objective of the newer designs is thrombus removal with a small-profile, over-the-wire device that can be introduced percutaneously. Most devices provide a small pilot lumen that leaves a substantial amount of residual thrombus. The debulking ability varies according to the device as well as the thrombus composition. The devices do not perform well with organized thrombus.13 The devices are geared to vessels less than 10 mm in diameter. Both over-the-wire and wireless versions are available. They are not steerable. Residual mural thrombus persists in most vessels, particularly larger veins such as the iliac and cava. The endothelium can be injured and result in rethrombosis as well as intimal hyperplasia. The potential for valve damage has been studied in animals but it is hard to determine in humans.14 In general, the debulking seems most appropriate in patients who cannot receive thrombolytics. However, many of these patients, such as elderly post-op patients, cannot receive heparin either. Without anticoagulation, rethrombosis occurs rapidly. In our experience, the debulking process rarely decreases the overall time of the procedure, since additional thrombolysis is necessary to remove residual thrombus for optimal results. Some devices combine mechanical and pharmaceutical properties to accelerate restoration of flow.15 The TrellisTM (Bacchus, Menlo Park, CA) device is a combination bipolar balloon, infusion catheter and ossilating wire.16 The thrombolytic agent is delivered between the occluding balloons. The perfused thrombus is then subjected to gentle mechanical disruption by an oscillating sinusoidal wire positioned between the balloons. This allows contained thrombolysis, thus limiting systemic exposure to the lytic agent. The device allows rapid aspiration of lysed thrombus through the dual lumen design, but anticoagulation is still necessary. Isolated thrombolysis is most useful in treating acute VT in patients with contraindications to lytic therapy. The advantage of significantly limiting the systemic effect of the drug allows treatment of post-op patients and patients with other risks of bleeding. The “power pulse-spray” concept of the AngioJetTM(Possis, Inc., Minneapolis, MN) is also a combination of powerful delivery of a lytic agent with a thrombectomy catheter.17 The device has undergone several evolutions to create a more
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effective debulking channel. Despite the reported contributions of mechanical thrombectomy, we find there is generally still a need for overnight thrombolysis. The devices are expensive and require set-up time and a technologist familiarity with each design. The use of mechanical thrombectomy may shorten the time until flow is restored, and they may lessen the overall time to completion, especially if catheter-directed thrombolysis is not needed after the debulking process.
The role of thrombolysis While investigators have shown that early thrombolysis effectively removes thrombus and preserves valve integrity,18 the early published reports of the risk of bleeding complications has prevented widespread acceptance of catheter-directed thrombolytic therapy for acute DVT.19 Catheter-directed thrombolysis of acute DVT could decrease the number of patients who develop PTS.20 However, this position is more advocated by interventionalists than referring physicians precisely because of the fear of complications. The main principle in thrombolytic therapy is effective and efficient delivery of an agent to the thrombosed vascular segment(s). In larger axial veins, this is best achieved with catheter delivery utilizing multi-side-hole infusion catheters and wires. When there is thrombus in deep calf veins and the popliteal, simultaneous flow-directed infusion, utilizing tourniquets, serves to improve flow in these areas. It is most important to optimize venous flow in the distal deep system. Persistent diversion of distal flow into the superficial system will place the newly opened and stented proximal segments at greater risk for rethrombosis. Optimizing resting flow velocities, by re-establishing continuity of flow from the foot to the cava, has proven to give the best hemodynamic and clinical results. Between 1980 and 1999, peripheral vascular thrombolysis was largely performed with urokinase (Abbokinase, Abbott Laboratories, Chicago, IL). This agent was preferred over streptokinase and alteplase for the safety margin relative to bleeding complications.21,22 Problems centered on manufacturing protocols led to a shortage of urokinase and indefinite withdrawal of this agent from the US market. Urokinase has, however, returned to the market, but remains relatively expensive (ImaRx, Tucson, AZ). Alternative lytic agents such as retaplase or RetavaseTM alteplase or ActivaseTM, and tenecteplase or TNKTM (Genentech Inc., South San Francisco, CA) are available for peripheral interventions. In our experience, there remains an increase in bleeding complications with alternative lytic agents compared to urokinase. Dose adjustments for concomitant heparin are advocated, but the fibrin-specific drugs are less well suited to the longer venous infusions. We prefer the low-dose, high volume infusions for DVT therapy, and when urokinase was available more DVT patients received catheter-directed thrombolysis.23 The formula for urokinase is one million international units (IU) per liter of normal saline infused at 50–100 cm3/hour. The higher volume promotes percolation of the drug through the occlusive thrombus. By pushing the drug through the thrombus, the volume aids in exposure of the drug to the clot. A low volume infusion just “sits there” and the progress is slower. The risk of complications, the cost of ICU care, and the length of treatment led to less use of catheter-directed
thrombolysis as well as the evolution of thrombectomy devices and combination therapies. Now, pharmacomechanical thrombectomy has become the preferred method of treating acute DVT. The value of thrombolysis appears well accepted by the interventional community, and therefore remains an important tool in therapy. However, the methods of application have evolved to decrease the risks. This includes more use of mechanical debulking tools, temporary IVC filters and intravascular ultrasound (IVUS). The cost may not be decreased, but thrombolytic agents are used less. The fibrinolytic action of the drugs is clear in the case of acute DVT, but it is not immediately obvious nor well understood how thrombolytic therapy functions in the case of chronic venous occlusion. It does, however, make a difference. Physicians attempting to recanalize chronic thrombus frequently fail to advance the wire or stay intraluminal if they do not infuse a thrombolytic agent prior to and during the wire recanalization phase. Only sub-total occlusions can be readily treated without lytic therapy. Even in these cases, we find that a 24-hour infusion permits greater expansion of the residual lumen prior to stenting. In treating subacute and chronic occlusions, we share, with Semba and Dake,24 the impression that a thrombolytic infusion can “soften” more organized thrombus and thereby facilitate passage of wires and catheters. Although catheterdirected thrombolytic therapy has been shown to be most successful in removing acute thrombus, in chronic conditions, clinical improvement observed after thrombolytic infusion is often greater than the image would suggest. That is because improvement of venous flow, particularly in the calf, depends on the cumulative effect of many unnamed veins remaining patent. Restoring flow in these small conduits can make a significant clinical difference. Analysis of National Venous Registry (NVR) data suggested thrombolysis of chronic thrombus was unsuccessful.25 In truth, images of distal veins often look as abnormal after lytic infusion as they do before. Whereas comparison images show dramatic differences when lysing acute DVT, the phlebographic appearance of chronic venous obstruction changes less, even though the venous flow can improve significantly. Interpretation of static contrast images fails to explain the clinical improvement in patients after thrombolytic infusion for chronic obstruction. Reducing venous resistance, by augmenting small and medium size venous channels, does not dramatically alter the post-infusion images, but it is an important adjunct to stenting larger veins. Video/digital phlebography, as mentioned above, can demonstrate a clear difference in rate of flow/ contrast clearance after thrombolytic infusion. Vascular physiology and fluid dynamics studies show how flow in a tubular conduit is proportional to r 4, where r represents the radius. If we apply this concept to venous flow, we see that augmenting multiple occluded or tiny lumens from < 1 mm to > 2–3 mm, significantly increases venous flow despite minimal changes on radiographic images. According to this principle, Pousseille’s Law, delivery of thrombolytic agents to the extremity via catheter or flow-directed techniques, can promote flow by enlarging the residual lumen. Although not restored to original caliber, lysing acute and subacute thrombus, superimposed upon chronic organized thrombus, increases the luminal diameter. This may not produce a dramatic change on x-ray images, but the increase in flow can be documented with
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis duplex and correlated with post-treatment clinical improvement. Ambulatory venous pressure, as indirectly measured with air plethysmography, should decrease as resistance to flow decreases. However, in our exams, the numbers often do not reflect the degree of clinical improvement. Reasons for this are complex and most likely involve the effects of long standing obstruction on valves and the calf muscle pump.
Technical aspects of catheter-directed DVT thrombolysis When treating an acute iliofemoral DVT, the popliteal approach is generally selected (Figure 19.3). If necessary, a bilateral approach is used simultaneously. Certain cases may require access from the contralateral or jugular approach. The advantage of the popliteal approach is that a patient may sit in bed. The jugular sheath is not well-tolerated for extended treatment. Thrombus around the jugular sheath is prone to lysis with the continuous motion from carotid pulsation. This can result in miserable oozing. Therefore, we prefer to reserve the internal jugular vein for short-term access. Although the baseline phlebogram is performed with the patient supine, the endovascular procedure requires placement of the patient in a prone position. A urinary catheter is advised. Initial deep venous access is safest utilizing ultrasound guidance of a 21-gauge micropuncture needle into the back wall of the popliteal vein or a superficial tributary, (Figure 19.3). Successful entry into the vein, in continuity with occluded proximal deep venous segment(s), permits placement of a working sheath for catheter exchange and
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contrast injection. A thrombosed popliteal vein can be cannulated as well. However, a pedal infusion of lytic agent is recommended for simultaneous treatment of the calf and popliteal segments. Spasm and missed passes are significantly less with the combination 3–5.5-French, co-axial, micropuncture dilators and 0.018-inch nitinol wire than with standard intravenous catheters. An angled 4–5-French hydrophilic catheter, in combination with a 0.035-inch GlidewireTM (Boston Scientific, Na, MA) or 0.035-inch RoadrunnerTM (Cook Inc., Bloomington, IN), is carefully advanced from the popliteal level, through the superficial femoral vein to the common femoral level. During the initial 24–48 hours, the goal is to place a multi-side-hole catheter along the length of the abnormal segments traversed by the wire. An overnight infusion of thrombolytic agent will decrease the intraluminal resistance and set the stage for subsequent catheter advancement, balloon dilatation, and stent placement. Following passage of a wire into the normal vein above the occlusion, a stiffer exchange-length wire that is positioned as the working wire during dilatation, and stent deployment. If necessary, sequential predilatation in the stenotic areas is conducted, from proximal to distal, using 8–14-mm balloons (4 cm length). Balloon selection depends on the estimated size of the native vessel and the observed resistance to balloon expansion. Overdilatation is avoided. Some vessels are very tenacious while others dilate with relative ease. Great care is taken to “feel” the balloon as one slowly proceeds to expand the residual lumen. Since venous angioplasty can cause thrombogenic dissection, anticoagulation is key during and after this therapy. We have come to learn that spontaneous flow through an irregular vein is better than stasis in a nice-looking stent. Therefore, good judgment is required in determination of a therapeutic endpoint. Stasis of contrast and
Figure 19.3 Popliteal puncture site. This is generally visualized with duplex to avoid puncture of the artery with is directly anterior to the popliteal vein. The ultrasound shows the compressible vein above and slightly medial to the artery. The leg can be rotated slightly to separate the vessels. It is important to see the puncture. With contrast, the needle presses against the posterior wall and widens the vein, as shown here (arrow). The skin entrance is slightly above the crease behind the knee, but he needle entry site is close to the top of the patella when the patient is prone. Left image show Site-Rite™ with needle guide.
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persistent collateral flow indicate an outflow problem, whereas stasis alone may indicate sub-optimal inflow. Patients are systemically heparinized (PTT > 50 and < 80 seconds) throughout the period of thrombolysis with urokinase and prothrombin time > 40 but < 60 seconds with alteplase. Oral anticoagulation is tapered before therapy (2 days off coumadin before admission) and restarted 1 day prior to stent placement. This allows removal of the sheath before the INR is therapeutic. Upon completion of thrombolysis, heparinization is continued until oral anticoagulation is consistent; PT > 20 seconds; and INR of 2.5–3.0. Oral anticoagulation is monitored cooperatively with the referring physician for several months, as inadequate anticoagulation is the most frequent cause of early failure. Younger patients with chronic conditions may have a hypercoagulable state. Whereas a minimum of 6–12 months of warfarin is standard in acute DVT, patients with chronic disease and/or multiple stents are placed on indefinite warfarin. A single iliac stent with excellent venous flow, in a patient without thrombophilia may not require warfarin. Compression stockings or leggings are prescribed and fitted for all patients with documented reflux before discharge. Patients are followed with clinic visits and duplex exams upon completion and at 3-month intervals for 1 year and yearly thereafter. Bleeding complications can occur with prolonged thrombolytic infusions, but they are relatively uncommon in the post-thrombotic patient population compared to cardiac patients. In reviewing the complications reported in the literature, clearly the most common problem is minor bleeding at the sheath site. Major bleeding, requiring transfusion, has been reported in 1–25% of patients. This is more likely to occur in obese patients; and the use of ultrasound guidance for initial puncture is strongly recommended. Pulmonary embolus occurred one time in our series, and continued thrombolysis
resolved all symptoms. It has been reported in < 1% of all reported cases. Therefore, IVC filters are not routinely used with catheter-directed thrombolysis. However, with mechanical thrombectomy, temporary filters are used, despite the lack of any controlled studies. Among more than 1000 iliofemoral venous endovascular patients reported in the literature, death has occurred in < 1% due to PE (1), sepsis (1), retroperitoneal hematoma (1) and intracranial hemorrhage (2) and MI (1)(6). With the use of fibrin-specific lytic agents, such as alteplase and tenecteplase, we note many more soft-tissue hematomas at automatic blood-pressure cuff sites and at venapuncture sites. This observation did not accompany use of urokinase. Rethrombosis < 30 days is generally due to poor outflow or inflow and/or subtherapeutic anticoagulation. When this occurs, retreatment with thrombolysis and additional stents is effective. Intimal hyperplasia, causing symptomatic restenosis occurred in approximately 10–20% of stented veins, and can be effectively treated with angioplasty.26
Flow-directed thrombolysis for calf DVT This technique is reserved for treating thrombus located in the tibial, soleus, gatrocnemius, and popliteal veins. It is more prevalent than thought.27 It may be more important than many believe, given the strategic location of the majority of venous valves in this area.28,29 If the baseline venogram reveals preferential flow in the superficial veins of the calf, strive to acquire an idea of where the thrombus is located by injecting contrast with tourniquets in place (Figure 19.4). The duplex may underestimate the amount of thrombus in the upper calf. If there is no continuity of flow in the deep veins
Figure 19.4 Tibial thrombus in patient with acute pancreatitis. This was treated effectively with a urokinase infusion through a pedal access, with application of the ankle tourniquet as shown in the image on the right. Contrast and lytic agent can be re-directed to the deep veins of the calf by compressing the saphenous vein against the malleolus.
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(b)
Figure 19.5 (a) Acute left lower extremity DVT in a 38-year old man hospitalized with pancreatitis. Immobilization, due to bed rest, combined with a classic iliac compression (Figure 19.6), led to iliofemoral and femoral-popliteal thrombosis. Additional tibial vein thrombus (Figure 19.4) was treated with flow-directed thrombolysis. (b) Acute femoral thrombus. Very few collaterals are evident. The femoral vein is engorged with thrombus and contrast tracks along the edge of the obstruction.
of the calf and the thigh, a lytic infusion from the level can be effective in reopening veins that are untreatable with catheter technique. Acute failure has been attributed to residual thrombus in the popliteal vein, below the sheath entry site. Unfortunately, some interventionists have recognized the importance of treating the distal vein, especially the entire
(a)
popliteal, after rethrombosis of successfully lysed iliofemoral segments. For this reason, we recommend a baseline and completion venogram from the foot. Unfortunately, duplex does not provide the same understanding of flow patterns, in the lower extremity venous system as real-time contrast venography.
(b)
Figure 19.6 (a) Pelvic venograms (seen supine) following thrombolytic therapy to remove acute thrombus from the iliofemoral segments. The classic absence of the left common iliac segment is due to chronic fibrosis where the right iliac artery crosses the vein. Ascending lumbar collaterals (double arrows) and trans-pelvic, left-right collaterals are seen. (b) Venogram following placement of a 12 mm X 60 mm self-expanding stent across the focal common iliac occlusion.
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A 22-gauge intercath placed in a dorsal pedal vein for the purpose of performing the baseline venogram is used for the flow-directed infusion. A single puncture in a pedal vein below the ankle is desirable. Although multiple punctures cannot be avoided in certain patients, we attempt to work from a distal to proximal direction to avoid infusing urokinase below multiple punctures. A small clear plastic dressing is placed over the 22-gauge catheter to maintain visualization of the site throughout the procedure. It is important to loop the IV tubing to prevent inadvertent loss of the site. Infection and/or bleeding are not problems but, as always, care is taken to observe for any extravasation of contrast during each injection. A short, clear plastic connecting tube is used with a three-way stopcock to facilitate interval injection of contrast for follow-up evaluation of progress of lytic therapy. A saline infusion is maintained through the pedal site if urokinase is not being infused. A Velcro-elastic tourniquet (Tiger Surgical, Portland, OR) is placed at the malleolar level in combination with a small disc positioned to provide focal compression of the saphenous vein against the medial malleolus. Under fluoroscopic visualization, a small amount of contrast is injected to ascertain focal compression of the saphenous vein and redirection of flow through a communicating vein into the deep system. The disc position, as well as the upper and lower margins of the tourniquet, is marked on the skin. This allows a nurse to release the tourniquet once every hour and replace it in the correct position. A folded 4 × 4 gauze is placed under the disc to protect the skin from pressure. The pedal pulse is marked and monitored with blood pressure and pulse; the tourniquet provides adequate redirection of venous flow without any compromise of arterial flow. It is released 10 minutes every hour and reapplied at a specifically marked level, which assures proper disc position and tightness. Normally, blood flows preferentially from the superficial to the deep system. However, in the presence of DVT, one may see contrast reflux through the perforating veins into the superficial system in the mid calf or above. When this is fluoroscopically recognized, a second tourniquet is placed at the knee to compress the greater saphenous vein against the femoral condyle to promote redirection of flow into the tibiopopliteal veins.
The role of metallic stents The interventionalist must have a working knowledge of stent properties and be familiar with a wide variety of commercially available products. The number of stents now on the market has grown significantly over the past decade and currently there are more than 40 different stents available for coronary use and more than 20 for use in the periphery. Current lists are available at the Endovascular Today website <www.evtoday. com>. Significant improvement in patency rates has been observed in iliac lesions treated with stents in addition to angioplasty. In the NVR, at one year, 74% of limbs treated with stents remained patent compared to 53% of limbs not receiving stents (p < 0.001).25 No stent possesses all the qualities of an ideal stent, for example good radio-opacity, ease of positioning, flexibility, tractability, fidelity of shape, and low restenosis rate. Evaluation of the characteristics of the properties of metallic stents is gained with experience as new stents are introduced
and compared to those in use. Clinical use of stents in the iliac vein was first reported by Zollikofer et al. in 1988.30 Migration and intimal hyperplasia were documented with early use of the Gianturco Z stent.31 Modifications were made to prevent slippage; modular stent units were connected with nylon suture and small hooks were added. Migration has been a rare event with all stent designs. When this does occur, misplaced or migrated Palmaz and Wallstents can be effectively retrieved using endovascular techniques.32 All stents have been shown to become endothelialized and/or covered with neointima.33 Sawada reported this in all Z stents observed at autopsy.34 The neointima appears rapidly and the endothelialization process occurs within 2–6 weeks. The amount of intimal thickening has been correlated to design. More rigid stents, exerting greater axial force on the vessel wall, seem to accelerate intimal hyperplasia. In these animal studies, and our experience, the Wallstent is less likely to induce compromising intimal hyperplasia due to the small wire size, pliability, and longitudinal flexibility. Zollikofer noted two important observations in animal studies: (1) regression of intimal hyperplasia occurred with time; and (2) restenosis is more common at a site of high pressure flow, for example arteriovenous fistula.35 This appears true for stented and non-stented vein segments. Intravascular ultrasound (IVUS) has allowed us to examine symptomatic patients and document restenosis caused by intimal hyperplasia. The majority of interventionalists use the Wallstent for venous stenting. In the common iliac location, with extrinsic pressure a factor in causing compression, flexibility and selfexpansion may give the Wallstent an advantage. A study comparing long-term patency of self-expanding versus balloon expandable stents, placed in the common iliac vein, has never been done. However, the general consensus is that the flexibility of the self-expanding stents is suited to the pelvic veins. The choice of lengths and diameters make this design suitable for 1–2 cm vein diameters. The newer nitinol stents have less foreshortening than the Wallstent, but they are less visible under fluoroscopy, especially in large patients. Currently available stents are used “off label”, as the 8–16 mm diameter stents are only FDA approved for biliary and iliac artery use. Covered stents, suitable for repair of venous tears, are generally not needed or recommended. In a low-pressure system, our limited use of covered stents has led to thrombosis. Another stent limitation is length. Many of the venous occlusions are long, and reconstruction requires tandem stent deployment. The fully expanded stent length ranges from 4.0 to 10.0 cm. Stents remain correspondingly longer if full expansion is not achieved. As in the arterial system, crossing the origin of branch vessels does not appear to be associated with problems. We have closely followed iliac vein Wallstents, in place for over 14 years, with duplex imaging. There is no indication of strut fracture or failure. Occasionally, we see separation of two stents by 1–2 cm. Patients with recurrent symptoms of edema or leg pain are scheduled for stent dilatation. Duplex imaging does not usually discern in-stent restenosis. This is better seen with IVUS. Approximately 15% of patients may return with intimal hyperplasia that can be effectively dilated. Clinically, they improve after this intervention. It is done via the jugular approach without reversal of warfarin. Although the majority of patients encounter restenosis within 12–24 months after
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis the initial procedure, we have treated patients anywhere from 2–10 years after the stents were placed. Progressive venous hypertension in the limb can be a sign of restenosis or rethrombosis. If there is no sign of thrombus, we advocate stent dilatation. Several technical points regarding venous stenting should be emphasized. Firstly, complete stenting of diseased segments promotes re-established continuity of deep venous flow which is imperative to stent patency. Under-stenting should be discouraged in view of the observation that tributary flow passes through Wallstent interstices and traversing the inguinal ligament with overlapping, self-expanding metallic stents is well tolerated (Figure 19.7). It is also important to not ignore stasis of contrast when stenting. This is a sign of inadequate spontaneous flow. This can be due to a sheath blocking flow, but contrast can obscure stenoses and dissections on digital imaging. So, stasis must be respected as a sign of poor flow which could cause the stents to fail. Moreover, neither the initial venographic appearance, the extent of the lesion nor the duration of the symptoms is a predictor of success or failure of guidewire passage through a venous obstruction. Some very chronic lesions are almost impossible and some are very easy. There must be genetic issues we do not yet recognize.
Acute left leg DVT: iliac compression or May–Thurner syndrome When Zollikofer first placed a stent in the iliac system, the indication was treatment of intimal hyperplasia, at the proximal anatamosis of a common femoral-to-common iliac bypass graft.30 Since then, stents have been shown to be an effective adjunct to surgery and balloon dilatation, particularly in the
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left common iliac segment.36 As in arterial disease, “culprit” lesions are frequently discovered after removal of acute thrombus. Verhaeghe et al. reported discovery of an underlying anatomical anomaly or lesion in 13/19 (68%) of limbs treated with catheter-directed rtPA for iliofemoral thrombosis.37 Ten of the venous lesions (77%) were unknown before lysis and eight (62%) were treated with stent therapy. For the most part, the condition is diagnosed in association with thrombosis, and as Cockett observed, early on, in acute cases, “mere removal of the clot does little good in these cases as it does not deal with the real cause of venous obstruction (i.e., the stricture).”38 Although the majority of large vein thromboses recanalize sufficiently, a certain percentage of iliofemoral DVT patients do not recover satisfactorily. Following standard therapy of heparin, bed rest, and oral anticoagulation, they remain symptomatic with pain and/or edema. Some develop ulcers. Unfortunately, it is not possible to predict which patients will develop a severe post-thrombotic syndrome. Cockett and Thomas, identified the relative lack of iliac recanalization and associated post-inflammatory perivenous scarring, as the main etiologies of serious post-thrombotic sequellae. The degree of uncompensated residual obstruction causes venous claudication, and the cutaneous changes associated with persistent venous hypertension. Patients in this category were among those first considered for surgical bypass.39 Left iliac compression (LIC) explains why deep vein thrombosis predominantly affects the left leg. Many persons with occult left iliac compression or occlusion are, in fact, asymptomatic. Prethrombotic venous hypertension may be present, but remains largely undiagnosed. Subtle asymmetry in leg or foot size may be noticed, but is mostly ignored. Iliac compression patients frequently present with associated femoral thrombosis. In fact, the condition should be suspected in anyone with acute left extremity DVT and/or symptoms of venous insufficiency. The youngest patient in whom we have seen venous claudication and edema, with a normal saphenous vein and Phlebographic confirmation of left iliac compression, was a 12-year-old girl. In addition, we have treated three young women, between 17 and 24 years old, with iliac stents to alleviate symptoms caused by May–Thurner compression not yet complicated by thrombosis. In their study of 94 patients with suspected iliac vein obstruction, Neglen and Raju have reported on primary stenting of May–Thurner compression as well as the prevalence of non-thrombotic iliac obstruction among patients with chronic venous insufficiency.40,41
Clinical experience: iliofemoral and iliocaval obstruction
Figure 19.7 Understenting demonstrated in the CTA scan. The aorta and iliac arteries are clearly seen the stent position is too low to open the common iliac vein. When the compression is tight, the large diameter, short stent can slip caudal if the leading upper edge is not deployed above the stenosis. Approximately one-two centimeters of stent must be positioned in the IVC to bridge the lesion. The lesion is very narrow in an AP diameter and wide in the transverse diameter.
In 1997, Bjarnason et al. reported on treatment of 77 patients. The majority of the patients, mean age 47 years (range 14–78 years) presented with acute DVT symptoms of < 14 days duration (69/86, 78%), while 9 (10%) had subacute thrombus (14–28 days) and 9 (10%) had thrombus older than 28 days. The mean length of symptoms prior to thrombolysis was 15 days (range 0–256 days). The average dose of urokinase was 10.5 million IU (range 4–24 million IU) and the average infusion time was 75 hours (range 8–247 hours). They reported greater technical success in treating iliac veins (79%) versus femoral veins (63%). We have seen this pattern as well. It reflects the
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fact that subclinical thrombosis is present prior to clinical presentation with acute iliofemoral DVT. Even though the initial technical success was similar between patients undergoing stent placement versus those who did not, it was less for patients with thrombus older than 4 weeks than those with more acute conditions. Thrombosed superficial femoral veins are often poorly recanalized and respond poorly to thrombolysis, alone. Eighty-six stents were placed in 38 (44%) of the 87 limbs treated for iliofemoral thrombosis. Seventy-five Wallstents were placed in 36 limbs and 11 Gianturco stents were placed in two limbs. Interestingly, they found a lower 6-month primary patency rate between stented (60%) and non-stented (75%) iliac veins and 54 vs. 75% at 1 year (p = 0.011). At one year, the secondary patency rate was 76% for stented and 82% for non-stented vessels (p = 0.46). They hypothesized that patients requiring stents presented with more severe chronic venous disease, accounting for the poorer long-term results. Stented patients were not uniformly maintained on warfarin longer than 6 months. An important report in the literature regards the National Venous Registry (1994–97).25 This was a multicenter registry that collected data on 473 iliofemoral DVT patients treated with endovascular techniques. The study included 287 patients with adequate follow-up. The majority had acute presentation of iliofemoral thrombosis (70%). The average dose of urokinase was 7.8 million IU and nearly 50% required placement of an iliac stent. Technical success, including placement of 104 stents, was 97%. Results were reported in terms of lysis grade. Complete lysis was achieved in 60% of patients presenting with acute thrombus (< 10 days). Among this group, 90% remained patent at 12 months compared to 70% of those with less than complete lysis. Patients were maintained on warfarin for 4–6 months. The study revealed greater 1-year patency in limbs with iliac stenosis treated with angioplasty
plus stent (74%) versus angioplasty alone (53%). A remarkably lower patency rate (20% at 2 months) was observed in the five stents placed in femoral segments. In our experience, stenting lower segments require careful assessment of flow patterns and intimal hyperplasia. The study was based on analysis of pre-and post-phlebograms and duplex ultrasound with minimal follow-up of 12 months. Between 1988 and 99, 116 patients received urokinase for lower extremity DVT at Creighton, in Omaha, NE. Eightyfour underwent endovascular therapy for chronic lower extremity thrombosis. The mean age was 47.5 years (range 12–90 years). Patients received a mean dose of 8.7 million IU (range 2–27 million IU with a minimum 24 hour infusion of urokinase (range 24–120 hours). Persistent venous stenoses, after thrombolysis, required stent placement in 53% (62 patients and 71 limbs) (Figure 19.8–19.10). Among these patients, 32 (51% of those stented and 28% of the total) had stents placed in the common femoral and/or superficial femoral veins. Sixteen patients had a single iliac stent placed for focal common iliac compression associated with acute thrombosis (L/15,R/1). In this subgroup, there is 100% primary patency with median follow-up of 24 months (range 8–50 months). Three patients have developed intimal hyperplasia within the stented segment causing increase in edema and discomfort compared to post-stenting. This occurred between 6 and 12 months and all were treated with balloon dilatation resulting in resolution of symptoms. All patients treated for chronic iliofemoral and iliocaval occlusion were examined before and after lysis/stenting with ultrasound. In 16 patients, peak velocities in diseased and non-affected iliac and femoral veins were suitable for analysis. We found the median common iliac velocity in the normal limb to be 44 cm/second (n = 16). Comparison of pre-stent mean (7.25 cm/second) and post-stent mean (41.3 cm/second)
Figure 19.8 Post thrombotic syndrome in a 42 year-old woman. Her right leg DVT first occurred 3 weeks after her first pregnancy, and reoccurred after her second delivery. She has a heterozygous prothrombin gene mutation. Following endovascular stent therapy, five years after the initial DVT, the right leg is significantly improved two weeks after discharge. Four years later, she remains Therapeutically anticoagulated and clinically improved with no further interventions.
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Figure 19.9 Early images (prone) during endovascular recanalization of the chronically occluded left common femoral and iliac segments. Left: Large iliolumbar and extensive hypogastric collaterals seen on day 3. Right: Finally, the close view of the classic narrowing of the common iliac segment. Several days of low-dose catheter delivered tPA required for traversing the common femoral vein.
common iliac vein velocity demonstrated a significant difference (p = < 0.0001) whereas the mean stented left iliac vein velocity (41.3 cm/second) was not significantly different from the untreated right iliac vein mean velocity (47 cm/second) (p = 0.4569).6 Bjarnason et al. also reported that velocities of less than 25 cm/second in the stented iliac segment correlated with poor patency.42 Further analysis of stented patients showed 19 required two iliac stents, 20 received three stents and three large patients (> 250 pounds) had more than three stents placed in the left iliac vein. Overall, 1-year primary patency of patients with iliac stents, including those with femoral stents, is 80% (57/71). Rethrombosis occurred within 30 days in 8/71 (11%). Six of these patients were retreated with thrombolysis and additional stents to improve inflow. This group included the three large patients with more than three stents in their long iliac veins. Symptomatic restenosis was documented and dilated in 6/71 (9%) limbs. In all, the restenosis became clinically apparent between 6 and 12 months. One-year secondary patency was 94% (67/71).
Neglen and Raju have reported on several large endovascular series in which thrombolysis was not used in treating chronic venous obstruction.36 They treated a highly selected group of patients suspected of having iliac vein occlusion. They reported placement of 118 Wallstents in 77 iliac veins, 43 of which were diagnosed with non-thrombotic iliac occlusion or stenosis. In the remaining limbs, there was evidence of prior DVT. As in the other large patient series, technical success was high (97%). Eighty-seven limbs were treated with a 1-year primary patency of 82% and assisted and secondary patency of 91 and 92%, respectively. Their data support the Creighton finding that focal iliac vein stenoses or occlusions can be opened effectively and safely stented with good 1-year patency rates. Clinical improvement usually parallels technical success. However, in severe chronic DVT, involving multiple venous segments, relief of large vein obstruction can produce clinical improvement even when chronic venous insufficiency remains. Raju reported similar experience with percutaneous recanalization of totally occluded iliac veins in 38 limbs and
Figure 19.10 Pelvic venograms (prone) pre and post-stent placement in the 42 year-old woman with a 5-year history of post thrombotic syndrome. Clinical improvement included decreased edema and resolution of right groin pain, leg heaviness and discoloration (Figure 19.8).
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Figure 19.11 IVC occlusion and endovascular reconstruction. The 40 year-old woman patient did not suspect IVC obstruction when she presented with a 2 year history of a non-healing right ankle ulcer. Her initial DVT occurred. After undergoing bilateral therapy for iliocaval occlusion, the ulcer healed in less than 4 weeks. She presented with recurrence of the ulcer two years after stent placement. Balloon dilatation of the right-side in-stent hyperplasia corrected the venous hypertension an allowed the ulcer to heal. Deep valve reflux, in the right femoral veins contributes to venous hypertension, as well. The patient remains anticoagulated.
the occlusion extended into the infrarenal IVC in nine cases.43 Two cava had an occluded filter. The median length of the occluded segment was 22 cm. The median number of 14– 16 mm diameter stents used per patient was three. Diffuse distal chronic venous changes were noted in 88% of treated limbs. The chronic, non-occlusive DVT involved femoral, popliteal, and tibial segments in 62% versus a single segment in 9%. However, distal segmental occlusions were noted in 52% of the limbs; the majority of such tandem occlusions were femoral. Distal femoral lesions were not stented. Mean follow-up was 24 months. He reported actuarial primary, assisted, and secondary patency rates of 49, 62, and 76%, respectively. Clinical improvement was gauged with the pain scale where a significant decrease from level 4 to level 0 (p < 0.0001) was reported. Sixty-six percent of limbs showed resolution of open ulcers or stasis dermatitis at 1 year. Reflux was documented in 87% of treated limbs and involved both superficial and deep systems in 65% of these individuals. Perhaps the differences in the long-term ilio-caval stent patency rates among separate series reflect variable treatment of distal and tandem obstructions as well as selective use of anticoagulation. We reported our initial IVC series at the American Venous Forum (AVF) in 1996 and in the Handbook for Venous Disorders.6 Then, 10 years later, the IVC occlusion patient data were presented at the AVF with long-term follow-up (Figure 19.11). Between Oct 1995 and June 2005, 26 patients (20 male/6 female, average age 41 years, range 17–73 years) underwent endovascular repair for IVC occlusion. Two patients with malignancy-related caval obstruction were successfully treated with relief of venous hypertension, but both died of their malignancy. Twenty-one patients had benign, chronic total infrarenal IVC obstruction and three had acute thrombotic occlusion of a partial, chronic caval stenosis. Mean duration of symptoms was 12.1 years (range 1–25 years). Six filters were occluded; Greenfield (3), Simon Nitinol (1) and Trapese (1). Three chronically occluded filters were successfully stented open. All patients had bilateral lower limb venous hypertension with the exception of two individuals aged 17 (left only) and 26 (right only). Thirteen out of twenty-four (54%) had a history of pulmonary embolus and 14/24 (58%)
had caval interruption with a filter (12) or surgery (2). The 48 limbs included prior BKA for venous disease and the following classifications: CEAP 1 (2), CEAP 3 (11), CEAP 4 (19), CEAP 5 (9), and CEAP 6 (5). The entire IVC was occluded in 7/24 (29%) and infrarenal in 16/24 (67%). Mean follow-up is currently 4 years (range 8 months–10 years). Primary patency among 22 surviving patients is 71%; seven patients have been redilated. Assisted patency is 23/24 (96%) and secondary patency is 100%. We concluded that endovenous reconstruction of the chronically occluded IVC can be accomplished with low morbidity and excellent technical and long-term clinical results.
Summary The success of endovascular therapy for venous occlusion is well known to a select group of interventionalists who care about patients with venous disease. It is a reality that venous disease continues to be regarded by too many physicians as a condition that is treated with anticoagulants or compression stockings. Venous disease treatment with new technology and pharmacotherapy represents an area of pioneering spirit among vascular specialists. While the majority still focuses on arterial disease, a few keep trying to teach the rest that chronic venous disease is far more prevalent than peripheral arterial disease. The growing awareness of possible treatments is slowed by the lack of randomized clinical trials. Many referring physicians consider the endovascular venous reconstruction and pharmacomechanical thrombolysis for acute DVT as anecdotal, unless level I data can substantiate recommendations for care. There are ongoing efforts to organize and fund such trials.44,45 In the meantime, the American Venous Forum and the European Venous Forum, along with other groups and industry, are expanding annual screening events and public awareness to diagnose and teach about venous disease. And, in the age of the Internet, patients search for solutions to their conditions. Still, the magnitude of venous disease remains overshadowed and underappreciated in the clinical arena. It truly is an important frontier in vascular medicine.
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REFERENCES 1. 2. 3. 4. 5.
6.
7.
8. 9. 10. 11. 12. 13.
14.
15. 16.
17.
18. 19. 20. 21.
22.
Heit JA. The epidemiology of venous thromboembolism in the community: implications for prevention and management. [Review] [96 refs]. J Thromb Thrombolysis 2006; 21(1): 23–9 Caprini JA, Tapson VF, Hyers TM et al. Treatment of venous thromboembolism: adherence to guidelines and impact of physician knowledge, attitudes, and beliefs. J Vasc Surg 2005; 42(4): 726–33 Tapson VF, Hyers TM, Waldo AL et al. Antithrombotic therapy practices in US hospitals in an era of practice guidelines.[see comment]. Arch Intern Med 2005; 165(13): 1458–64 Raju S, Owen S Jr, Neglen P. The clinical impact of iliac venous stents in the management of chronic venous insufficiency. J Vasc Surg 2002; 35(1): 8–15 Bjarnason H, Kruse JR, Asinger DA et al. Iliofemoral deep venous thrombosis: safety and efficacy outcome during 5 years of catheter-directed thrombolytic therapy. J Vasc Interv Radiol 1997; 8(3): 405–18 Thorpe P, Osse F, Dang H. Endovascular reconstruction for chronic iliac vein and inferior vena cava obstruction. In: Gloviczki P, Yao J, eds. Handbook of Venous Disorders. 2nd ed. London: Arnold; 2001; 347–61 Carpenter JP, Holland GA, Baum RA, Owen RS, Carpenter JT, Cope C. Magnetic resonance venography for the detection of deep venous thrombosis: comparison with contrast venography and duplex Doppler ultrasonography. J Vasc Surg 1993; 18(5): 734–41 Neglén P, Hollis KC, Olivier J, Raju S. Stenting of the venous outflow in chronic venous disease: long-term stent-related outcome, clinical, and hemodynamic result. J Vasc Surg 2007; 46(5): 979–90 Sharafuddin MJ, Hicks ME. Current status of percutaneous mechanical thrombectomy. Part I. General principles. [Review] [88 refs]. J Vasc Interv Radiol 1997; 8(6): 911–21 Sharafuddin MJ, Hicks ME. Current status of percutaneous mechanical thrombectomy. Part II. Devices and mechanisms of action. [Review] [105 refs]. J Vasc Interv Radiol 1998; 9 (1 Pt 1): 15–31 Sharafuddin MJ, Hicks ME. Current status of percutaneous mechanical thrombectomy. Part III. Present and future applications. [Review] [151 refs]. J Vasc Interv Radiol 1998; 9(2): 209–24 Stainken BF. Mechanical thrombectomy: basic principles, current devices, and future directions. Tech Vasc Interv Radiol 2003; 6(1): 2–5 Gu X, Sharafuddin MJ, Titus JL et al. Acute and delayed outcomes of mechanical thrombectomy with use of the steerable Amplatz thrombectomy device in a model of subacute inferior vena cava thrombosis. J Vasc Interv Radiol 1997; 8(6): 947–56 Sharafuddin MJ, Gu X, Han YM, Urness M, Gunther R, Amplatz K. Injury potential to venous valves from the Amplatz thrombectomy device. J Vasc Interv Radiol 1999; 10(1): 64–9 HYPERLINK "http://www.jvir.org/cgi/external_ref?access_num=9540903&link_ type=MED" Vedantham S, Vesely TM, Sicard GA et al. Pharmacomechanical thrombolysis and early stent placement for iliofemoral deep vein thrombosis. J Vasc Interv Radiol 2004; 15(6): 565–74 O'Sullivan GJ, Lohan DG, Gough N, Cronin CG, Kee ST. Pharmacomechanical thrombectomy of acute deep vein thrombosis with the Trellis-8 isolated thrombolysis catheter. J Vasc Interv Radiol 2007; 18(6): 715–24 Allie DE, Hebert CJ, Lirtzman MD et al. Novel simultaneous combination chemical thrombolysis/rheolytic thrombectomy therapy for acute critical limb ischemia: the power-pulse spray technique. Catheter Cardiovasc Interv 2004; 63(4): 512–22 Schweizer J, Kirch W, Koch R et al. Short- and long-term results after thrombolytic treatment of deep venous thrombosis. [see comment]. J Am Coll Cardiol 2000; 36(4): 1336–43 Meissner AJ, Misiak A, Ziemski JM et al. Hazards of thrombolytic therapy in deep vein thrombosis. Br J Surg 1987; 74(11): 991–93 Peden E, Zhou W, Bush RL, Lumsden AB, Lin PH. The case for thrombolysis for iliofemoral venous thrombosis. [Review] [76 refs]. Semin Vasc Surg 2005; 18(3): 139–47 Ouriel K, Gray B, Clair DG, Olin J. Complications associated with the use of urokinase and recombinant tissue plasminogen activator for catheter-directed peripheral arterial and venous thrombolysis. J Vasc Interv Radiol 2000; 11(3): 295–8 Ouriel K, Kandarpa K. Safety of thrombolytic therapy with urokinase or recombinant tissue plasminogen activator for peripheral arterial occlusion: a comprehensive compilation of published work. J Endovasc Ther 2004; 11(4): 436–46
23.
24. 25.
26. 27. 28. 29. 30. 31. 32. 33. 34. 35.
36. 37. 38. 39. 40. 41. 42.
43. 44.
45.
Sugimoto K, Hofmann LV, Razavi MK et al. The safety, efficacy, and pharmacoeconomics of low-dose alteplase compared with urokinase for catheter-directed thrombolysis of arterial and venous occlusions. J Vasc Surg 2003; 37(3): 512–7 Dake MD, Semba CP. Thrombolytic therapy in venous occlusive disease. J Vasc Interv Radiol 1995; 6(6 Pt 2 Su): 73S–77S Mewissen MW, Seabrook GR, Meissner MH, Cynamon J, Labropoulos N, Haughton SH. Catheter-directed thrombolysis for lower extremity deep venous thrombosis: report of a national multicenter registry.[erratum appears in Radiology 1999 Dec; 213(3):930]. Radiology 1999; 211 (1): 39–49 Neglen P, Raju S. In-stent recurrent stenosis in stents placed in the lower extremity venous outflow tract. J Vasc Surg 2004; 39(1): 181–7 Ouriel K, Green RM, Greenberg RK, Clair DG. The anatomy of deep venous thrombosis of the lower extremity. J Vasc Surg 2000; 31(5): 895–900 Masuda EM, Kessler DM, Kistner RL, Eklof B, Sato DT. The natural history of calf vein thrombosis: lysis of thrombi and development of reflux. J Vasc Surg 1998; 28(1): 67–73 Raju S, Fredericks R, Lishman P, Neglen P, Morano J. Observations on the calf venous pump mechanism: determinants of postexercise pressure. J Vasc Surg 1993; 17(3): 459–69 Zollikofer CL, Largiader I, Bruhlmann WF, Uhlschmid GK, Marty AH. Endovascular stenting of veins and grafts: preliminary clinical experience. Radiology 1988; 167(3): 707–12 Irving JD, Dondelinger RF, Reidy JF et al. Gianturco self-expanding stents: clinical experience in the vena cava and large veins. Cardiovasc Intervent Radiol 1992; 15(5): 328–33 Slonim SM, Dake MD, Razavi MK et al. Management of misplaced or migrated endovascular stents. J Vasc Intervent Radiol 1999; 10(7): 851–9 Duprat G, Jr., Wright KC, Charnsangavej C, Wallace S, Gianturco C. Self-expanding metallic stents for small vessels: an experimental evaluation. Radiology 1987;162(2): 469–72 Sawada S, Fujiwara Y, Koyama T et al. Application of expandable metallic stents to the venous system. Acta Radiol 1992; 33(2): 156–9 Zollikofer CL, Antonucci F, Stuckmann G, Mattias P, Salomonowitz EK. Historical overview on the development and characteristics of stents and future outlooks. Cardiovasc Intervent Radiol 1992; 15(5): 272–8 Neglen P, Thrasher TL, Raju S. Venous outflow obstruction: An underestimated contributor to chronic venous disease. J Vasc Surg 2003;38(5): 879–85 Verhaeghe R, Stockx L, Lacroix H, Vermylen J, Baert AL. Catheterdirected lysis of iliofemoral vein thrombosis with use of rt-PA. Eur Radiol 1997; 7(7): 996–1001 Cockett FB, Thomas ML. The iliac compression syndrome. Br J Surg 1965; 52(10): 816–21 Thomas ML, Fletcher EW, Cockett FB, Negus D. Venous collaterals in external and common iliac vein obstruction. Clin Radiol 1967; 18(4): 403–11 Neglen P, Raju S. Angioplasty and stenting of the obstructed iliac vein. Hawaii Med J 2000; 59(6): 276–8 Raju S, Neglen P. High prevalence of nonthrombotic iliac vein lesions in chronic venous disease: a permissive role in pathogenicity. J Vasc Surg 2006;44(1): 136–43 Bjarnason H, Kruse JR, Asinger DA et al. Iliofemoral deep venous thrombosis: safety and efficacy outcome during 5 years of catheter-directed thrombolytic therapy. J Vasc Intervent Radiol 1997; 8(3): 405–18 Raju S, Hollis K, Neglen P. Obstructive lesions of the inferior vena cava: clinical features and endovenous treatment. J Vasc Surg 2006; 44(4): 820–7 Vedantham S, Rundback JH, Khilnani NM et al. Development of a research agenda for endovenous treatment of lower-extremity venous reflux: proceedings from a multidisciplinary consensus panel. [13 refs]. Journal of Vascular & Interventional Radiology 1575; (12): 2005 Vedantham S, Rundback JH, Comerota AJ et al. Development of a research agenda for endovascular treatment of venous thromboembolism: proceedings from a multidisciplinary consensus panel. J Vasc Interv Radiol. 2005; 16(12): 1567–73
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Stents RR Heuser, KL Waters, CW Hatler, and LM Kelly
Introduction Peripheral artery disease is characterized by diffuse disease affecting 12% of the adult population and up to 20% of elderly persons. These patients have significant functional disability. Although effective, the concept of treating with focal stents or focal balloon angioplasty clearly is not the panacea for this clinical problem nor is it the panacea for coronary artery disease. Endovascular stenting does avoid the problem of early elastic recoil, residual stenosis, and flow-limiting dissection after balloon angioplasty. Judicious use of stents in the peripheral tree can be the treatment of choice for many of the challenges of treating peripheral arterial disease.1,2 When describing this stent technology, it would be preferable if one stent would be effective for all of these applications. Please see the appropriate chapter for the vessel location application of specific anatomic stent applications. See Table 20.1 where we have compiled a list from manufacturers on many of the peripheral stents available and approved in the US. The ideal stent would have the following characteristics: ● ● ●
●
● ● ●
●
low profile, perhaps a few microns in diameter; high tensile strength; highly radio-opaque (but not so radio-opaque to obscure arteriographic images); highly compatible with MRI and totally visible with imaging modalities; pharmacologically coated to inhibit intimal hyperplasia; no polymer covering; torque resistant and fracture resistant to thousands of pounds of pressure; biodegradable, reabsorbable (there should be absolutely no inflammatory reaction when it breaks down and the degradation can be modified after placement of the stent).
It can be surmised from this list, that not one stent meets all of the ideal characteristics. Peripheral vascular lesions are even more heterogenous than coronary lesions. Furthermore, each application will have to be modified for the anatomy.
10 mm or greater in diameter. The balloon’s expandable nature makes it possible to be more accurate in placement to make sure there is no extension of the stent into the aorta or across the vertebral or internal mammary artery. The expansible strength of a self-expanding stent may make this more durable. For the aorta, many stents are not large enough and in a patient with stenosis combined with an aneurysm, an aorta cuff as part of an endoluminal graft may be a better option.
Renal, iliac, femoral, and popliteal arteries When treating renal artery lesions, balloon expandable stents are preferred over the self-expanding stents since accuracy of placement is necessary. It must be noted that a main renal artery stenosis differs from the ostial lesion. The ostial lesion will not only need to be treated with a device with significant radial strength but length must be taken into consideration. Many manufacturers have made the shorter stents to accommodate many of these lesions that are quite minimal in length. The iliac arteries have been treated with both selfexpanding and balloon expandable stents. For lesions effecting the bifurcation, the kissing balloon technique necessitates a balloon expandable stent, but in areas not affected by branches, the self-expanding stent is quite adequate. Iliac stents require the ability to dilate up to 8–9 mm. The femoral artery in many cases is not amenable to stenting simply because of the length of lesions. However recent studies suggest focal stenting with nitinol devices are preferable to balloon angioplasty.2,3 The popliteal arteries in general are usually not treated with stents unless a flow-limiting dissection is present.4–7 The anterior tibial, peroneal, and posterior tibial arteries in general are not treated by stenting. If so, coronary stents are usually applied although dedicated peripheral stents for these applications are used by some investigators.
Coronary stents for peripheral arteries Carotid, subclavian and aortic arteries Carotid arteries have traditionally been treated with selfexpanding stents. In the subclavian, balloon expandable stents are necessary and should be dilated to at least 8 mm up to even 132
The coronary stent application in the peripheral arteries is limited. Coronary stents have to be fairly large. The drug-eluting stent in particular would not be large enough. In lieu of the current controversy about coronary thrombosis, drug-eluting stents may prove not to be an ideal alternative to consider. There may
Table 20.1
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(a) Biliary stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))
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(a) Biliary stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))—cont’d
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Stents Table 20.1 (b) Carotid stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))—cont’d
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(c) Peripheral stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))
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Table 20.1
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(c) Peripheral stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))—cont’d
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Table 20.1
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Stents be situations where a carotid dissection in the internal carotid may be small enough that only a coronary stent can make the turn or make access possible. With the renal arteries, the vessels are too small for consideration of coronary stents and the tensile strength is not great enough with current coronary devices. Below the knee, it is not advantageous to use coronary stents; however, in patients with critical limb ischemia or patients with flow-limiting dissections, these can be very effective.
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Conclusion In the case of peripheral stenting it is clear that neither one size nor one type of stent fits all. In peripheral arterial disease stenting needs to be modified toward the patient’s arteriosclerosis with a common knowledge that the diffuse nature of peripheral vascular disease makes stenting an adjunct and not always a requirement.
REFERENCES 1. 2. 3. 4.
Yadav J, Wholey M, Kuntz R et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004; 351: 1493–501 Schillinger M, Sabeti S, Loewe C et al. Balloon angioplasty versus implantation of nitinol stents in the superficial femoral artery. N Engl J Med 2006; 354: 1879–88 Cejna M, Turnher S, Illiasch H et al. PTA versus Palmaz stent in femoropopliteal artery obstructions: a multicenter prospective randomized study. J Vasc Interv Radiol 2001; 12: 23–31 Vroegindeweij D, Vos LD, Tielbeek AV, Buth J, van de Bosch HC. Balloon angioplasty combined with primary stenting versus balloon angioplasty alone in femoropopliteal obstructions: a comparative randomized study. Cardiovasc Intervent Radiol 1997; 20: 420–5
5. 6.
7.
8.
Grimm J, Muller-Hulsbeck S, Jahnke T et al. Randomized study to compare PTA alone versus Palmaz stent placement for femoropopliteal lesions. J Vasc Interv Radiol 2001; 12: 935–42 Zdanowsmki Z, Albrechtsson U, Lundin A et al. Percutaneous transluminal angioplasty with or without stenting for femoropopliteal occlusions? A randomized controlled study. Int Angiol 1999; 18: 251–5 Becquemin JP, Favre JP, Marzelle J et al. Systematic versus selective stent placement after superficial femoral artery balloon angioplasty: a multicenter prospective randomized study. J Vasc Surg 2003; 37: 487–94 Reilly Communications Group. Diagnostic & Invasive Cardiology Sept/Oct 2006; 46(5), www.dicardiology.net.
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Role of covered stents in peripheral arterial diseases M Henry, I Henry, and M Hugel
Introduction During the past 40 years, surgery has been established as a reliable treatment for peripheral diseases in all peripheral regions. Endovascular therapy is a relatively new field of vascular medicine and has continued to expand over the past two decades, thanks to the advancement of technical developments. This new concept has become widely recognized and accepted. The applications of endovascular procedures have been expanded dramatically throughout the human body for both occlusive and aneurysmal diseases, not only at iliac and femoropopliteal levels but also at aortic, renal, and supra-aortic levels. Angioplasty is now the first treatment proposed for peripheral vascular diseases and the treatment of choice for simple arterial lesions. Yet angioplasty alone is limited and has several complications (dissections, acute thromboses, etc.). The problem of restenosis remains and for long lesions the initial success and the long-term results are not as good as they are for short lesions, particularly in femoropopliteal arteries, in which surgery is often preferred.1–3 The concept of vascular stenting originated with Charles Dotter in 1969,4 but it did not become a clinical reality until the late 1980s. Expandable metallic stents have proved their usefulness in the management of complications related to angioplasty and possibly restenosis;5,6 for the later, however, this benefit is debated. Stenting is controversial, particularly at infrainguinal location. Its use is considered acceptable in the aortoiliac vessels and in the majority of published series in the literature, and the immediate and long-term results are encouraging.7–14 A primary or a direct stenting could be envisaged for these lesions if we consider the meta-analysis reported by Bosch and Hunink.15 Nevertheless, stenting is more in dispute for the femoropopliteal vessels and the results are very disparate in the literature with a primary patency between 22 and 77%.16–24 Three randomized trials showed no difference between PTA alone vs. PTA and stent,25–27 and according to TASC recommendation 36,28 femoropopliteal stenting as a primary approach to the interventional treatment of intermittent claudication or arterial limb ischemia is not indicated. Stents may have a limited role in salvage of acute PTA failure or complications. These recommendations were based on studies performed with the old generations of stents and it is the same with the randomized studies. New stents are now available, nitinol and covered stents, which seem to give better results.28–31 140
Endoluminal stent grafts and covered stents are now being investigated for treatment of both aneurysmal and occlusive peripheral arterial diseases.32–45 For occlusive diseases, it is postulated that an endoluminal bypass with a stent graft may limit the ingrowth of intimal hyperplasia along the length of the treated segment thereby improving patency as compared to conventional angioplasty and stenting. For an aneurysmal disease, the stent graft may be used to bridge the aneurysmal segment and therefore occlude the aneurysm from the native circulation. Several covered stents are either currently available or in clinical experiment: ●
● ●
● ● ●
● ●
The Cragg Endopro System 1/Passager (Boston Scientific, Natick, MA) The Corvita endoluminal graft (Boston Scientific) The Hemobahn or the new Viabahn (WL Gore & Associates, Flagstaff, AZ) The Wallgraft (Boston Scientific) The Jostent (Jomed International AB, Helsinberg, Sweden) The aSpire covered stent (Vascular Architects, San José, CA) The Cordis covered nitinol stent (Cordis, Warren NJ) The Adventia V12 (Atrium Medical Corporation, Hudson, NH)
We describe below these different covered stents, the results obtained, and their clinical applications in different locations.
The different types of covered stents: description and techniques of implantation The Cragg Endopro System 1/Passager Stent-graft construction The Cragg Endopro System 1/Passager (Figure 21.1) consists of a flexible, self-expandable nitinol stent covered with ultrathin woven polyester fabric. It has the property of shape memory.46–48 The design and construction of the stent have been previously described.47–50 The fabric is of low porosity and is attached to the stent framework by polyester ligatures. The stent graft is presented in a compressed form in a loading cartridge. Stent grafts range from 5 mm to 12 mm in diameter
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Figure 21.1
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Cragg/Passager.
and from 3 cm to 10 cm in length. They are delivered through 50-cm-long introducer sheaths ranging in diameter from 7French to 10-French, depending on the size of the stent-graft to be implanted. Stent-graft introduction technique Device delivery is usually accomplished using an ipsilateral retrograde or antegrade femoral artery approach. A retrograde popliteal approach has been used in cases in which femoral artery access was not possible. The rigidity of the delivery device limits the possibilities of implantation using contralateral access. For occlusive disease, balloon angioplasty is always performed first in order to enlarge the arterial lumen. Occasionally, debulking techniques such as rotational atherectomy are used in case of calcified arteries. The stent graft is delivered through the 50-cm-long introducer sheath, which is placed across the lesion to be treated. The stent-graft diameter is usually selected to be equal to or 1 mm greater than the nominal arterial diameter. The stent graft is positioned fluoroscopically across the treated segment. Platinum markers at each end of the stent assist in positioning the device. Once the stent graft is in position, the sheath is withdrawn, and an internal positioning catheter is used to fix the stent graft in place. The stent graft expands using the thermal memory characteristics of its nitinol frame. The graft is usually then dilated with an angioplasty balloon at high pressure (14–16 atmospheres); this fixes the graft against the arterial wall and helps unwrinkle the fabric. When several grafts are needed to cover a long lesion, it is important to overlap the prostheses by at least 5–10 mm so that the fabric portion of the graft covers the entire arterial lumen. In the middle part of the femoral artery, an overlapping of 1 cm may be better to avoid disjunction of the stents. The Corvita endoluminal graft51 This prosthesis was formerly developed by Schneider/Boston Scientific but is no longer available. Stent-graft construction The Corvita Endoluminal Graft (Figure 21.2) is a self-expanding endoluminal vascular prosthesis with an introducer system that makes it a low-profile device and permits percutaneous delivery and deployment. The integrated endoluminal graft consists of two components:
Figure 21.2
● ●
Corvita covered stent.
a self-expanding cylindrical wire structure; a highly porous and elastic coating of spun 13-µm-thin Corethane (polycarbonate urethane; The Polymer Technology Group Inc., Berkeley, CA) fibers in which blood can coagulate and seal the Corvita endoluminal graft to form a new blood-tight vessel wall. The Corethane coating is glued on the inside of the metallic structure.
Stent-graft implantation The endoluminal graft can be cut to length by the user with surgical scissors and mounted in the tip of an introducer sheath. For that purpose, the Corvita endoluminal graft is manually compressed to one-fifth or one-sixth of its original, expanded diameter and simply inserted by the user into the introducer sheath. Then it is loaded into and deployed from a delivery system consisting of an internal sheath and a coaxial catheter, which is introduced inside the sheath and therefore helps to release the endoluminal graft precisely at the predetermined placement site. The introducer sheath with the compressed Corvita endoluminal graft in the tip can be introduced transfemorally as well as over a guidewire into the arterial system and advanced under continual fluoroscopic visualization to the site of the lesion. The Corvita endoluminal graft can be released from the introducer sheath at the intended site by coaxial introduction of a “holding” catheter and by slowly withdrawing the introducer sheath. The exact placement of the Corvita endoluminal graft can still be corrected during the initial release process. The flexibility of this device allows its implantation using various approaches such as the ipsilateral femoral, the contralateral, or the popliteal approach, and in tortuous arteries. The Hemobahn/Viabahn (Gore and Associates, Flagstoff, AZ) This endoprosthesis (Figure 21.3) is constructed with a durable, reinforced biocompatible, expanded polytetrafluoroethylene (PTFE) liner attached to the external nitinol stent structure. This self-expanding prosthesis is designed to allow
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Figure 21.4
Figure 21.3
Viabahn covered stent.
relining of luminal surfaces in tortuous arterial anatomy. Its extreme flexibility enables it to better traverse tortuous areas such as the SFA and conforms more closely to the complex anatomy of the artery. Along with its superior flexibility, the Viabahn endoprosthesis is engineered for exceptional strength and durability. Radio-opaque markers enhance visualization to facilitate accurate placement. The catheter-based system allows for rapid, accurate deployment without device lengthening or shortening. The Viabahn is compressed and attached to a dual-lumen polyethylene delivery catheter available in lengths of 75 cm and 110 cm. The device is available in diameters from 4.5 mm to 13 mm and lengths of 25, 50, 100, and 150 mm. The delivery system is ≤ 10 French in diameter and it requires a 0.025-inch or 0.035-inch guidewire. The deployment consists of untwisting and slowly pulling the deployment knob. After deployment, the device must be smoothed against the arterial lumen wall by inflating an appropriately sized angioplasty balloon within it. The flexibility of the device allows easy contralateral approach. In comparison with Hemobahn, Viabahn has some refinements (0.035-inch guidewire instead of 0.025-inch and deployment from proximal to distal). The Wallgraft endoprosthesis This endoprosthesis (Figure 21.4) is composed of a braided polyester graft, which is bonded to the outside of a commercially available Wallstent with a thin layer of a Corethane (Boston Scientific Corporation). Radio-opaque tracer wires are braided with the stent wires to distinguish the Wallgraft from a Wallstent under fluoroscopy. This design configuration is flexible and self-expanding. The Wallgraft is available in diameters of 6 mm to 14 mm and lengths of 20, 30, 50, and 70 mm. The premounted Wallgraft is available on a Unistep Plus delivery system. The delivery system is equal to or less than 11 French in diameter, has a 90-cm working length and a central lumen that can accommodate a 0.035-inch guidewire.
Wallgraft covered stent.
The deployment is achieved by withdrawing the protective sheath. The self-expandable endoprosthesis is then expanded further by inflating the appropriately sized angioplasty balloon. The flexibility of this prosthesis allows its use in tortuous arteries, even through a contralateral approach. Its shortening, however, may render precise placement difficult. The Jostent stent The Jostent stent (Figure 21.5) is a balloon-expandable prosthesis. It is available in lengths ranging from 28 mm to 58 mm and its expansion diameter ranges from 5 mm to 10 mm. It consists of double thin stainless steel prosthesis. There is a PTFE coating between the two prostheses. An implantation in a flexion area such as the popliteal artery should be avoided because of potential compression and its rigidity. The aSpire covered stent (Vascular Architects, San José CA, USA) This stent (Figure 21.6) is a double-spiral helical nitinol selfexpanding stent completely covered by a thin layer of PTFE, which provides significantly greater vessel wall coverage than metallic stents. Unlike other covered stent grafts, the aSpire stent preserves many of the native vessel’s desired elements including side-branch access. It is available in lengths of 2.5, 5.0, and 10.0 cm and in diameter from 6 mm to 14 mm.
Figure 21.5
Jostent peripheral stent graft.
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●
Figure 21.6
aSpire covered stent.
It provides good radial strength, flexibility, and conformability. The spiral design preserves smooth laminar flow, maintains natural compliance, and withstands torsional stress. If the stent position is not in optimal position it can be “wrapped down,” repositioned, and re-expanded. Cordis covered nitinol stent (in experiment) The Cordis covered nitinol stent is a PTFE tube encapsulated between two nitinol self-expanding, laser-cut stents. The PTFE graft material is located on the inner lumen of the outer stent and is cuffed and bonded at the ends of the outer stent framework. The inner framework supports the inner lumen of the graft to prevent any draping or sagging. Covered stents were available in lengths between 40 mm and 80 mm and diameters between 6 mm and 10 mm. Stents were constrained in a 9French or 10-French delivery system consisting of an inner shaft and an outer sheath designed to accept a 0.035-inch guidewire. Radio-opaque markers were located on the inner shaft at the proximal and distal ends of the undeployed stent and at the tip of the outer sheath for monitoring stent deployment. New stents Other stents will be developed by different companies: ●
The Advanta V12 covered stent (Atrium Medical Corporation, Hudson NH). It is a low-profile balloon-expandable
Figure 21.7
Bard Fluency covered stent.
143
stent made of stainless steel with low foreshortening, covered with a microporous PTFE film for improved biocompatibility and to protect the blood from undesirable vessel wall lesions. It controls tissue prolapse and helps to minimize in stent restenosis due to vascular wall injury. It is available in diameters from 5 mm to 12 mm and fit through 6-French and 7-French introducers. We are waiting for the first studies in peripheral field. The Fluency developed by Bard Peripheral Vascular Inc. (Tempa, AZ, USA) (Figure 21.7). It is a low-profile selfexpanding stent with an ultrathin PTFE covering, exceptional radial force, highly radio-opaque stent graft ends, a soft atraumatic tip, and minimal shortening. It has an excellent trackability, pushability, and flexibility allowing implantation in the main peripheral arteries, with placement accuracy with an 8-French or 9-French delivery system.
The different locations for covered stents Iliofemoropopliteal angioplasty and stenting: results with the different covered stents Cragg Endopro System 1/Passager (Figures 21.8–21.12) Our experience Patient population. One hundred and fifty-six patients (134 males, 22 females), mean age 63.4 ± 10.5 years (range 38–88 years) were selected for treatment with the stent graft. According to Rutherford’s classification, 136 patients were in grade I (8 in category 2, 128 in category 3), 12 patients in grade II, and 8 in grade III (category 5). The mean ankle–brachial index (ABI) was 0.56 ± 0.11. Three tibial vessels were patent in 72, two in 74, and one in 10 patients. Results. Table 21.1 shows the locations and the types of lesions. Ninety-three lesions were heavily calcified (21 were treated with rotational atherectomy), and 17 ulcerated. Tables 21.2 and 21.3 detail the lesion characteristics including the mean lesion length, the mean percentage stenosis before angioplasty and graft placement, and the mean arterial diameter. A total of 266 stent grafts were placed. Lengths ranged from 3 cm to 10 cm and diameters ranged from 5 mm to 10 mm. Indications for stent-graft placement were postangioplasty residual stenoses (n = 70), dissections (n = 22), restenoses (n = 21), ulcerated lesions (n = 17), and aneurysms (n = 26).
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STENT FEMORAL G.
(a) Figure 21.8
(b)
(a) Long SFA occlusion; (b) recanalization: final result after Cragg/Passager stent implantation.
Technical success was achieved in all cases but one at the iliac level (98%) and the femoropopliteal level (99%) (83 cases of 84). In this one case, the patient had a large femoral aneurysm, and partial success was achieved but with persistent arterial leak at the distal part of the aneurysm. This patient was in poor general condition and died from an acute myocardial infarction 4 days after the procedure. Post-angioplasty percent stenoses decreased from 43 ± 3.9% to 0.6 ± 3% after stent-graft implantation, with no significant difference in the iliac and femoropopliteal location (Table 21.4). No significant residual stenosis was seen even in calcified lesions. The mean length of stent segments was significantly greater at the femoropopliteal level in comparison with the iliac level for occlusions and stenoses (Table 21.5).
The mean stent-graft length for all lesions was 114.7 ± 65.7 mm. Immediate clinical success was obtained in all uncomplicated cases with an increase in the ABI from 0.56 ± 0.11 to 0.95 ± 0.14. All patients were given ticlopidine (250 mg/day) or clopidogrel (75 mg/day) and aspirin (100 mg/day) for 1 month, and aspirin alone thereafter. Complications. In the first 30 days there were 18 major complications. At the puncture site, five complications occurred: ● ● ●
two hematomas, one requiring surgery; two pseudoaneurysms both requiring surgery; one local thrombosis treated by thrombolysis.
At the iliac level, four complications occurred (6.2%): ●
●
●
One stent-graft thrombosed within 24 hours (this was associated with distal embolization, treated by surgical thrombectomy). One patient who had two stent-grafts placed for treatment of a right iliac occlusion presented 15 days post-procedure with left-leg claudication. Angiography demonstrated partial obstruction of the left common iliac artery by one of the stent grafts, which protruded slightly into the aorta. A new stent-graft was placed in the left common iliac artery with a good result. Two arteries thrombosed and were treated with success by new PTA.
At the femoropopliteal level: (a)
(b)
Figure 21.9 (a) Total occlusion right iliac artery; diffuse stenoses left iliac artery; (b) final results after Cragg/Passager stent implantation.
●
One patient developed distal embolization after recanalization of an 8-cm-long femoral occlusion, treated by thrombolysis and thromboaspiration. This patient died from an acute myocardial infarction on the third postoperative day.
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(a) Figure 21.10
(b)
(c)
AFTER STENTING
(a) Popliteal artery aneurysm; (b) Cragg/Passager covered stent; and (c) final result after Cragg/Passager stent implantation.
(a) Figure 21.11
CRAGG/PASSAGER
(b)
(a) SFA aneurysm; (b) treatment with Cragg/Passager stent.
BEFORE ANGIOPLASTY
RUPTURE OF THE ARTERY AFTER ANGIOPLASTY
AFTER STENTING
CRAGG/PASSAGER
(a) Figure 21.12
(b)
(c)
(d)
(a, b) Right external iliac artery stenosis; (c) arterial rupture after angioplasty; and (d) treatment with Cragg/Passager stent.
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Lesion characteristics: locations and types of lesions
Location
No.
Iliac Femoral Popliteal Total
64 82 10 156
Stenoses
Occlusions
Aneurysms
33 28 1 62
18 46 4 68
13 8 5 26
Table 21.2 Location
Calcified
Ulcerated
27 63 3 93
10 6 1 17
Lesion characteristics: mean lesion length Stenoses
Iliac 52.2 ± 26.4 Femoral 112.5 ± 69.8 Popliteal 80
Occlusions
Aneurysms
Range
86.7 ± 36.1 161.1 ± 85.3 67.5 ± 15
38.5 ± 13.9 125 ± 93.3 114 ± 80.5
20–150 20–300 30–200
Table 21.3 Lesion characteristics: mean percentage stenosis before PTA and mean arterial diameter Mean percent stenosis before PTA SFA Iliac Popliteal Mean arterial diameter SFA Iliac Occlusion Stenosis Popliteal
Table 21.4
70–100% 70–100% 75–100%
5.95 ± 0.6 mm
5–7 mm
7.8 ± 1.1 mm 7.9 ± 1.1 mm 5.5 ± 0.6 mm
6–10 mm 7–10 mm 5–6 mm
Results before and after PTA
Global population Iliac Femoral Popliteal
Table 21.5
93 ± 4.1% 89 ± 3.7% 92 ± 4.6%
Stenosis before PTA
Stenosis after PTA
Stenosis after stent
92 ± 3.7 89 ± 3.7 93 ± 4.3 92 ± 4.6
43 ± 3.9 48 ± 4.3 45 ± 3.8 37 ± 2.7
0.6 ± 0.3 0 0.8 ± 0.8 0.8 ± 0.8
Results before and after stent Lesion length before stent (mm)
Global population Iliac Femoral Popliteal
104.1 59.2 140.9 92
Stented lesion length (mm) 114.7 63.8 155.2 112
Mean percent of covering (%) 110.2 107.8 110.1 121.7
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●
Seven stent-graft thromboses occurred within 24 hours of the procedure. Three were treated by thrombolysis and thromboaspiration and four required surgical bypasses. Five of the lesions were longer than 15 cm. One stent-graft thrombosis occurred on day 8, requiring surgical bypass.
Finally, a complication that appears to be directly linked with this type of endoprosthesis is the rapid development of fever along with pain in the region of the implant that can last from 2 to 3 weeks; however no infection has been found in these cases. Consequently, the etiology of this phenomenon is still uncertain. This was observed 29 times (18.6%): 25 times at the femoropopliteal level (occlusion n = 15, stenosis n = 7, aneurysm n = 3) and 4 times at the iliac level (occlusion n = 1, stenosis n = 3). There could be a relation between this phenomenon and lesion length, as it appears to be more frequent as the lesion length increases; however, the condition appears to be self-limiting. Follow-up. All patients were followed up by duplex scan on day 180 and every 6 months thereafter. At 6 months, a followup angiography was performed. The maximum follow-up was 60 months, the mean follow-up 36.9 ± 17.9 months. Restenosis. At the iliac level, one restenosis occurred outside the stent and was treated with success by new PTA. At the femoropopliteal level eight patients (8.6%) developed a restenosis, regardless of the stents placed at this extremity. Restenosis inside the stent was not observed. Of these eight restenoses, seven were treated by new angioplasty and three had an additional stent-graft placement. One patient was treated surgically with a bypass. Pseudoaneurysms. In three patients small pseudoaneurysms were detected at the end of the stent graft. In two cases they were treated by the placement of an additional short stent graft. The third patient, however, was only monitored medically due to the small size of the aneurysm. Late thrombosis. At the iliac level, no late thrombosis was observed. At the femoropopliteal level, 18 patients (19.6%) had graft thrombosis. One was recanalized percutaneously, three were treated by surgical thrombectomy, ten required bypass graft placement, and four refused surgery and were treated medically. Of these lesions, twelve were longer than 15 cm. Long-term follow-up. The long-term patencies at 60 months are summarized in Table 21.6. In the literature Several series were published with the Endopro/Passager. Scheinert et al.52 analyzed the primary and long-term results of 48 endoprostheses implanted in iliac artery in 39 patients for long iliac occlusions (n = 22), aneurysms (n = 16), perforation (n = 1). The primary patency was 89.7% at 6 months, 87.1% at 12 months and 84.2% at 24 months. The secondary patency was 94.9% at 6, 92.1% at 12 and 24 months, respectively. Link et al.53 treated an iliac occlusion and 15 high-grade iliac stenoses with a cumulative patency rate of 71% at 12 months. Dorffner et al.54 reported a series of 15 aneurysms in 13 patients (common iliac artery n = 6, external iliac artery: n = 1, hypogastric artery: n = 1, femoral artery: n = 2, popliteal artery: n = 4). In all cases, the aneurysm was successfully
Table 21.6
147
Long-term patencies at 60 months Primary patency (%)
Iliac Global Lesions ≥ 10 cm Lesions > 10 cm Occlusions Stenoses Aneurysms Femoropopliteal Global Lesions ≥ 10 cm Lesions < 10 cm Occlusions Stenoses Aneurysms Femoral Popliteal
Secondary patency (%)
88 85 89 88 92 84
100 100 100 100 100 100
62 51 75 61 63 55 65 40
70 59 85 72 73 55 73 50
occluded after stent implantation. The primary and secondary patency rates at 6 months were 93 and 100% respectively. An arterial rupture of the external iliac artery during balloon angioplasty was treated successfully with the prosthesis by Formichi.55 Beregi JP et al.56 reported a series of 19 aneurysms (iliac: n = 7, subclavian: n = 5, femoral: n = 3, popliteal: n = 3, carotid: n = 1) treated with the same prosthesis with a successful aneurysm occlusion in 18 of 19 patients. At 1 year, the stent was patent in 13 patients (68%) and the aneurysm excluded in 17 (89%). Scheinert et al.32 reported a series of 48 iliac aneurysms treated with 53 endoprostheses. Complete occlusion of the aneurysm was achieved in 47 of 48 cases (97.9%). Primary patency rates were 100% after 1 year, 97.9% after 2 years, 94.9% after 3 years and 87.6% after 4 years. No secondary leaks were observed. Cormier et al.33 treated 34 iliac aneurysms (mean diameter 42 mm). Three procedures were carried out under emergency conditions after acute rupture. The technical success was 97.6%. Scheinert et al.34 reported a series of 20 catheter-included iliac artery injuries treated with these covered stents. An immediate exclusion of the lesion was achieved in all cases, but within 24 hours after, fever (55%), elevations in white blood cell count (50%) and C-reactive protein (65%) were seen in the majority of patients. Two restenoses appeared at the outlet of the endografts and were successfully treated with balloon angioplasty, achieving primary and secondary patency rates of 87 and 100% respectively for a median 21-months follow-up. Ahmadi et al.35 reported a series of 30 patients who underwent covered stent implantation because of post-PTA recurrent stenosis in the SFA. Technical success was 100%. At 6, 12, 36, and 72 months, respectively primary patency rates were 27, 23, 17, and 17%, and secondary patency rates were 63, 60, 34, and 34%. All these published series showed much better long-term results at iliac level than at femoropopliteal level, but for some types of lesions the results appear encouraging.
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The Corvita endoluminal graft (Figure 21.13–21.16) Our experience Population. Sixty-four patients (51 males, 13 females), mean age 65.1 ± 9.8 years (range 39–86) were treated with the Corvita endoluminal graft. According to Fontaine’s classification, 10 were in stage IIa (patients with aneurysms), 52 were in stage IIb, and 2 were in stage III. At the distal arterial level, 6 patients had only 1 patent leg vessel, 36 had 2 patent vessels, and 22 had 3 patent vessels. Lesion characteristics. Table 21.7 summarizes the localization of the lesions following their etiology. We treated 27 stenoses (iliac n = 18, femoropopliteal n = 9), 20 occlusions (iliac n = 8, femoropopliteal n = 12), and 17 aneurysms (iliac n = 12, femoropopliteal n = 5) (Figure 21.6–21.13). The mean length of the lesions was 80.5 ± 55.2 mm (range 20–300). At the iliac level, the mean length was 60.5 ± 28.3 (range 20–150) and at the femoropopliteal level it was 109.7 ± 70.7 (range 20–300). Long-term follow-up. Primary patency and secondary patency rates at 3-year follow-up are listed in Table 21.8. The Hemobahn/Viabahn stent An initial feasibility study36 addressing iliac and femoral artery occlusive disease was performed at three investigational sites in the US and in twelve European centers. In total, 93 patients had 100 lesions treated (iliac n = 58, femoral n = 42). The current mean implant duration was 5.4 months. The primary technical success in this group was 99%. The primary and secondary iliac patency at 1 month (n = 49), 3 months (n = 43), and 6 months (n = 24) was 96% at all intervals. The primary patency for treated femoral arteries at 1 month (n = 37), 3 months (n = 24) and 6 months (n = 7) was 100%, 91%, and 80% respectively. The corresponding secondary patency in the femoral region was 100, 94, and 82% at 1 month, 3 months, and 6 months of follow-up. Our experience We have implanted ten prostheses in the SFA to treat nine long occlusions (mean length 14.5 cm) and one aneurysm with good short- and mid-term results. All the prostheses remain patent at a mean of 12.5-month follow-up.
(a) Figure 21.13
BILATERAL ILIAC ANEURYSM
(b)
In the literature Procedure-related complications have included distal embolization in 5%, groin hematoma in 2%, and iliac artery rupture in 1%. The last case was successfully managed with deployment of a second stent graft without clinical sequelae. Lammer et al.57 reported a study of 127 patients treated for symptomatic peripheral arterial occlusive disease (iliac, n = 61 limbs; femoral, n = 141 limbs). Endoprosthesis deployment was successful in all patients. Primary patency rates in iliac arteries were 98 ± 3% and 91 ± 4% at 6 and 12 months respectively, and at femoral level 90 ± 3% and 79 ± 5% at 6 and 12 months respectively. Secondary patency rates were 95 and 93% for iliac and femoral arteries respectively at 12 months. Bauermeister37 treated 25 patients with long segment occlusions of the femoropopliteal arteries with the Hemobahn stent graft (median occlusion length 22 cm). Primary and secondary patency rates were 73.2 and 82.6% respectively at 1 year. Bleyn38 reported a series of 65 patients (67 limbs) with a mean femoral occlusion length of 14.3 cm. The primary patency rates were 80% at 1 year and 55.6% at 4 years; secondary patency rates were 88.7% at 1 year and 77.8% at 4 years. Saxon et al.39 published a 70% primary patency rate and 93% secondary patency rate at 4-year follow up for lesions of SFA with an average length > 10 cm using Hemobahn or Viabahn. Jahnke et al.40 reported a series of 63 Hemobahn stents used in 52 patients with occlusion (82.7%) or stenosis (17.3%) of the SFA. Mean length of vessel segments covered 10.9 cm ± 5.1. Technical success was 100%. Primary patency rate at 12 and 24 months were 78.4 and 74.1% respectively. Secondary patency was 88.3% at 12 months and 83.2% at 24 months. Chopra et al.41 reported a series of 60 patients (70 lower limbs) with SFA lesions. A total of 158 Hemobahn/Viabahn were implanted. Mean lesion length was 20 cm (2.38 cm). Technical success was 98%. The primary patency rates at 6, 12, 18, and 24 months were 97, 93, 89, and 87% respectively.
RESULT AFTER STENTING
(c)
RESULT AFTER 1 YEAR
(a) Bilateral iliac aneurysm; (b) result after placement of Corvita stents; and (c) results after 1 year.
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(a) Figure 21.14
(b)
(d)
(a) Long SFA occlusion; (b) recanalization; (c, d) final results after covered stents implantation (Corvita).
The secondary patency rates were 99, 96, 91 and 89% respectively. Recently, Fisher et al.42 reported a series of 57 patients treated with 82 Hemobahn or Viabahn for stenoses (13%) or occlusions (87%) of the SFA in 60 limbs. The average length of the treated lesions was 10.7 cm (3–34). Technical success was 98%. Early thrombosis (within 30 days) occurred in 10%. Late thrombosis or reocclusion was observed in 22 arteries (37%) up to 5 years after prosthesis placement (14 in the first year). Primary–secondary patency rates were 90, 95% at 30 days, 67–81% at 1 year, 57–80% at 2 years and 45–69% at 5 years. In a subgroup analysis of 48 patients with “optimal” conditions for implantation (no heavy calcifications, popliteal obstruction, or complete SFA occlusion) minimum 1 vessel run-off, and adequate antiplatelet therapy or anticoagulation, the primary-secondary patency rates were 80–91% at 1 year, 71–89% at 3 years, 62–90% at 5 years. The authors concluded
(a)
(c)
149
(b)
Figure 21.15 (a) SFA popliteal aneurysm; (b) treatment with Corvita covered stent.
that this prosthesis seems to be suitable for SFA so long as ideal indications and prophylaxis against secondary thrombosis are strictly observed. All these reported data with Hemobahn/Viabahn showed good long-term results even at femoropopliteal level. Primary and secondary patencies were similar to those reported for open synthetic femoropopliteal bypass procedures. The Wallgraft stent (Figure 21.17) Our experience We have used this prosthesis in 11 patients to treat occlusive or aneurismal diseases in the iliac (n = 3), femoral (n = 4), popliteal (n = 2), radial (n = 1) and carotid (n = 1) arteries. All prostheses remain patent at a mean of 16 months follow-up (3–41 months). In the literature Steinkamp et al.43 implanted 24 prostheses in 16 patients in iliac arteries to treat large dissections (n = 9), arterial perforations (n = 4), and aneurysms (n = 3). The secondary patency rate was 94.1%. Kumins et al.44 successfully treated three iliac embolic lesions responsible for blue toe syndrome with no recurrence after 16 months. Rzucidlo et al.45 reported the results of stent grafting to treat diffuse aortoiliac occlusive diffuse. Thirty-four patients were treated (Wallgraft: 88%, Hemobahn: 12%). Mean lesion length 13.7 ± 8 cm. Technical success was 100%. At 1 year primary patency was 70% and primary assisted patency 88%. For the authors, early results of stent graft placement to treat this type of lesion appear better than with stenting alone. The Wallgraft was also used to treat traumatic vascular injury as reported by White et al.58 Sixty-two patients were treated: iliac (n = 33), subclavian (n = 18), and femoral (n = 11). Post-procedure exclusion was achieved in 93.5%. One-year exclusion rates were 91.3% iliac, 90% subclavian and 62.3% femoral. One year primary patency rates were 76.4% iliac, 85.7% subclavian, and 85.7% femoral. Freedom from bypass was achieved in 74.3% iliac and 100% femoral and subclavian injuries. The Wallgraft for the treatment of traumatic arterial injuries offers a promising alterative to conventional operative
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(a)
(b)
(c)
(d)
Figure 21.16 (a) Left external iliac artery occlusion; (b, c) recanalization after fibrinolysis/ angioplasty; and (d) final result after stent implantation (Corvita).
The Jostent stent This balloon-expandable stent (Figures 21.18 and 21.19) is useful to treat small lesions at different locations and particularly in emergency to solve complications, which could appear after any PTA. Our experience We have implanted this stent with success in the iliac and femoral arteries in 20 patients to treat ulcerated plaques, small aneurysms, arterial perforations or ruptures, and pseudoaneurysms. In the literature Liistro et al.61 reported a case of thrombus containing iliac lesion treated with a Jostent stent with good follow-up at 6 months.
repair with comparable patency and less major morbidity and mortality. Femoropopliteal aneurysms have been treated with this prosthesis. Howell et al.59 reported a series of 17 patients with a technical success of 100% for femoral aneurysms and 92.3% for popliteal aneurysms. The one-year primary and secondary patency rates were both 100% for femoral, and 69 and 92% respectively for popliteal aneurysms. Lagana et al.60 published a series of 17 femoropopliteal aneurysms (14 treated with Wallgraft) with a 3-year primary patency of 63% and an assisted primary patency of 73%.
Table 21.7
Corvita endomunial graft: lesion characteristics
Location
No.
Iliac Femoral Popliteal Bypass Total
38 22 3 1 64
Stenoses 18 8 — 1 27
Occlusions 8 12 — — 20
Aneurysms 12 2 3 — 17
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Role of covered stents in peripheral arterial diseases Table 21.8 Primary patency & secondary patency at 3-year follow-up Primary patency (%) Global Iliac Global Lesions ≥ 10 cm Lesions > 10 cm Occlusion Stenoses Aneurysms Femoropopliteal Global Lesions ≥ 10 cm Lesions < 10 cm Occlusions Stenoses Aneurysms
Secondary patency (%)
74
86
87 100 85 88 83 92
95 100 94 88 94 100
55 55 54 31 78 57
72 64 82 64 78 78
Cil et al.62 published a case of arteriovenous fistula, which occurred after femoral arterial catheterization and treated with a Jomed stent, with an excellent result at 4-year follow-up. The aSpire covered stent Rosenthal et al.63 reported the results of remote SFA endarterectomy in conjunction with distal aSpire stenting in 210 patients. Mean length of endarterectomized SFA: 28.3 ± 6.2 cm (15–43). At 33 months the primary patency was 60.6% and the primary assisted patency 70.2%. Lenti et al.64 published a multicentric study including 152 patients (168 limbs) with 118 occlusions and 50 stenoses of the SFA. The mean length of the vessel segments covered was 104.35 ± 73.7 mm. The primary patency rates at 12 and 24 months were 64 and 57% respectively and the primary assisted patency rates 76 and 71% respectively. These studies showed good mid-term results but a high number of reinterventions were necessary in order to obtain an optimal assisted primary patency.
(a) Figure 21.17
(b)
(c)
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The Cordis covered nitinol stent Wiesinger et al.65 reported a multicenter prospective nonrandomized COVENT study involving 98 patients who received 130 stents in 107 arteries (60 iliac and 47 SFAs) after predilatation. Mean lesion length was 50 mm in the SFA and 45 mm in the iliac arteries. Technical success was 99%. Primary patency rates were 92% at 6 months and 89.8% at 1 year for the entire cohort. Secondary patency rates were 98 and 95.6% respectively. No statistically significant differences were observed in the primary patency rates for the SFAs (89.3% at both 6 and 12 months) versus the iliac arteries (94.3% at 6 months and 90.7% at 12 months). Carotid angioplasty and stenting: indications for covered stents Self-expandable stents have been providing excellent results when treating most cases of carotid stenosis. With cerebral protection, the neurological complication rate is reduced by 60%. However, brain embolisms may occur even with brain protection, and delayed embolic post-procedure events may also occur. With soft plaques we may have protrusion of cholesterol material through the net of the metallic stent. The migration of the plaque material through the mesh may go on for several days after the insertion of the stent, and produce these delayed embolisms and strokes. Covered stent grafts have been proposed to treat these high-risk embolism plaques.66 They can seal the plaque completely and also eliminate the risk of the stent being crossed by the cholesterol material. Covered stents can also exclude thrombi from the lumen of a vessel.61 Several covered stent grafts may be used. The Jostent stent graft is a balloonexpandable stent and its precise delivery makes it preferable when treating lesions at the ostium of the common carotid and brachiocephalic trunk. Self-expandable stents such as Wallgraft are more resistant to external compression and adapt better to areas where flexion may occur such as carotid bifurcation. Moreover, if this stent is delivered across the bifurcation, the flow of the external carotid artery may be jeopardized. Designs are therefore being developed to provide partial covering of the stent, which
(d)
(a, b) Ulcerated SFA lesion; (c–e) treatment after Wallgraft stent implantation.
(e)
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(a) Figure 21.18
(b)
●
carotid aneurysms with their risk of brain embolism;68 carotid pseudoaneurysms which are more common than true aneurysms, being usually iatrogenic or posttraumatic.69,70
(a) Figure 21.19
(d)
Jostent peripheral stent graft; (a,b) ulcerated, aneurismal lesions; (c,d) treatment with Jostent stent.
will maintain the flow toward the external carotid artery, while sealing the internal carotid plaque.66 Recently, Schillinger et al.67 published a study done to investigate when filter-protected carotid angioplasty stenting using a covered self-expanding stent reduces the risk of cerebral embolization. A significant reduction in ipsilateral microembolic signals by transcranial Doppler was observed with the covered versus the bare stent but a restenosis occurred in 38% of patients treated with covered stents, and none treated with bare stents. The trial was stopped. So, covered stents potentially reduce the risk of cerebral embolism but the problem of in-stent restenosis has to be resolved. Covered stents have also been proposed in other indications: ●
(c)
(b)
A covered stent has also been used to seal a pseudoaneurysm, which had developed at the site of an infected anastomosis between the carotid and the subclavian artery71 as well as in the following situations: ● ● ● ●
severe or extensive disruption of the vessel wall;72 arteriovenous carotid to jugular fistula;73 aneurysms in Behcet’s disease;74 dissection, which may occasionally follow iatrogenic catheter injury or spontaneous trauma.
Subclavian and vertebral angioplasty and stenting: indications for covered stents Covered stents may be indicated to treat specific lesions of the subclavian and vertebral artery: ●
(c)
aneurysm74 or pseudoaneurysm;75
(d)
(a, b) Left iliac artery complex lesion (stenosis + ulceration); (c) treatment with Jostent covered stent.
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traumatic artery injury;76 spontaneous arterial rupture or dissection.77
Other indications for covered stents Covered stents may be indicated for: ●
●
●
Renal arteries in case of aneurysms not involving a large collateral branch, or pseudoaneurysm or arteriovenous fistula, or in case of arterial rupture during renal angioplasty.78 We have used a Jomed covered stent to treat successfully three cases of rupture of a renal artery avoiding surgery. Digestive visceral arteries with the same indications as for renal arteries.79 Hemodialysis access. Covered stents are effective in controlling angioplasty-induced rupture and sometimes for maintaining patency after restenosis in another stent like a Wallstent, but they do not prevent restenosis for de novo lesion. Aneurysm or pseudoaneurysm of hemodialysis access may also be treated with covered stents.
Techniques and treatment The role of covered stents in the treatment of arterial occlusive diseases is controversial, but the last generation of prostheses seems to give promising results, which are competitive with surgery even for long occlusions of the SFA where a primary patency greater than 80% has been reported in several series at long-term follow-up. Stent grafts have potential advantages. They may help to improve the technical success rate by permanently compressing atheromas, repairing obstructive flaps or dissections, and preventing elastic recoil. In the long term the stent structure may prevent remodeling and the fabric tube may prevent tissue infiltration and intimal hyperplasia.42 The latter hypothesis had been proven in several studies and particularly by Virmani et al.80 who found 75% endothelialization of the flow surface in PTFE nitinol stents after 3 months and almost complete coverage after 6 months. The main disadvantage of these endoprostheses is their thrombogenicity, particularly in the first months. Reocclusions can occur suddenly and mostly during the first month, whereas the mean occlusion time of bare stents is a few months or years. In addition the progression of atheromatous lesions outside the stent increases the possibility of reocclusion. In-stent restenosis and stenosis at the distal end of the stent may occur which can also lead to reocclusion. To expect good results and good patency with these prostheses, it is important to know some important variables to optimize stent graft use. Our technique for graft placement has evolved with practice. The following are important points that we have learned during our initial stent-graft experience. Prior to stent-graft implantation, the target lesion should be predilated with a balloon approximately 1 mm larger than the nominal arterial diameter. In some cases, such as calcified fibrous lesions, it could be useful to debulk the arteries before balloon angioplasty. Atherectomy devices, like the Rotablator
153
may be used. It is important to cover the entire lesion with the stent graft and, if possible, to implant a long stent graft so that both ends are implanted in a relatively normal segment of the artery. Angioplasty should not be performed outside the target lesion to avoid restenosis. Accurate placement of the endoprosthesis can be obtained with some prostheses like Cragg Endopro System I/Passager and the Hemobahn/Viabahn due to the minimal shortening, but can sometimes be difficult with other stents because of significant shortening during expansion. After stent implantation, it is important to dilate the stent graft to its nominal diameter. This helps to fully expand the stent and to remove any wrinkles in the fabric that may have occurred during compression and delivery of the graft. An aggressive balloon dilatation is preferable and requires high pressures to achieve the true diameter of the graft within the vessel. High-pressure angioplasty with shorter (2–4 cm) balloons allows for improved deployment and outcomes over long 10-cm balloons. When long lesions must be treated with several prostheses, grafts should overlap by approximately 10–15 mm to prevent them from separating from each other. Separation may lead to a false aneurysm that could thrombose. Adequate inflow to the proximal graft is of utmost importance. Thus it appears important to place a stent graft only after ensuring that proximal iliac and common femoral disease has been adequately addressed. The patency status of the run-off vessels has been shown to affect both surgical bypass and endovascular procedure patency. Patency of tibial vessel run-off has been shown to be a strong predictor of long-term success in endovascular procedures, with two or three vessel run-off associated with two or three times the patency of patients with zero to one vessel runoff. Fischer et al.42 found significantly lower patency in patients with poor run-off. However for Hartung et al.81 poor run-off does not affect the long-term patency because most of the time outflow lesions are improved during catheter intervention. The fact that reocclusions mostly occur in the first year after stent graft placement correlates with the nearly complete endothelialization after 12 months.80 About 71% of all reocclusions occur in the first year after graft implantations, 21% in the first 30 days, which underscores the importance of consistent antiplatelet therapy. A powerful anti-aggregant protocol associating ticlopidine or clopidogrel and aspirin given several days before the procedure seems to have limited early thromboses. Aspirin plus ticlopidine or clopidogrel for 3–6 months are recommended. The treatment of aneurysms with covered stents in the iliac and femoropopliteal arteries seems rather easy. The results of our series are very favorable at the iliac level but less favorable at the femoropopliteal level, regardless of the graft used. The simplicity of their use should make these covered grafts the treatment of choice for aneurysmal lesions. We wish to insist that even after a stent occlusion at the femoropopliteal level, there have been no serious ischemic complications or limb loss in our experience. The phenomenon of pain and fever encountered after implantation of Cragg Endopro System/Passager is a complication that we still do not fully understand. The phenomenon does not seem to be related to local infection, but it is clearly an inflammatory response to graft implantation. It is likely that the stent graft itself or one of its fabric or metal components may be an inducer of cytokinins from neutrophils.
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We have seen that covered stents may also have good specific indications at other levels: supra-aortic vessels, renal and abdominal arteries, and hemodialysis fistula. More specific devices should be developed to enlarge their indications. The indications for covered stents are still debated; however, the following indications are not debatable: aneurysms; arteriovenous fistulae; arterial traumas; arterial rupture.
● ● ● ●
Covered stents should be available in all catheterization laboratories in order to quickly treat arterial ruptures that may occur during an angioplasty procedure and thus avoid surgical repair. Certain indications are more questionable, such as long occlusions or stenoses, long dissections, and ulcerated lesions. Fischer et al.42 pointed out patients with “optimal” conditions for a good long-term arterial patency: no heavy calcifications, popliteal obstruction or complete SFA occlusion, minimum one vessel run-off, and adequate antiplatelet therapy or anticoagulation.
Results obtained with covered stents seem encouraging and the use of new prostheses, with lower thrombotic risks, should allow the treatment of long lesions with success rates and results that are at least as good as those obtained with surgery, and results obtained with the Hemobahn/Viabahn stent seem promising. A continuous follow up is necessary to prevent reocclusions owing to poor compliance or progression of atheromatous disease. Intensive surveillance using objective testing followed by prompt repeat intervention are mandatory to maintaining patency and quality of life.
Conclusion Covered endoprostheses allow the operator to perform true internal bypass using percutaneous access. The indications for their use should broaden and they could become an alternative to surgery. Improvements should come about, particularly with respect to thrombogenicity and the method of implantation. Randomized studies versus surgery and other types of stents are expected in order to confirm the interest of these new prostheses and their place as compared to non-covered prostheses.
REFERENCES 1. 2. 3. 4. 5.
6. 7. 8. 9. 10. 11. 12. 13.
14. 15.
Johnson KW. Femoral and popliteal arteries: Reanalysis of results of balloon angioplasty. Radiology 1992; 183: 767–71 Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty. Factors influencing long-term success. Circulation 1991; 83 (Suppl I): 170–80 Moore WS. Therapeutic options for femoropopliteal occlusive disease. Circulation 1991; 83(Suppl I): 191–93 Dotter CT. Transluminally placed coil-spring endarterial tube grafts: Long-term patency in canine popliteal artery. Invest Radiol 1969; 4 329–32 Richter GM, Roeren TH, Loeldge G et al. Superior clinical results of iliac stent placement versus percutaneous transluminal angioplasty: Four-year success rates of a randomised study (Abstract). Radiology 1991; 181(Suppl): 161 Henry M, Amor M, Ethevenot G et al. Palmaz-Schatz stent in the treatment of peripheral vascular diseases: Two year follow up. A single center experience (Abstract). Circulation 1992; 86: 4 Henry M, Amor M, Cragg A et al. Occlusive and aneurysmal peripheral arterial disease: assessment of a stent-graft system. Radiology 1996; 201: 717–24 Henry M, Amor M, Henry I et al. Application of a new covered endoprosthesis in the treatment of occlusive and aneurysmal peripheral arterial diseases (in French). Arch Mal Cœur Vaiss 1997; 90: 953–60 Strecker EP, Hagen B, Liermann D et al. Iliac and femoropopliteal vascular occlusive disease treated with flexible tantalum stents. Cardiovasc Intervent Radiol 1993; 16: 158–64 Vorwerk D, Guenther RW, Schurmann K et al. Primary stent placement for chronic iliac artery occlusions: follow-up results in 103 patients. Radiology 1995; 194: 745–9 Vorwerk D, Guenther RW, Schurmann K et al. Aortic and iliac stenoses: follow-up results of stent placement after insufficient balloon angioplasty in 118 cases. Radiology 1996; 198: 45–8 Palmaz JC, Laborde JC, Riviera FJ et al. Stenting of the iliac arteries with the Palmaz stent: experience from a multicenter trial. Cardiovasc Intervent Radiol 1992; 15: 291–7 Henry M, Amor M, Ethevenot G et al. Palmaz stent placement in iliac and femoropopliteal arteries: primary and secondary patency in 310 patients with 2–4 year follow-up. Radiology 1995; 197: 167–74 Henry M, Amor M, Ethevenot G et al. Percutaneous endoluminal treatment of iliac occlusions: long-term follow-up in 105 patients. J Endovasc Surg 1998; 5: 228–35 Bosch JL, Hunink MG. Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease. Radiology 1997; 204: 87–96
16.
17.
18. 19. 20. 21. 22.
23. 24. 25. 26.
27. 28. 29. 30.
Dake MD, Semba CP, Kee ST et al. Early results of Hemobahn for the treatment of peripheral arterial disease. In: Ninth International course book of peripheral vascular intervention. Endovascular Therapy Course, May 5–8 1998, Paris. Toulouse: Europa Organization, 1998; 259–260 Ohki T, Veith FJ. Endovascular grafts for the treatment of arterial lesions. In: Ninth International course book of peripheral vascular intervention. Endovascular Therapy Course, May 5–8 1998, Paris. Toulouse: Europa Organization, 1998; 269–282 Sapoval MR, Long AL, Raynaud AC et al. Femoropopliteal stent placement: long-term results. Radiology 1992; 184: 833–9 Rousseau HP, Raillat CR, Joffre F et al. Treatment of femoropopliteal stenoses by means of self-expandable endoprostheses: midterm results. Radiology 1989; 172: 961–4 Lierman D, Strecker EP, Peters J. The Strecker stent: Indications and results in iliac and femoropopliteal arteries. Cardiovasc Intervent Radiol 1992; 15: 298–305 Damajaru S, Cuasay L, Le D et al. Predictors of primary patency failure in Wallstent self-expanding endovascular prostheses for iliofemoral occlusive disease. Tex Heart Inst J 1997; 24: 173–8 Gray BH, Sullivan TM, Childs MB et al. High incidence of restenosis–reocclusion of stents in the percutaneous treatment of long segment superficial femoral artery disease after suboptimal angioplasty. J Vasc Surg 1997; 25: 74–83 Cikrit DF, Dalsing MC. Lower extremity arterial endovascular stenting. Surg Clin North Am 1998; 78: 617–29 Criado FJ. Endovascular treatment of occlusive lesions in the femoropopliteal territory. In Criado FJ, ed. Endovascular Intervention: Basic Concepts and Techniques. Armonk NY: Futura, 1999: 105–14 CÈjna M, Schoder M, Lammer J. PTA vs stent in femoropopliteal obstruction (in German). Radiologie 1999; 39: 144–50 Vroegindeweij D, Vos LD, Tielbeek AV et al. Balloon angioplasty combined with primary stenting vs balloon angioplasty alone in femoropopliteal obstructions: a comparative randomized study. Cardiovasc Intervent Radiol 1997; 20: 420–5 Zdanowski A, Albrechtsson U, Lundin A. Percutaneous transluminal angioplasty with or without stenting for femoropopliteal occlusions? A randomized controlled study. Int Angiol 1999; 18: 251–55 TASC Document. J Vasc Surg 2000; 31: S1–296 Henry M, Henry I, Klonaris C et al. Clinical experience with the OptiMed sinus stent in the peripheral arteries. J Endovasc Ther 2003; 10: 772–79 Hayerizadeth BF, Zeller T, Krankenberg H et al. Superficial femoral artery stenting using nitinol stents. A German multicenter experience. In the Paris Course on Revascularization, Paris, May 2002
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37. 38. 39. 40.
41. 42.
43. 44. 45. 46. 47. 48. 49. 50. 51.
52.
53. 54.
55. 56.
Mewissen M. Nitinol stents in the femoropopliteal arterial segment. Endovasc Today 2005; 4: 29–34 Scheinert D, Schroder M, Steinkamp H et al. Treatment of iliac artery aneurysms by percutaneous implantation of stent grafts. Circulation 2000; 102: 253–8 Cormier F, Alayoubi A, Laridon D et al. Endovascular treatment of iliac aneurysms with covered stents. A Vasc Surg 2000; 14: 561–566 Scheinert D, Ludwig J, Steinkamp HJ et al. Treatment of catheter induced iliac artery injuries with self-expanding endografts. J Endovasc Thur 2000; 7: 213–20 Ahmadi R, Schillinger M, Maca T et al. Femoropopliteal arteries: immediate and long-term results with a Dacron-covered stent graft. Radiology 2002; 223: 345–50 Dake MD, Semba CP, Kee ST et al. Hemobahn: Results of a multicenter feasibility study. Presented at the International Symposium on Vascular Diagnosis and Intervention. Miami, January 11–15, 1998 Bauermeister G. Endovascular stent grafting in the treatment of superficial femoral artery occlusive disease. J Endovasc Thur 2001; 8: 315–20 Bleyn J. Superficial femoral artery stenting with Hemobahn. International Stenting Congress XV. Scottsdale, February 2002 Saxon AR, Coffman JM, Gooding JM et al. Endograft used in the femoral and popliteal arteries. Tech Vasc Interv Radiol 2004; 7: 6–15 Jahnke T, Andresen R, Muller-Hulsbeck S et al. Hemobahn stentgrafts for treatment of femoropopliteal arterial obstructions: midterm results of a prospective trial. J Vasc Interv Radiol 2003; 14(1): 41–51 Chopra P. Use of the Viabahn stent graft for PVD in the femoropopliteal arterial segment. Endovasc Today 2005; 5(Suppl): 4–8 Fisher M, Schwabe C, Schulte KL. Value of the Hemobahn/Viabahn endoprosthesis in the treatment of long chronic lesions of the superficial femoral artery: 6 years of experience. J Endovascular Ther 2006; 13: 281–90 Steinkamp HJ, Werk M, Seibolds et al. Treatment of arterial traumas by the Wallgraft endoprosthesis. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfahr 2001; 173: 97–102 Kumins NH, Owens EL, Oglevie SB et al. Early experience using the Wallgraft in the management of distal microembolism from common iliac artery pathology. Ann Vasc Surg 2002; 16: 181–6 Rzucidlo EM, Powell RJ, Zwolak RM et al. Early results of stentgrafting to treat diffuse aorto iliac occlusive disease. J Vasc Surg 2003; 37: 1175–80 Cragg AH, Lund G, Rysavy JA et al. Non-surgical placement of arterial endoprostheses: A new technique using nitinol wire. Radiology 1983; 147: 261–83 Cragg AH, De Jong SC, Barnhart WH et al. Nitinol intravascular stent: Results of pre-clinical evaluation. Radiology 1993; 189: 775–8 Cragg AH, Dake MD. Percutaneous femoropopliteal graft placement. J Vasc Intervent Radiol 1993; 4: 445–63 Henry M, Amor M, Ethevenot G, et al. Initial experience with the Cragg Endopro System 1 for intraluminal treatment of peripheral vascular disease. J Endovasc Surg 1994; 1: 31–43 Henry M, Amor M, Cragg A et al. Occlusive and aneurismal peripheral arterial disease: assessment of a stent-graft system. Radiology 1996; 201: 717–24 Dereume JP, Ferreira J El Douaihy M et al. Clinical experience with an integrated self-expandable stented graft (Corvita) for the treatment of various arterial lesions. In Veith FJ, ed. Current Critical Problems in Vascular Surgery, Vol. 6. St. Louis: Quality Medical Publishing, 1995 Scheinert D, Ragg JC, Vogt A et al. The value of a fabric coated selfexpanding stent in iliac arterial occlusions or aneurysms. the primary and long-term results. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfarh 1998; 169: 302–9 Link J, Muller-Hulsbeck S, Hackethal S et al. Midterm follow up after Cragg stent placement in iliac arteries. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfarh 1997; 167: 412–7 Dorffner R, Thurnher S, Puig S et al. Treatment of arterial aneurysms of the pelvic leg vessels using dacron covered nitinol stents. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfarh 1998; 168: 275–80 Formichi M, Raybaud G, Benichou H et al. Rupture of the external iliac artery during balloon angioplasty: endovascular treatment using a covered stent. J. Endovasc Surg 1998; 5: 37–41 Beregi JP, Prat A, Willoteaux S et al. Covered stents in the treatment of peripheral arterial aneurysms: Procedural results and mid-term follow up. Cardiovasc Intervent Radiol 1999; 22: 13–9
57.
58. 59. 60. 61. 62.
63. 64.
65.
66.
67.
68. 69. 70. 71. 72. 73. 74. 75. 76. 77.
78. 79. 80.
81.
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Lammer J, Dzkr MD, Bleyn J et al. Peripheral arterial obstruction, prospective study of treatment with a transluminally placed selfexpanding stent graft. Interventional Trial Study Groups. Radiology 2000; 8: 315–20 White R, Krajcer Z, Johnson M et al. Results of a multicenter trial for the treatment of traumatic vascular injury with a covered stent. J Trauma 2006; 60: 1189–95 Howell M, Kracjer Z, Diethrich EB et al. Wallgraft endoprosthesis for the percutaneous treatment of femoral and popiteal artery aneurysms. J Endovasc Ther 2002; 9: 76–81 Lagana D, Carrafiello G, Mangini M. Endovascular treatment of femoropopliteal aneurysms: a five years experience. Cardiovasc Intervent Radiol 2006; 29: 819–25 Liistro F, Stankovic G, Dimario C et al. Covered stent to exclude intravascular thrombus. J Endovasc Ther 2002; 9: 246–49 Cil BE, Akmangit I, Peynircioglu B et al. Iatrogenic femoral arterioveinous fistula: endovascular treatment with covered stent implantation and 4 year follow-up. Diagn Interv Radiol 2006; 12: 50–2 Rosenthal D, Martin JD, Smeets L et al. Remote superficial artery endarterectomy and distal aSpire stenting: results of a multinational study at three year follow-up. J Cardiovasc Surg 2006; 47: 385–91 Lenti M, Cieri E, Derango P et al. Endovascular treatment of long lesions of superficial femoral artery: results from a multicenter registry of aSpiral covered PTFE stent. Vascular Annual Meeting. Baltimore, May 30–June 4, 2006 Wiesinger B, Beregi JP, Oliva VL et al. PTFE covered self-expanding nitinol stents for the treatment of severe iliac and femoral artery stenoses and occlusions: final results from a prospective study. J Endovasc Ther 2005; 12: 240–46 Inglese L, Calabrese E. Extracranial carotid aneurysm: Interventional treatment. In: Henry M et al, eds. Angioplasty and Stenting of the Carotid and Supra-aortic Trunks. London: Martin Dunitz, 2004 Schillinger M, Dick P, Wiest G et al. Covered versus bare self-expanding stents for endovascular treatment of carotid artery stenosis: a stop randomized trial. J Endovasc Ther 2006; 13: 312–9 Mukherjee D, Roffi M, Yadav JS. Endovascular treatment of carotid artery aneurysms with stent grafts. J Endovasc Cardiol 2002; 14: 269–72 Simionato F, Righi C, Melissano G et al. Stent-graft treatment of a common carotid artery pseudoaneurysm. J Endovasc Ther 2000; 7: 136–40 Scavee V, De Wispelaere JF, Mormont E et al. Pseudoaneurysm of the internal carotid artery: treatment with a covered stent. Cardiovasc Intervent Radiol 2001; 24: 283–5 Battaglial, Barolucci R, Minacci S et al. Stent graft repair the rupture of the subclavian artery secondary to infection of a subclavian carotid bypass graft. Ann Vasc Surg 2001; 15: 474–76 Parodi JC, Ferreira LM, Bergan J. Endovascular stent-graft treatment of traumatic arterial lesions. Ann Vasc Surg 1999; 13(2): 121–9 Geremia G, Bakon M, Brennecke L, et al. Experimental arteriovenous fistulae: treatment with silicone-covered metallic stents. Am J Neurorad 1997; 18(2): 271–7 Eggebrecht H, Bruch C, Haude M et al. Transluminal exclusion of a subclavian artery aneurysm with stent graft implantation. Z Kardiol 2000; 89: 761–5 Hernandez JA, Pershad A, Laufer N et al. Subclavian artery pseudo aneurysm: successful exclusion with a covered self expanding stent. J Invas Cardiol 2002; 14: 278–9 Stecco K, Meier A, Seiver A et al. Endovascular stent graft placement for treatment of traumatic penetrating subclavian artery injury. J Trauma 2000; 48: 948–50 Chiaradio JC, Guzman L, Padilla L et al. Intravascular graft stent treatment of a ruptured fusiform dissecting aneurysm of the intracranial vertebral artery: technical case report. Neurosurgery 2002; 50: 213–16 Schneidereit NP, Lee S, Morris DC et al. Endovascular repair of ruptured renal artery aneurysms. J Endovasc Ther 2003; 10: 71–4 Larson RA, Solomon J, Carpentier JP. Stent graft repair of visceral artery aneurysms. J Vasc Surg 2002; 36: 1260–63 Virmani R, Kolodgie FD, Dake MD et al. Histopathologic evaluation of an expanded polytetrafluoroethylene nitinol stent endoprosthesis in canine ilio femoral arteries. J Vasc Interv Radiol 1999; 10: 445–56 Hartung O, Oterd A, Dubuc M et al. Efficacy of Hemobahn in the treatment of superficial femoral artery lesions in patients with acute or critical ischemia: a comparative study with claudicants. Eur J Vasc Endovasc Surg 2005; 30: 300–6
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Embolic protection devices M Henry, I Henry, A Polydorou, and M Hugel
Introduction Percutaneous endoluminal interventions have revolutionized the contemporary management of atherosclerotic arterial disease in a variety of vascular beds. Beginning with coronary circulation and quickly spreading to the peripheral and cerebral vessels, balloon angioplasty, with and without stenting, has been remarkably successful in treating arterial occlusive disease, and is currently the first treatment to be proposed to patients suffering from atherosclerotic diseases. Over the past few years, the vascular interventionist has managed to treat increasingly complex lesions in high-risk patients using a combination of new techniques and new devices. One of the problems remaining is the occurrence of embolic debris liberated during vascular manipulation. It is now clear that atheroemboli are the rule in any intervention in atherosclerotic disease and seem the root cause of many procedural complications whenever atherosclerotic lesions are treated. Contrary to earlier beliefs that atheroembolization is a “non-issue” during percutaneous catheter intervention, there is now mounting evidence that distal atherosclerotic debris commonly embolize from lesions in many vascular territories during percutaneous intervention. The role of distal embolization was well demonstrated at first in coronary arteries, saphenous vein grafts1,2 and in carotid angioplasty,3–14 but has been increasingly demonstrated in other territories such as the renal15–19 and peripheral arteries.20–23 Embolic protection devices (EPD) have been developed to reduce the complications due to atheroembolism in different territories. These EPDs currently on the market or in clinical experiments can be classified under three main groups, each with its own working principle: ● ● ●
distal occlusion devices; distal filters; proximal occlusion devices.
These three types of EPD can be used in carotid angioplasty stenting (CAS), yet there are some specific cases or locations for which a certain type is more advantageous when compared to the others. This article lists the main EPDs and outlines our device selection criteria. 156
Different types of EPDs Distal occlusion The different devices The concept here is based on blockage of distal blood flow by placement of a sealing balloon downstream from the lesion of interest and inflated at low pressure. This redirects blood flow towards the external carotid artery (ECA) and results in a stagnant column of blood during intervention. The brain is protected from any embolic migration during the occlusion and the potential embolic debris trapped within it can be removed before releasing downstream occlusion. These debris generated by the dilatation and stent placement are then eliminated using one or two techniques such as aspiration or cleaning depending on the device used. Three devices employ this approach. The Percusurge Guardwire (Medtronic Inc., Santa Rosa, CA) (Figure 22.1) ●
This device has been widely used in CAS24–28 and more recently in renal angioplasty stenting.15–17
Description. The Percusurge GuardWire system is constructed as a 0.014-inch hollow nitinol (nickel–titanium alloy) wire with a shapeable floppy distal tip (190 or 300 cm). Proximal to the floppy tip is a compliant elastomeric polyurethane occlusion balloon with a maximal crossing profile of 0.036-inch when deflated. Once the stenotic lesion is crossed with the GuardWire, the occlusion balloon is inflated to a variable size, ranging from 3 to 6 mm in diameter, using the handheld Microseal Adaptor and EZ Flator. The handheld system is then removed from the proximal end of the wire while the occlusion balloon remains inflated. This coaxial exchange set-up allows for over-the-wire (OTW) delivery of angioplasty balloons and stent systems. Any embolic particles released during this portion of the procedure remain in the stagnant pool of blood below the occlusion balloon in the distal internal carotid artery (ICA). This column of blood is aspirated through the large bore lumen of the Export catheter connected to a vacuum syringe. Two or three aspirations can be done through the stent and below the balloon to eliminate the maximum of debris. At the conclusion of the procedure, the occlusion balloon is deflated with the handheld device. Total occlusion times typically range from 5 to 15 minutes.
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Figure 22.1 Rosa, CA).
157
The Percusurge Guardwire (Medtronic Inc., Santa
Published results. The PercuSurge GuardWire currently has US FDA approval for use in the treatment of degenerated saphenous vein grafts following coronary artery bypass surgery. In 1999, we reported our initial experience treating 53 carotid stenoses on 48 patients.24 Immediate technical success rate was 100% with mean balloon occlusion time of 542 ± 243 seconds. One patient developed amaurosis, yielding an overall neurological event rate of 1.8%. More recently, we published our midterm results, 268 procedures performed under cerebral protection on 242 patients.25 Technical success rate was 99.3%, mean occlusion time was 410 ± 220 seconds, five patients suffered neurological events (1.9%) for a combined 30-day stroke, and death rate was 2.3%. With the EPD, visible debris were extracted from all patients. Mean diameter was 250 µm (52–2652 µm), with the mean number per procedure being 74 (7–145). Different types of particles were found: atheromatous plaques, cholesterol crystals, calcified crystals, necrotic cores, fibrin, recent and old thrombi, platelets, macrophage foam cells, lipoid masses, and acellular material. Al-Mubarak and colleagues reported their results following stenting of 37 patients with carotid stenosis. One patient suffered a non-disabling stroke and another died from consequences of hyperperfusion syndrome resulting in a peri-operative combined stroke and death rate of 5.4%. The same group has also reported the occurrence of ipsilateral cerebral embolization via ECA collaterals using the distal balloon protection system.27,28 We have used the Percusurge Guardwire in renal angioplasty stenting in 46 patients. We aspirated visible debris in all patients. The mean particle number was 98.1 ± 60 (13–208) and the mean particle diameter 201 ± 76 m (38–6206). The Tri Active FX (Kensey Nash, Exton, PA) (Figure 22.2) This device has the ability to block, flush, and aspirate the debris generated during CAS. It consists of a 0.14-inch hypotube attached to an inflatable balloon (3–5 mm). This hypotube, like the PercuSurge Guardwire, serves as the interventional guidewire over which balloon and stents can be placed. The current version of the Triactive FX system uses a rapid CO2 exchange system, allowing for quick inflations and deflations. This allows for rapid re-establishment of antegrade flow. After the procedure is completed, the stagnant column of blood is removed using a distal saline infusion catheter (Flushcath) and active extraction. This active flush system allows for more aggressive particle removal from the walls of the vessel, stent struts, and area surrounding the distal balloon before the downstream vasculature is exposed
Figure 22.2
The Tri Active FX (Kensey Nash, Exton, PA).
to restoration of flow. Recently, Franke29 reported a prospective, non-randomized multicenter pilot study. Fifty patients were included with a procedural success of 94 and 2% of neurological complications at hospital discharge (one minor stroke). The Guard Dog (Possis Medical Inc., Minneapolis MN) (Figure 22.3) This was recently approved for work in the periphery and consists of a 0.035-inch guidewire that incorporates a 3–6-mm CO2-filled compliant balloon at the tips. The balloon requires 0.7 atmospheres of pressure to be inflated and is used to seal off the distal vasculature. Removal of debris can then be performed using another device (Possis Angiojet) as desired. The Twin-One (Minvasys, Gennevilliers, France) (Figure 22.4) This new system was recently proposed by Theron and is an evolution of his cerebral protection concept described many years ago.30–32 For this author, as well as for Castriota et al.,33 the only moment of a real risk of embolic complication is the time of post-dilatation of the stent when the plaque is broken. The goal of this new protection device is therefore to focus the problem on the carotid bifurcation and to concentrate, from the beginning to the end of the procedure, all manipulations on a very limited anatomical space (Figure 22.4a). The various phases of the technique are as follows: ●
●
●
●
●
After having positioned the guiding catheter in the common carotid artery, the stenosis is passed with a 0.014inch wire (Figure 22.4b). When a predilatation is necessary, it is performed with a 2-mm balloon without cerebral protection (Figure 22.4c). The stenosis is passed with the stent without cerebral protection. The stent is auto-expandable and its length is 4 cm or more. It can be rapid-exchange or over-the-wire. Its diameter is 7–9 mm according to the artery. It is a delicate moment and the manipulations must be extremely soft (Figure 22.4d). The stent is deployed without cerebral protection. It is positioned covering the origin of the external carotid (Figure 22.4e). The guiding catheter is introduced in the stent (Figure 22.4f).
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(b) Figure 22.3
●
●
(c)
The Guard Dog (Possis Medical Inc., Minneapolis MN).
The delivery system of the stent and the wire are withdrawn (Figure 22.4g). The protection system is introduced (TwinOne) in the stent. It is a device combining a catheter loaded with an occlusion balloon with a rapid exchange angioplasty catheter. Introduced as one tool, it is possible – after peeling away the sheath – to move each catheter separately to ensure the best positioning of each item. There is no wire and the progression is particularly fast and simple when continuous frame stents are used. For the open cell stents, a torquer facilitates the progression of the balloon.
4a
4b
4h
Figure 22.4
4c
4i
●
●
●
●
The system is positioned at the distal extremity of the stent (Figure 22.4h). The occlusion balloon is inflated in the stent and the angioplasty balloon is positioned at the narrowing of the stent (Figure 22.4i). An angiographic series is performed. Contrast should be gently injected to avoid forcing the contrast around the occlusive balloon and give a false impression of incomplete occlusion. The contrast must remain at the origin of the internal carotid if the closure is efficient (Figure 22.4j). The post-stenting dilatation is achieved.
4d
4j
The Twin-One (Minvasys, Gennevilliers, France).
4e
4k
4f
4l
4g
4m
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●
The angioplasty balloon is pulled back and withdrawn from the femoral or radial introducer. The guiding catheter is repositioned when necessary on the site of the angioplasty and blood (one or two 20-cm3 syringes) is aspirated quickly through the guiding catheter (Figure 22.4l). A flush is not performed. The occlusion balloon is deflated and retrieved. The mean occlusion time is less than 5 minutes in most cases and may reach only 3 minutes in some cases. The guiding catheter is positioned, again in the common carotid artery, and control angiographic series are performed (Figure 22.4m).
●
A first series of 45 CAS performed with this technique has been reported without complications and without any cerebral intolerance. This system can be used via a femoral or radial approach. Advantages of distal occlusion These devices have a very low crossing profile (<3 French), high flexibility, good steerability, and radio-opacity. It behaves similarly to the steerable coronary guidewires, allowing the lesion to be crossed easily and decreasing technical failures. Protection balloons are rapidly inflated or deflated. They do not require a very large landing zone (9–10 mm) so there does not need to be much clearance distal to the lesion in order for the device to be placed properly. With these devices, we can aspirate particles of all sizes, and they are not limited in the amount of debris collected because there is no basket to fill up or become clogged. These devices give adequate support as the inflated balloon facilitates stent implantation and balloon dilatation.
●
●
Disadvantages of distal occlusion During CAS under protection with occlusion balloon, the flow is totally interrupted and oriented towards the external carotid artery (ECA). Particles are blocked in the ICA. Nevertheless, some problems remain and embolic events may occur at all steps of the procedure. ●
●
● ●
The balloon protection device offers protection against embolism only after the lesion has been crossed by the wire. Some embolisms may occur during lesion crossing. The occlusion balloon may deflate or may be non-occlusive during the procedure, sometimes only during systole or after dilatation of the stenosis (the increased flow may result in dramatic enlargement of the artery). So, some particles can migrate to the brain. It is very important to verify by contrast injection that the blood flow is totally blocked. In case the flow is not interrupted, it is better to place the balloon high in the ICA at the base of the skull. Some particles could be too large for suction (very rare). Below the inflated balloon there is a shadow zone where some particles may remain blocked and are difficult or impossible to aspirate with the aspiration catheter. These particles may migrate to the brain when the balloon is deflated. This area may be cleaned up by flushing with the aspiration catheter or with the Flushcath. But flushing vigorously at high pressure during the cleaning procedures may lead to reflux to the origin of the common carotid artery (CCA) (this is more critical on the right side since
●
●
159
the length of the CCA is usually shorter) and/or to the right vertebral artery, with the risk of neurological deficit in this territory. The shadow zone may need to be flushed carefully in some circumstances, particularly in patients with a high risk of neurological complications. During ICA balloon occlusion, blood flow is redirected to the ECA with the potential for cerebral and retinal embolization through large collaterals (to the mid-cerebral artery and vertebral artery). Collateral circulation exists between the ECA and ICA through the ophthalmic artery, ascending pharyngeal artery, and internal maxillary artery, and between the ECA and vertebral artery through the occipital and ascending pharyngeal arteries. The risk of brain embolism due to this collateral circulation must be recognized. It is important to obtain a good cerebral angiogram before the procedure to identify this collateral circulation, so that a different protection strategy can be envisaged (e.g. filters or flow reversal). Al-Mubarak et al.28 have described this complication well. Even after meticulous aspiration some debris may remain in the treated area, which may be cleaned up by flushing. However, this technique may lead to ischemic complications in cases of collateral circulation, as previously described. In our series, one neurological complication (amaurosis) appeared after flushing, after which flushing was discontinued. Intolerance to balloon occlusion could sometimes appear quickly after the beginning of the procedure with convulsions, syncope, and neurological deficit. Deflation of the balloon (after quick aspiration) to restore the flow could be necessary and after an adequate recovery time, reblockage of the ICA is often possible and the procedure is completed under protection. In our series, we always observed a complete neurological recovery after balloon deflation in a few minutes. These intolerances are seen in 4 to 8% of the cases (12/268 in our series), and in particular in patients with extensive intracranial disease or absence of adequate collateral flow from other vascular beds. These patients must be detected before choosing the protection device with a good four-vessel angiogram and a good imaging of the intracranial circulation. Some complications have to be mentioned: 䊊 Spasms could appear at the site of the balloon, which are easily treated with antispasmodic drug (3.8% in our series). 䊊 Dissection of the ICA has been rarely reported. We have to mention that angiographic assessment of the lesion is not possible during balloon inflation.
Filters Characteristic of a filter34 Filters offer the opportunity to trap the larger embolic debris while potentially maintaining perfusion of the ICA during angioplasty and stenting procedure. The majority of the distal filters incorporate very similar designs with minor modifications. These devices which are essentially small basket filters mounted on 0.014-inch guidewire with a floppy, shapeable
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distal tip, that can be easily torqued and passed across the stenosis offer the advantage of continued visualization by contrast injection during stent placement as well as the obvious perfusion advantage. The frame of the filter basket is typically constructed of expandable nitinol covered with a porous polyurethane membrane. The pores in the membrane are laser cut and range from 70 to 140 µm. Although the crossing profiles are variable, the designs are such that the filter is collapsed within a delivery sheath, which is retracted and discarded once the filter is in position beyond the stenotic arterial segment in the distal ICA. Two primary configurations of the delivery systems exist, over-the-wire (OTW) and monorail. Once the delivery sheath is retracted, the filter device “springs” open. The guidewire is then used for subsequent balloon angioplasty and stent placement. Ideally, the filter is designed to conform to the vessel lumen upon deployment and capture emboli released during angioplasty and stent placement. At the end of the procedure, a separate recovery or retrieval catheter is passed over the wire and used to envelop or capture the filter system (including trapped debris). The entire device is then removed. Different filters Several filters are proposed, some are available on the market and FDA approved, while others are still being tested. The AccuNet system (Guidant, Indianapolis, IN) (Figure 22.5) This was the first to gain FDA approval based on the results of the ARCHER trial.35 This filter system comprised a 0.014-inch guidewire with a 3.5-cm-long shapeable floppy tip. Integrated on the guidewire is the deployable filtration element comprising a four-wire nitinol basket. A thin, porous, polyurethane membrane with 120-µm pore size is fixed to the basket to capture emboli. The crossing profile ranges from 3.5 to 3.7. The size of the basket ranges from 4.5 mm to 7.5 mm in diameter (adapting to vessel lumen of 3.5–7.0 mm). The retrieval catheter (5.5-French) has a shapeable end, allowing the operator to deflect the tip away from stent struts during the recapturing step (working length 141 cm). This device is 6-French compatible.
Figure 22.6
The Angioguard XP (Cordis, Warren, NJ).
The deployable filtration element is made out of an eight-wire nitinol basket attached to a 0.014-inch guidewire with a 3.5-cm-long shapeable platinum coil floppy tip. The basket has six radio-opaque markers for better visualization, one distal and one proximal to the basket for checking its position and four markers on the struts for checking whether the basket is open or closed. The filter membrane has a pore size of 100 µm. The crossing profile ranges from 3.2 to 3.9 French depending on the filter sizes. The filter diameter ranges from 4 to 8 mm. The crossing profile of the retrieval catheter is 5.1 French. This device is 7-French guide compatible with a landing zone of 18 mm. It is important to stress that the filter cannot be completely withdrawn into the pod.
The Angioguard XP (Cordis, Warren, NJ) (Figure 22.6) This filter is currently available in an OTW and monorail configuration. This device was used for the Sapphire trial.36,37
The Filter Wire EZ (Boston Scientific, Natik, MA) (Figure 22.7) This has FDA approval for coronary angioplasty. A unique feature of this filter is the suspended loop filter (“fish mouth”) frame. The nitinol ring supports the polyurethane membrane “butterfly net,” which theoretically provides for complete circumferential contact with the arterial wall. The ring expands to accommodate a vessel diameter range of 3.5–5.5 mm. To improve the alignment with the vessel wall, the wire is kept in the center of the filter by a horizontal strut. A Spinner tube underlying filter assembly allows the wire to rotate independently from the delivery sheath to enhance the system’s steerability.
Figure 22.5
Figure 22.7
The AccuNet system (Guidant, Indianapolis, IN).
The Filter Wire EZ (Boston Scientific, Natik, MA).
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The pore size of the membrane is 110 µm, and the 150-cm delivery catheter has a crossing profile of 3.2 French. This device is 6-French-guide compatible with a landing zone of 18 mm. The retrieval catheter has a crossing profile of 4.3 French. This filter wire has been validated in the Beach study.38 The Emboshield (Abbott) (Figure 22.8) It is a device featuring a bare wire configuration. This allows crossing of the lesion with an independent filter delivery wire (0.014-inch) available in two lengths (190 and 315 cm). The filter is then separately delivered and deployed on the wire. This design allows the filter element to “float” freely on the wire below a distal stop. Guidewire movement is possible while the filter is in place. The crossing profile ranges from 3.7 to 3.9 French. The pore size of the membrane is 140 µm. This device is 6-French compatible. The filter diameter ranges from 3 to 6 mm and the retrieval catheter has a 6-French crossing profile. A new device was recently proposed, the Emboshield Pro, with a crossing profile ranging from 2.8 to 3.2 French, 19 and 22.5 mm landing zone (for 2.5 to 4.8 mm and 4 to 7 mm sizes respectively). The pore size is 120 µm. The effectiveness of the Emboshield filter has been validated in the Security study.39 The Spider RX (EV3, Plymouth, MN) (Figure 22.9) This filter permits the use of a guidewire of choice for crossing the target lesion. In a second step, the delivery catheter with a crossing profile of 2.9 or 3.2 French is introduced over the wire and placed distal to the lesion in the ICA. A stylet is used to create a transition from the delivery catheter to the primary guidewire. After removal of the central guidewire, the filter, which is mounted on a 0.014-inch guidewire (175 or 320 cm) is advanced through the delivery catheter and is strictly maintained in the same landing position distal to the lesion. After placement of the filter, the delivery catheter is withdrawn. In contrast to the systems previously mentioned, the basket of this device consists of a nitinol wire braid filter with “pores” ranging from 167 to 209 µm. The diameter of the basket ranges from 3 to 7 mm. This device is 6-French compatible and the filter heparin coated. A clasp at the entrance of the frame may ensure a better vessel wall apposition of the “fish mouth” opening filter with a radio-opaque gold ring. The retrieval catheter has a diameter of 4.2 French for filters of 3, 4, and 5 mm; and 4.9 F for the
Figure 22.8
The Emboshield (Abbott).
Figure 22.9
The Spider RX (EV3, Plymouth, MN).
6 and 7 mm filters. If necessary, the snap wire feature permits conversion of the 320-cm-long wire to a 17-cm rapid exchange length. This device has been validated in the Protect trial.40 The Interceptor Plus (Medtronic Inc., Santa Rosa, CA) (Figure 22.10) This filter consists of a braided nitinol basket attached to a 0.014inch steerable guide wire. Four pores are located at the entrance of the basket. Minimal pore size is 100 µm. The filter features a simplified, intuitive delivery system that does not require the use of a sheath for deployment. The filter system is offered in sizes to fit vessel diameters from 4.25 to 6.25 mm with a lesion-crossing profile of only 0.036 inches. This filter features excellent conformity to vessel walls. It is 6-French guide compatible. The Rubicon Filter (Rubicon, Salt Lake City, UT) (Figure 22.11) This device has a unique design and is the only filter without a dedicated delivery catheter. It has a very low profile of 2.4 to 2.7F. It is mounted on a 0.014-inch guidewire and deployed via a coaxial actuating wire at the proximal end of the guidewire. The pores have a size of 100 µm. The filter basket is supported by floating nitinol struts for optimal apposition. It is 6-French guide compatible. The Rubicon filter is available in sizes from 4 to 6 mm. The long toper design of the filter increases the volume to capture debris. The large bore catheter retrieval system actuator (6 French) shows the exact status of the filter as it is being captured for removal, minimizing the risk of debris loss. To reduce snagging of the stent, it has a dilator-style inner sheath, which telescopes over the filter basket to minimize movement of the filter during its retrieval. Advantages of the filters The major advantage is the preservation of the flow, allowing their use in patients with poor collateral circulation, total contralateral ICA occlusion, severe contralateral ICA stenosis, intracranial stenosis, or a poor circle of Willis. The ability to perform angiography during the procedure allows accurate placement of the stent. The new generation of filters has a very low profile that allows crossing the majority of the lesions without predilatation. Two filters, Emboshield and Spider, have an independent guidewire allowing crossing of the lesion with the guidewire at first, which is an advantage with tight lesions and tortuous vessels.
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Figure 22.10
The Interceptor Plus (Medtronic Inc., Santa Rosa, CA).
Disadvantages and limitations of filters Some filters have a large crossing profile, leading to difficulties in crossing tight, tortuous lesions. Some published series reported that it was impossible to cross the lesion with the filters in 2–12% of cases.41,42 Predilatation of the lesion with a coronary balloon can facilitate the placement of the filter but with a risk of brain embolism. A “buddy wire” can straighten the artery and facilitate the crossing of the lesion in tortuous arteries. With the new generation of filters, failure to cross the lesion is rare, and in our experience, less than 1% of the cases (1 failure in 305 procedures). A filter engulfment with consequent distal slow flow may occur. A filter may also plug up with a static column of blood with suspended particles that will embolize if we retrieve the filter. In these cases before retrieving the filter we have to aspirate very carefully the blood below the filter and to clean the dilated area with either an aspiration catheter or the guiding catheter we advance inside the stent. The filter may thrombose: effective anticoagulation with activated coagulation time (ACT) > 250 to 300 seconds is recommended. The filter may cause spasm or dissection of
Figure 22.11
The Rubicon Filter (Rubicon, Salt Lake City, UT).
the distal ICA, which could possibly lead to restenosis. Closure and retrieval of filters can dislodge their content collected during the procedure. Some difficulties in retrieving the filters have been reported, for example in 8.4% of cases.4 We may have difficulties getting the retrieval catheter in and the filter could get caught on the struts of the stents during retrieval. These problems occur more frequently with open cell stent design. As with occlusion balloons, filters cannot prevent all neurological embolic events. The filter can protect the brain only after the filter has crossed the lesion and has been deployed. This maneuvre and the initial positioning of the guide catheter in the CCA can release embolic material. Some emboli may occur during the procedure if the filter is not well deployed or if the diameter of the filter is not sufficient during systole and diastole, and after predilatation of the lesion, which could increase the flow and the diameter of the artery. It is important to deploy the filter in a straight part of the vessel to have a good wall apposition of the filter to avoid embolism. Inadequate filter vessel apposition is not always angiographically detectable and complete protection from embolization may not be possible in oval or eccentric vessels. A filter can generally retrieve debris > 100 µm, most of the devices have a pore size of 100 µm or larger, which can allow smaller particles to go to the brain with the possibility of micro infarcts. Only a small number of particles are removed43 and macroscopically visible particles are retrieved in only 35.0–83.7% of the filters.42,44 Filters reduce the risk of brain embolism as demonstrated by TCD or diffusion weighted magnetic resonance imaging (DW-MRI) but do not prevent all emboli from reaching the cerebral circulation. Asymptomatic or “silent” ischemic lesions detected with DW-MRI have been reported more frequently after CAS than after endarterectomy.45–47 Recently, Flach et al.48 published
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Embolic protection devices a 9% frequency of new hyperintense lesions in surgically treated patients and a 43% frequency in the CAS group. Although the clinical importance of silent lesions is yet unclear, Vermeer et al. recently found that silent brain infarcts are associated with cognitive dysfunction in the general population. An increased frequency of dementia, and neuropsychomatic changes could also be a consequence of these lesions.49–52 With all protection devices, all stents we may observe periprocedural or delayed embolic events. Most of the time, these complications are due to plaque protrusion through the stent struts and embolization of plaque material. To avoid these problems, we can aspirate this debris inside the stent and below the filter with an aspiration catheter or the guiding catheter. It is better to aspirate and clean the dilated area for at least all symptomatic lesions and all echolucent plaques. Other issues have been demonstrated with current EPD. Recently, Vos et al.53 published interesting data showing that the role of some filters is unclear and associated with potential problems. By means of TCD, he detected a higher number of microemboli during filter-protected CAS but the number of particulate macroemboli was higher in the unprotected group. Distal thrombus formation occurred only in patients with filter protection. MacDonald et al.54 published similar data with the EmboShield filter. New generation of filters (Figure 22.12) To overcome some problems encountered with current filters, a new filter was recently proposed and is in experiment. This filter, the FiberNet (Lumen Biomedical Inc., Plymouth, MN) consists primarily of polyester fibers located coaxially around the distal tip of a guidewire assembly. This filter is soft, conformable and when activated, expands radially to fill the vessel, providing excellent apposition to the vessel wall. Contained and captured emboli are recovered/removed both by aspiration through the retrieval catheter and also by retention within the filter fibers when the filter is closed and retracted into the retrieval catheter. Aspiration is achieved through the retrieval catheter using vacuum syringes to provide suction. This filter enables capture of emboli as small as 40 µm without compromising the flow through the filter, and can be delivered as a standard coronary guidewire.
Figure 22.12
New generation of filters.
163
The possibility of suction through the retrieval catheter during device removal is probably one of the major improvements with this device, allowing cleaning of the dilated area and of the inner part of the stent. This technique allows aspiration of the debris, which can protrude through the struts of the stent after stent placement and dilatation and which could be one of the causes of the delayed embolic events. We performed the first human study in carotid and renal arteries with this new protection device. Fifty-three patients (49 carotid and 4 renal) were treated. Visible debris comprising atheroma was detected in each case. It is important to state that nearly 30% of the debris was aspirated from inside the stent, which could potentially reduce delayed embolic events. We compared this device with other filters. With the FiberNet, we removed five times more debris. Thirty-four patients underwent CT or MRI before and at 30-day post-procedure. No changes were noted in the follow-up tests when compared to the baseline.55
Flow reversal technique Parodi antiembolization catheter (Gore and Associates Inc., Flagstaff, AZ) (Figure 22.13) Description of the device56,57 The Parodi antiembolization catheter (PAEC) is a guiding sheath with an occlusion balloon attached at the distal end of the catheter. The main lumen has an inner diameter of 7.3 French that allows the passage of balloons and stents. Once the PAEC has been inserted in the CCA, a Parodi external balloon (PEB) is inserted and inflated in the ECA. Then, the occlusion balloon attached on the outer surface of the PAEC is then connected to a sheath that is percutaneously inserted into the femoral vein to create a temporary arteriovenous shunt. This shunt, along with the PEB, creates reversal of flow in the ICA. The deployment of the PEB is required to prevent retrograde flow from the ECA, which may cause prograde flow in the ICA. Particles of all sizes flow through the PAEC and are captured by a filter placed at the arteriovenous connection. The new device is 9-French-sheath compatible. The working length of the Gore balloon sheath (0.035-inch-guidewire compatible) is 91 cm.
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GORE Balloon Wire GORE Balloon Sheath
Figure 22.13
Parodi antiembolization catheter (Gore and Associates Inc., Flagstaff, AZ).
Advantages ●
●
●
● ●
● ●
●
Complete protection can be achieved before manipulating the lesion. The risk of complications is reduced by never crossing the lesion unprotected. The lesion can be crossed with any guidewire of our choice under protection, avoiding brain embolism during this step. Embolization to the brain is not possible during reversed flow. Particles of all sizes can be captured. Tight, tortuous lesions, and stenosis with limited landing zone can be treated with any wires. The PAEC provides a treatment option for patients whose anatomy is unsuitable for the use of a distal filter. No damage is caused to the fragile intima of the distal ICA. The technique avoids flushing through the ECA with the risk of brain embolization in the case of collateral circulation between the ECA and ICA or vertebral artery. Complications associated with filter retrieval and filter related vasospasm in the ICA are eliminated.
Disadvantages and limitations ●
●
●
●
The interruption of flow during protection may not be tolerated in some patients (5%), as with distal occlusion balloon. The new generation of PAEC need a 9-French introducer. With the previous device a larger puncture side-hole was needed (11-French). The technique has the potential to cause spasm or dissection in the ECA or CCA. As with other protection devices, a brain embolism may occur during placement of the catheter in the CCA. This step cannot be protected.
Seatbelt and airbag technique This technique was described by Parodi et al.58 in two patients. They used a flow-reversal system (Parodi anti-embolism system), which was first placed with a 260-cm exchange wire in the CCA 3 cm below the carotid bifurcation. Flow reversal was achieved by inflating the balloon in the ECA and CCA. Via an external connector a guidewire and an E Trap Filter (MSD, Pittsburgh, PA) were delivered to the distal ICA with active suction from a syringe on the PAES catheter. Once the filter was above the stenosis, the flow reversal was discontinued and the procedure proceeded under cerebral protection with the filter. The combination of these existing cerebral protection devices could, at least in theory, achieve what neither of them could independently. Moreover, it may be feasible to avoid some drawbacks of the various systems. Because distal protection devices must cross the lesion, which may account for about 12% of all emboli generated during a procedure,12 Parodi et al. sought to provide protection during this step by initiating flow reversal through the ICA to prevent distal embolization. No cerebral embolization has been demonstrated on TCD monitoring during these procedures. This technique could be indicated for carotid stenoses that demonstrate a high potential for embolization or in patients with an aberrant or a non-functioning circle of Willis or contralateral ICA occlusion, which may be intolerant to balloon occlusion.
MOMA Device MOMA Device is a “proximal flow blockage” cerebral protection device. Cerebral protection occurs by interruption of antegrade blood flow from the common carotid artery and
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Embolic protection devices retrograde blood flow through the ipsilateral ECA. This is achieved by a low-pressure balloon occlusion of the two vessels by means of a single device integrating the two occlusive balloons and a working channel for the delivery of interventional devices to the target lesion. One balloon occludes the ECA and the second balloon the CCA, so that passing the target lesion with the embolic protection system before starting the procedure can be avoided. Debris are thus stopped at the carotid bifurcation and prevented from dislodging to the brain. Removal of debris is performed by spot (active) syringe aspiration which can be performed any time during the intervention through the working channel of the device.
Choice of the protection device Device selection for carotid angioplasty and stenting Table 22.1 summarizes advantages and disadvantages of the different protection devices. We know that all CAS should be performed under cerebral protection. The choice of the protection device depends on the interventionist, the lesion, the anatomy of the different vessels (aortic arch, carotid arteries, etc.), the intracranial circulation and the collateral circulation. Before deciding which protection device to use it is indispensable to assess carefully the anatomy at intracerebral level, the access site and the lesion itself. Intracerebral circulation To decide on which protection device to use, a good angiography of the intracranial circulation is mandatory with fourvessel angiography and a good assessment of the collateral circulation. Without sufficient collateralization, only distal filters can be used. Distal and proximal occlusion systems should not be used because cerebral perfusion will be inadequate during the procedure and intolerance episodes could happen. It could be the case in patients with severe contralateral carotid stenosis or occlusion. Distal occlusion is also contraindicated in patients with anastomosis between ICA, ECA, and vertebral territories. With sufficient collateralization distal occlusion can be used. Access site assessment Patients presenting with tortuous vessels, or type III aortic arch, require low-profile flexible protection systems, as it is
Table 22.1
165
difficult to reach the lesion site. Low-profile, steerable, flexible devices should be used, like the distal occlusion system, and some filters we have to choose carefully. But proximal occlusion systems seem inadequate due to their larger profile. Lesion site assessment ●
●
●
●
Severe stenoses and irregular lesions can be treated under any kind of protection but we have to choose very lowprofile, steerable devices. With a very tortuous ICA, a severely angulated ICA or when there is little space between the lesion site and the cerebrum, with lake of landing zone for the device, it is better to use proximal occlusion devices. If thrombotic lesion or thrombi are suspected, proximal occlusion devices are the only possibility of avoiding a brain embolism. Some authors advise proximal occlusion system to treat plaques with very high risk of brain embolism (soft, dishomogenous plaques, plaques with GSM < 25). However, very low-profile, flexible, soft-tipped filters or distal occlusion systems can be used and the generation of protection devices like FiberNet seems also very promising for these lesions with a greater tendency to embolize.
Device selection for renal angioplasty and stenting We have the choice between distal occlusion and filters. The limitation with filters as in CAS is the pore size with the possibility of small emboli going to the kidney. The landing zone is also a concern. For these reasons, the new three-dimensional filter FiberNet seems a good indication. Device selection for peripheral angioplasty Any filters of distal occlusion systems can be used in peripheral arteries. Device selection for vertebral artery If a protection is indicated for a vertebral angioplasty stenting, low-profile, flexible filters or occlusion balloons can be used and placed in the vertebral artery. Another possibility is to place a Parodi device at the ostium of the subclavian artery to block the flow and create a reversal flow inside the vertebral artery.
Advantages and disadvantages of the different concepts
Embolization Flow ICA Ability to during decrease protection perform guidewire/catheter from angiography lesion crossing emboli during protection Filters +++ + + Occlusion ++ ++ ++ Flow reversal –– +++ +++ ECA: external carotid artery; ICA: internal carotid artery
Embolization through ECA
Potential Tolerance Easy to spasm/damage use to ICA
+++ –– +++
–– +++ ––
+++ +++ ––
+++ + +
+++ ++ +
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Conclusion Several protection devices have been developed and are currently available on the market. All are not equivalent and have some limitations and drawbacks. When performing CAS it is mandatory to have a good knowledge of the three kinds
of protection device to choose the best system suited to the patient, the lesion, and the anatomy to avoid some problems, which can lead to dramatic neurological complications. New generations of protection devices are proposed. They should widen the indications of CAS and other peripheral angioplasties and limit their potential complications.
REFERENCES 1. 2.
3. 4. 5. 6. 7. 8. 9. 10. 11.
12. 13. 14. 15. 16. 17. 18. 19. 20. 21.
22.
Piana RN, Paik GY, Moscucci M et al. Incidence and treatment of “no-reflow” after percutaneous coronary intervention. Circulation 1994; 89: 2514–18 Grube E, Gerckens U, Yeung AC et al. Prevention of distal embolization during coronary angioplasty in saphenous vein grafts and native vessels using porous filter protection. Circulation 2001; 104: 2436–41 Bicknell CD, Cowling MG, Clark MW et al. Carotid angioplasty in a pulsatile flow model: factors affecting embolic potential. Eur J Vasc Endovasc Surg 2003; 26: 22–31 Bicknell CD, Cheshire NJ. The relationship between carotid atherosclerotic plaque morphology and the embolic risk during endovascular therapy. Eur J Vasc Endovasc Surg 2003; 26: 17–21 Roubin GS. Carotid Angioplasty and Stenting under Cerebral Protection: The Standard of Care. International Congress XV. Scottsdale, February 11–14, 2002 Ohki T, Veith FJ. Carotid stenting with and without protection device: Should protection be useful in all patients? Semin Vasc Surg 2000; 13(2): 144–52 Ohki T, Roubin GS, Veith FJ, Iyer SS, Brady E. Efficacy of a Filter Device in the Prevention of Embolic Events during Carotid Angioplasty and Stenting. An ex-vivo Analysis. J Vasc Surg 1999; 30(6): 1034–44 Wholey MH, Al-Mubarak N, Wholey MH. Updated review of the global carotid artery stent registry. Cathet Cardiovasc Interv 2003; 60: 259–66 Reimers B, Schlueter M, Castriota F. Routine use of cerebral protection during carotid artery stenting: results of a multicenter registry of 753 patients. Am J Med 2004; 116: 217–22 Kastrup A, Groschel K, Frapf H et al. Early outcome of carotid and stenting with and without cerebral protection devices: a systematic review of the literature. Stroke 2003; 34(3): 813–19 Henry M, Polydorou A, Henry I, et al. Carotid angioplasty under protection with the Percusurge Guardwire device. In: Henry M and Ohki T, eds. Angioplasty and Stenting of the Carotid and Supraaortic Trunks. London: Taylor and Francis, 2004; 485–96 Ohki T, Veith FJ. Embolization during carotid stenting: experimental models and results. Carotid Intervent 2000; 3: 66–74 Ohki T, Marin ML, Lyon RT et al. Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potentials. J Vasc Surg 1998; 27: 463–71 Henry M, Polydorou A, Henry I et al. Carotid angioplasty and stenting under protection. Techniques, results and limitations. J Cardiovasc Surg 2006; 47: 519–46 Henry M, Klonaris C, Henry I. Renal stenting with the Percusurge Guardwire device: a pilot study. J Endovasc Ther 2001; 8: 227–37 Henry M, Henry I, Klonaris C et al. Renal angioplasty and stenting under protection. The way for the future? Catheter Cardiovasc Interv 2003; 60: 299–312 Henry M, Henry I, Polydorou A et al. Renal angioplasty and stenting: long-term results and the potential role of protection devices. Expert Review Cardiovasc Ther 2005; 3: 321–34 Holden A, Hill A. Renal angioplasty and stenting with distal protection of the main renal artery in ischemic nephropathy: early experience. J Vasc Surg 2003; 38: 962–68 Holden A, Hill A, Jaff MR et al. Renal artery stent revascularization with embolic protection in patients with ischemic nephropathy. Kidney Int 2006; 70: 948–55 Freeman HJ, Rundback JH. Embolic protection in femoropopliteal artery intervention. Endovasc Today 2006; 5: 65-70 Wholey MH, Toursarkissian B, Postoak D et al. Early experience in the application of distal protection devices in treatment of peripheral vascular disease of the lower extremities. Catheter Cardiovasc Interv 2005; 64: 227–35 Siablis D, Karnabatidis D, Katsanos K et al. Outflow protection filters during percutaneous recanalization of lower extremities arterial occlusions: a pilot study. Eur J Radiol 2005; 55: 243–49
23.
24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
34. 35.
36. 37. 38. 39.
40. 41.
42. 43.
Konig C, Pusich B, Tepe G et al. Frequent embolization in peripheral angioplasty: detection with an embolism protection device (Angioguard) and electron microscopy. Cardiovasc Intervent Radiol 2003; 26: 334–9 Henry M, Amor M, Henry I et al. Carotid stenting with cerebral protection: First clinical experience using the Percusurge Guardwire system. J Endovasc Surg 1999; 6: 321–31 Henry M, Henry I, Klonaris C et al. Benefits of cerebral protection during carotid stenting with the Percusurge Guardwire system: Mid-term results. J Endovasc Ther 2002; 9: 1–13 Mehran R, Roubin GS, New G et al. Neurologic events after carotid stenting with distal protection using an occlusion balloon: final results from the café USA trial. AHA Meeting, Anaheim, November 12, 2001 Al Mubarak N, Roubin GS, Vitek JJ et al. Effect of the distal-balloon protection system on microembolization during carotid stenting. Circulation 2001; 104: 1999–2002 Al Mubarak N, Vitek JJ, Iyer S et al. Embolization via collateral circulation during carotid stenting with the distal balloon protection system. J Endovasc Ther 2001; 8: 354–7 Franke J, Bauer C, Ghamzemzadeh A5L5 et al. Distal occlusion with flushing and aspiration: the Kensey Nash device. Presented at the ICCA 06, Frankfurt, November 23–25, 2006 Theron J, Cosgrove R, Melançon D, Ethier R. Embolization with temporary balloon occlusion of the internal carotid artery and vertebral arteries, Neuroradiology 1986; 28: 246–53 Theron J, Raymond J, Casasco A et al. Percutaneous angioplasty of atherosclerotic and post-surgical stenosis of carotid arteries. ANJR 1987; 8: 495–500 Theron J, Courtheoux P, Alachkar F, Maiza D. New triple coaxial catheter system for carotid angioplasty with cerebral protection. ANJR 1990; 11: 869–74 Castriota F, Manetti R, Liso A et al. Cerebral protection: can only the poststenting dilatation phase be protected? In: Henry, Ohki, Polydorou, Strigaris, Kiskinis, eds. Angioplasty and Stenting of the Carotid and Supra-aortic Trunks. Informa, London, 2004, 381–90 Eskandari MK. Design and development of mechanical embolic protection devices. Expert Rev Med Devices 2006; 3: 387–93 Wholey MH. The ARCHER trial: prospective clinical trial for carotid stenting in high surgical risk patients, preliminary thirtyday results. Presented at the 52nd Annual Meeting of the American College of Cardiology, Chicago, IL, March 30, 2003 Yadav JS, Wholey MH, Kuntz RE et al. Protected carotid artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004; 351: 1493–501 Ouriel K. SAPPHIRE study. Vasc News 2004; 22: 1–2 White CJ, Iyer SS, Hopkins LN et al. Carotid stenting with distal protection in high surgical risk patients: the Beach Trial 30 day results. Catheter Cardiovasc Interv 2006; 67: 503–12 Whitlow PL. SECURITY: Multicenter registry in high-risk symptomatic and asymptomatic carotid disease with the Abbott Xact stent and MedNova filter. Presented at Transcatheter Cardiovascular Therapeutics (TCT), Washington, DC, September 15–19, 2003 Cremonesi A. The Spider Embolic protection device performance evaluation in the carotid artery during percutaneous transluminal angioplasty and/or stenting. J Invasive Cardiol 2005; 17: 463–67 Castriota F, Cremonesi A, Manetti R. Carotid angioplasty and stenting with and without cerebral protection: single center experience in 275 consecutive patients. International Congress XV, Scottsdale, February 11–14, 2002 Reimers B, Corvaja N, Moshiri S et al. Cerebral protection with filter devices during carotid artery stenting. Circulation 2001; 104: 12–15 Coggia M, Goeau-Brissonnière O, Duval JL et al. Embolic risk of the different stages of carotid bifurcation balloon angioplasty: an experimental study. J Vasc Surg 2000; 31: 550–7
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Embolic protection devices 44. 45. 46. 47. 48. 49. 50. 51. 52.
Angelini A, Reimers B, Dellabarbara M. Embolized debris during carotid artery stenting with cerebral protection device: a histopathologic survey. AHA Meeting, Anaheim, 13 November 2001 Jaeger H, Mathias K, Drescher R et al. Clinical results of cerebral protection with a filter device during stent implantation of the carotid artery. Cardiovasc Interv Radiol 2001; 24: 249–56 Barth A, Remonda L, Lovblad KO et al. Silent cerebral ischemia detected by diffusion-weighted MRI after carotid endarterectomy. Stroke 2000; 31: 1824–8 Tomczak R, Wunderlich A, Liewald F et al. Diffusion weighted MRI: detection of cerebral ischemia before and after carotid thromboendarterectomy. J Comput Assist Tomogr 2001; 25: 247–50 Flach H, Ouhlous M, Hendricks J et al. Cerebral ischemia after carotid intervention. J Endovasc Ther 2004; 11: 251–57 Vermeer SE, Prins ND, Den Heijer T et al. Silent brain infarcts and the risk of dementia and cognitive decline. N Engl J Med 2003; 348: 1215–22 Heyer EJ, Adamas DC, Somon RA et al. Neuropsychometric changes in patients after carotid endarterectomy. Stroke 1998; 29: 1110–15 Heyer EJ, Sharma R, Rampersad A et al. A controlled prospective study of neuropsychological dysfunction following carotid endarterectomy. Arch Neurol 2002; 59: 217–22 Vanninen E, Vanninen R, Aikia M et al. Frequency of carotid endarterectomy related subclinical cerebral complications. Cerebrovasc Dis 1996; 6: 272–80
53.
54.
55. 56. 57.
58.
167
Vos AJ, Vandenberg JC, Ernst SM. Carotid angioplasty and stent placement: comparison of transcranial Doppler vs data and clinical outcome with and without filtering cerebral protection devices in 509 patients. Radiology 2005; 234: 493–9 MacDonald S, Cleveland TJ, Evans D, Griffiths PD, Gaines PA. A comparison of the high-intensity signal rate using transcranial Doppler during unprotected and protected carotid stenting (Neuroshield) with a randomised controlled trial. Presented at the Annual Meeting of the Cardiovascular and Interventional Radiology Society of Europe, Antalya, Turkey, September 20, 2003 Henry M, Polydorou A, Henry I et al. New distal embolic protection device. The FiberNet 3-dimensional filter. First carotid human study. Cath Cardiovasc. Intervent (in press) Parodi JJC, Lamura R, Ferreira LM et al. Initial evaluation of carotid angioplasty and stenting with three different cerebral protection devices. J Vasc Surg 2000; 32: 1127–36 Parodi JC, Bates MC, Schonholz C. Parodi embolization system: description and first results. In: Henry M, T. Ohki, eds. Angioplasty and Stenting of the Carotid and Supra-aortic Trunks. Taylor & Francis, London, 2004; 523–30 Parodi JC, Schonholz C, Ferreira MC et al. Seat belt and airbag technique for cerebral protection during carotid stenting. J Endovasc Ther 2002; 9: 20–4
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Vascular closure devices ZG Turi
Introduction After Seldinger contributed a method for percutaneous puncture of the femoral artery a half century ago,1 relatively little changed in vascular access and closure until the late 1970s. Standard percutaneous femoral access technique required multiple passages through the skin and thigh muscles by catheters over exchange wires, a method that occasionally resulted in loss of access, accumulation of debris in the tips of catheters, and a variety of secondary complications. Most importantly, repeated passage of catheters through the femoral puncture site resulted in fraying of the arteriotomy edge. The introduction of vascular sheaths was a significant step forward,2 allowing simultaneous pressure monitoring through a Y connector (or later a sidearm), and resulted in smoother arteriotomy edges because it eliminated the need for multiple catheter introductions though the vessel wall. Closure was entirely by external compression (Figure 23.1), largely manual but in some laboratories with mechanical compression devices, several of which remain in use (Figure 23.2). The state of the art for vascular closure remained largely unchanged for four decades. Patients undergoing percutaneous access, whether from the arm or leg, typically had compression applied, while open arteriotomy was accompanied by suture closure. The paradigm shifted in the early 1990s with the introduction of VasoSeal (Datascope, Montvale, NJ), a collagen plug device, which was the first of the vascular closure devices (VCDs) to be commercialized. Vascular closure is now a 500-million-dollar medical device market, accounting for some 30–40% of femoral catheterizations in the US, but < 10% of vascular closure in the rest of the world. The evidence base to justify routine use of VCDs is extremely limited, and adoption has been largely by physician and patient preference. Nevertheless, these devices are an important consideration in the everexpanding armamentarium of endovascular technologies.
Vascular access The sine qua non of vascular closure is good vascular access. Although not the primary focus of this chapter, good vascular access technique can prevent most of the vascular complications associated with femoral procedures and with VCDs. Four techniques that may reduce complications, facilitate access, and prevent VCD complications are largely 168
ignored by much of the vascular intervention community. These include: ●
●
adjunctive use of fluoroscopy and/or ultrasound for access to the common femoral artery, with confirmation that needle position is below the center of the femoral head and over the medial half of the bone prior to arterial entry (Figure 23.3); arterial puncture in the “safe zone” for vascular access (Figure 23.4);
Figure 23.1 The most common closure technique, manual compression, is utilized in 70% of cases in the US and well over 90% in the rest of the world, despite the need for prolonged bed rest, greater patient discomfort and delay in ambulation and discharge. Besides cost considerations, the perception of a higher complication rate with vascular closure devices has resulted in continued preference for manual compression by most hospitals and operators.
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(a)
(b)
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(c)
Figure 23.2 Three types of mechanical compression: (a) the Compressar (Advanced Vascular Dynamics, Portland, OR) has an adjustable arm and a flexible hinged diaphragm deployed on top of the arteriotomy; (b) the FemoStop (Radi Medical Systems, Uppsala, Sweden) utilizes a bladder inflated to sufficient pressure to control hemorrhage; and (c) SafeGuard combines an inflatable bulb and a sterile dressing to apply local pressure to the arteriotomy site (Datascope, Montvale, NJ).
above the bottom of the femoral head eliminates approximately 75% of punctures into the femoral bifurcation vessels;3 䊊 puncture below the middle of the femoral head eliminates much of the retroperitoneal bleeding risk because it nearly guarantees arterial entry below the inguinal ligament;4 angiography to assess femoral artery size, location of puncture, and presence of disease in the common femoral or low external iliac artery, regardless of whether VCDs are used; 䊊
●
(a)
●
avoidance of anticoagulation if the femoral puncture is outside the “safe zone,” most importantly if it is above the inferior reflection of the inferior epigastric artery (IEA).5 This means that in elective or ad hoc intervention cases, the patient should be brought back for intervention in a separate sitting if the femoral puncture is suboptimal.6
Use of a single anatomic landmark for femoral puncture, most commonly the inguinal crease, is not optimal, since the inguinal crease is on average 6 mm below the femoral bifurcation and
(b)
Figure 23.3 (a) Hemostat placed over the medial portion of the femoral head just below the center identifies a landmark for targeting the common femoral artery prior to skin puncture; (b) after skin puncture and advancement of needle until pulsation is felt just prior to arterial entry, repeat fluoroscopy is used to ascertain that the tip is over the target (light blue circle) at a point just below the centerline of the femoral head (dashed red line). (See Color plates.)
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Manual compression
Figure 23.4 The safe zone for femoral access. Note the location of the bottom loop of the inferior epigastric artery (IEA, red arrow) and the femoral bifurcation (back arrow). The safe zone begins above the femoral bifurcation or at the bottom of the femoral head (whichever is higher) and extends to a point below the IEA’s lowest excursion. About one-quarter of patients have the femoral bifurcation above the bottom of the femoral head. Since neither the location of the femoral bifurcation or IEA is known at the time of puncture, we recommend a site approximately where the light blue circle is shown. This image is in the RAO view for clarity – the blue circle would be over the common femoral artery in the AP view. (See Color plates.)
not, as generally assumed, over the center of the common femoral artery.7 Nevertheless, the inguinal crease remains the most common landmark (Figure 23.5), resulting in femoral puncture being outside the “safe zone” in a large percentage of patients (74% in our series3). Puncture outside the “safe zone” is associated with a significant increase in closure complications,
Pulse/Bone 7%
All Three 1%
Crease/Bone 1% Crease/Pulse 13%
Crease 40%
Manual compression (MC) is invariably effective if adequate compression is applied proximal to the femoral puncture, the femoral puncture is located over the femoral head and below the inguinal ligament, the clotting cascade and platelet function are intact, the compression is carried out over a long enough period of time, the fenestration is small, and only a single anterior wall puncture of the artery has occurred. Because all of those criteria are frequently not met, and because the technique has inherent limitations, a complication rate for MC of approximately 2% for diagnostic catheterizations and 4% for interventions remains in the modern era.8 These rates may also represent an underestimation (see the later section on “Complications”). MC itself lends to certain complications related to prolonged compression, including venous stasis and potential venous thrombosis, and there is evidence, albeit weak, that deep vein thrombosis and pulmonary embolism may be related to prolonged groin holds and immobilization.9 The technique is also painful, and engenders significant delay before patients are allowed to ambulate. The delay is exacerbated in the setting of periintervention anticoagulation; most laboratories do not allow sheaths to be pulled until the activated clotting time has decreased below 150–180 seconds. This leads to patients leaving the catheterization laboratory with indwelling vascular sheaths, potentially causing a variety of complications in addition to bleeding, including infection. Nevertheless, the lowest complication rates have typically been associated with MC, and it remains the standard of care for the majority of diagnostic and interventional cases, with wide geographic variation. An alternative to MC, assisted compression with a variety of compression devices (Figure 23.2), has a good safety record, although some devices have been associated with pain, occasional injury from tissue necrosis owing to excess and prolonged compression of the skin, and some infrequent but rare complications primarily associated with incorrect placement or inadequate attention to the puncture site during device deployment, among others.10 Comparison between MC and compression devices have generally favored the latter,11 and between compression devices and VCDs have been equivocal,12–14 although design issues limit the applicability of these studies and the findings have not been consistent.15
Closure devices
Bone 13%
Pulse 25%
Figure 23.5 Results of a survey of 200 interventional radiologists and cardiologists asking what landmarks they use for femoral puncture. Note that the inguinal crease is the primary landmark, an unfortunate choice (see text). Based on data from Grier et al.7 (See Color plates.)
It is helpful to categorize VCDs by their mechanism of action and mechanical properties. In general devices can be classified as invasive or non-invasive based on whether they are introduced through the skin into the tissue track or applied topically. Active approximation of the arteriotomy edges, either by bringing the edges of the fenestration together with sutures, clips or staples, or sandwiching the arteriotomy closed, is differentiated from devices deployed only outside the artery; the latter works by passive approximation. For active
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Angio-Seal Clotting/Sealing
No C/S
Clotting/Sealing
No C/S
Intraluminal Active Approximation
Passive
Extraluminal Perclose
StarClose
Boomerang
Permanent Foreign Body
Invasive
No Foreign Body
No Foreign Body
EpiclosePlus
Temporary Foreign Body
Temporary Foreign Body
VasoSeal
(a)
No C/S
Clotting/Sealing
No C/S
Passive
Active Approximation
Syvek Patch
Noninvasive
Therus
No Foreign Body
(b)
No Foreign Body
FemoStop
Figure 23.6 (a) The invasive vascular closure devices can be subcategorized by whether or not they provide active or passive approximation, incorporate a clotting or sealing agent, reside intra- or extraluminally, and whether or not a temporary or permanent foreign body is left behind. By way of an example, among the invasive closure devices shown, Angio-Seal is an active approximator, incorporates a clotting agent, leaves behind an intraluminal anchor, and resorbs over time, thus it is a temporary foreign body; (b) the non-invasive vascular closure devices include topical patches, compression devices, and a novel experimental ultrasound closure system.48 C/S = clotting or sealing agent. (See Color plates.)
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approximators, devices can be differentiated by whether a foreign body is left inside the arterial lumen (intraluminal) as opposed to buried in the vessel wall only (extraluminal). Further subclassification depends on whether a sealing or thrombosing agent is used. Finally, some devices leave behind a foreign body, which either resorbs (temporary) or remains permanent. Figure 23.6 shows an algorithm for classification and an example of each of the subcategories described above. Thrombosing agents in VCDs have been either collagen or a thrombin–collagen mixture. The use of collagen for hemostasis was well established in the surgical literature16 prior to its introduction by Datascope as a vascular closure plug in the early 1990s.17 Collagen exerts its thrombotic effect by inducing both platelet adhesion and activation.18 Collagen is also part of the vessel wall, ordinarily protected from blood by an endothelial layer but triggering clotting when endothelial disruption occurs. Gelatin foam has been used in lieu of collagen as a VCD thrombosing agent. Sealing agents are being utilized in several devices in lieu of collagen; these do not actively promote thrombosis, potentially decreasing the risks associated with inadvertent intravascular placement. In general, closure devices have required a system for ascertaining the exact depth of the arteriotomy. An inner locator has been common to virtually all of the devices with the exception of first-generation VasoSeal, a device that used a clip placed on the original needle used for femoral access to mark the arteriotomy depth. The locator used in various devices has been in the form of an anchor, wings, or a balloon. The diameter of these locator devices is an important consideration given the relatively small size of the common femoral artery. The minimal luminal size varies with demographics: for women the mean is approximately 5.0 mm, and for men approximately 6.3 mm (Figure 23.7). The 5.0–6.0 mm size of most locator devices (the notable exception is the smaller profile of the Angio-Seal anchor) used inside the common femoral artery can be seen to eliminate a fair percentage of women (particular those with diabetes) and a minority of men from safe VCD deployment.
Closure devices either deploy through the procedural sheath or require placement of a separate assembly in exchange. The former approach has two advantages: first, it allows introduction of the closure device through an existing conduit rather than through a new exposure of the tissue tract, simplifying the procedure and perhaps decreasing infection risk. Second, it avoids upsizing of the tissue tract, a drawback of most available VCDs that likely increases complication rates due to bleeding and trauma, especially when the arteriotomy itself is upsized.19
Passive approximators (Figure 23.8) VasoSeal, a passive collagen plug, was relatively effective in diagnostic catheterization and to a lesser degree in interventional procedures. When compared with MC in metaanalyses, it had a higher failure rate than other devices20 and was associated with an overall higher complication rate.21 The device, and possibly the passive closure approach in general, may have intrinsic drawbacks, particularly in interventional cases with full anticoagulation and antiplatelet therapy. However, much of the VasoSeal literature is from an earlier intervention era, when larger sheaths, excessive anticoagulation, post-procedure heparin, and non-weight adjusted heparin were widely used – all markers for increased vascular complications, particularly bleeding.22 In addition, there is an overall learning curve associated with vascular closure generically as well as individual closure devices; complication rates during the first 50 deployments have been shown to be up to four times higher than seen after 100 cases23 with an inflection point for decreasing complications requiring as many as 350 cases in individual institutions24 (see “Complications”). VasoSeal, as the first device to market, suffered a disproportionate disadvantage in these respects and is no longer actively marketed. A similar fate was suffered by the Duett (Vascular Solutions, Minneapolis, MN), which remains available from
n=200
25
Study population %
20
15
10
5
0 2
3
4
5 6 7 8 9 Femoral artery minimal luminal diameter (mm)
10
11
12
Figure 23.7 Minimal luminal diameter of the common femoral artery in 200 patients undergoing diagnostic cardiac catheterization. Superimposed are three vascular closure device technologies, with a dotted line showing the minimal luminal diameter for deployment. Note that a 4-mm locator wing would exclude a relative minority of primarily female patients while a 6-mm-diameter balloon would potentially exclude the majority of women in the particular population studied. Adapted from Schnyder G et al.3 (See Color plates.)
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(b)
(c)
(e)
(f)
173
(d)
Figure 23.8 A gallery of passive approximation vascular closure devices: (a) Syvek patch; (b) VasoSeal; (c) Duett; (d) Boomerang ClosureWire; (e) Mynx (previously Finale); and (f) ExoSeal*. * = Not FDA approved as of fall 2007. (See Color plates.)
the manufacturer. This device features a procoagulant combination of thrombin mixed with collagen, deposited in the tissue track through the sheath used for the procedure after the latter is withdrawn to just outside the artery. The delivery system was relatively complex, and it carried an inherent risk of intra-arterial injection of thrombin with consequent iatrogenic arterial occlusion25 with rare but occasional catastrophic consequences. A review of the FDA MAUDE database demonstrates a small but disproportionate percentage of complications associated with arterial occlusion due to injection of thrombin/collagen into the vessel. Because the resorption rate of the coagulant foam is relatively rapid, this device has rarely been associated with infection. The marker balloon deployed inside the arteriotomy, 6 mm in diameter, limits the use of this device to arteries that are relatively large. Like VasoSeal, it does not actively approximate the arteriotomy edges. Several other passive approximators using sealants rather than thrombosing agents are currently under investigation or recently FDA approved. These include the Mynx (AccessClosure, Mountain View, CA) and ExoSeal (Johnson and Johnson, New Brunswick, NJ). The former utilizes a polyethylene glycol wafer, while the latter incorporates a biopolymer. Although pivotal trials of polyethylene glycol sealant were performed in the US and Europe, and were reported as successful in abstract presentations, these have not been published to date. Another passive approximator, the Boomerang Closurewire (Cardiva Medical, Mountain View, CA), works by a novel approach: a nitinol disk is deployed inside the blood vessel and brought back against the arteriotomy; traction is then applied until hemostasis occurs, at which point the disk is collapsed and removed from the tissue track. The device leaves no foreign body behind. The inherent disadvantage in the
concept, the withdrawal through the freshly formed clot, is mitigated to an extent by the low profile of the collapsed disk as it is withdrawn, but it does require additional compression at that point. It has been evaluated primarily for diagnostic catheterizations,26 although it is FDA-approved for intervention as well. A large number of topical patches are available. These accelerate hemostasis by a variety of mechanisms, with the active agents being a wide range of substances with apparent procoagulant properties. The ability of these devices to facilitate clotting inside the tissue track down to the arteriotomy level has not been demonstrated convincingly, and despite wide availability and some 20% of the vascular closure market, no significant evidence base for effectiveness exists.
Active approximators (Figure 23.9) Angio-Seal, the second VCD to be released, could be characterized as a “belt and suspenders” VCD. It provides active rather than passive approximation, sandwiching the arteriotomy between a resorbable anchor and a collagen plug held together by a cinched resorbable suture. In addition, the collagen plug serves as a thrombosing agent. Overall, it has a high (and possibly the highest overall) success rate of deployment and closure with a short learning curve.23,27 Potential disadvantages relate to the anchor, particularly inside an atherosclerotic femoral artery, causing vascular obstruction; in addition there is rare dislodgement of the anchor resulting in obstruction of the infrainguinal vessels. The device leaves a foreign body inside the tissue track to serve as a potential nidus for infection, and on occasion the collagen sponge has been
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Textbook of peripheral vascular interventions (a)
(b)
(c)
(e)
(f)
(d)
(g)
Figure 23.9 A gallery of active approximation vascular closure devices: (a) Angio-Seal; (b) Perclose; (c) StarClose; (d) AngioLink; (e) SuperStitch; (f) Therus*; and (g) Epiclose Plus*. * = Not FDA-approved as of fall 2007. (See Color plates.)
inserted inside the artery resulting in arterial thrombosis. It dominates the VCD market with over two-thirds of the VCDs used. Perclose was the next of the VCDs released. It provides active approximation with suture. It has a high success rate, but somewhat lower than Angio-Seal28 (large true randomized device-to-device comparisons without major design flaws are essentially non-existent). Because there is no clotting or sealing agent, oozing from the tissue track in interventional cases is the most common disadvantage. Unlike Angio-Seal, there is a permanent foreign body in the form of suture material; however the intra-arterial profile of the suture is substantially less than that of the Angio-Seal anchor. The learning curve for earlier generations was substantial,24 but modifications in design have largely eliminated this issue. The device has significant advantages for “preclosure.” Use of the preclosure technique as well as a version of the device designed for large caliber arterial punctures has been successful for a variety of interventions with devices > 18 French, including abdominal aortic endograft placement.29 Preclosure of large bore venous access sites is also effective,30 although care should be taken with this technique, since inadvertent trans-section of the common femoral vein can occur; the latter is both highly morbid and difficult to treat. Perclose has held about onequarter of the vascular closure market. Similar to Perclose is the Sutura SuperStitch (Sutura, Fountain Valley, CA). A new class of active approximators, the percutaneous metal arterial closure devices, have several features in common. Both StarClose (Abbott Vascular, Redwood City, CA) and AngioLink (Medtronic, Santa Rosa, CA) actively approximate the arteriotomy edges, and both are designed to penetrate only as far as the media, with no metal exposure inside the arterial lumen. The StarClose device is a nitinol clip while AngioLink is a titanium staple; both result in upsizing, with StarClose upsizing the tissue tract to 12 French but leaving the arteriotomy itself intact, while AngioLink upsizes the arteriotomy to 10 French. Neither incorporates a thrombosing
or sealing agent, and both leave a permanent foreign body behind. StarClose has taken an increasing portion of the VCD market, primarily from Perclose; both devices share the same classification system (and manufacturer) except for the extraluminal nature of StarClose. Finally, two novel concepts of active closure, both acting by heating of the arterial puncture site to denature collagen and seal the vessel, are under development. Therus (Therus, Seattle, WA) beams ultrasound energy at the arteriotomy from the skin surface using tracking technology to identify the exact location of puncture. Epiclose Plus (Cardiodex, TiratHacarmel, Israel) uses a balloon placed inside the tissue track on top of the arteriotomy to deliver local heat for the same purpose. Several issues remain to be clarified in this promising approach, most prominently the effectiveness of the targeting algorithms and reliability of heat sealing in fully anticoagulated patients.
Complications In general, the causes of vascular access complications, whether or not related to VCDs, have been variable across studies. A number of common though not consistent associations include female gender, small or very large body habitus, diabetes, presence of peripheral vascular disease, aggressive anticoagulation (high doses, non-weight-based dosing, postprocedure continuation of anticoagulation), poor access techniques (multiple, high, low, or back wall punctures), large sheath size, small vessel size, poor sterility control, glycoprotein IIb/IIIa use, and operator learning curve. The specific role of VCDs in these complications is muddled. Because the clinical trials are generally flawed by a weak evidence base31 that includes changing device platforms, selection bias, cohort mismatch, learning curve issues and lack of essential information such as predeployment femoral angiography and extent of anticoagulation, the answer to whether or not the
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Vascular closure devices complication rate of VCDs is higher has been elusive. Compared with MC, the complications of VCDs have been variously reported as equivalent,20,32 greater,33,34 or lower overall,21,35 with meta-analyses and propensity scoring having been used to attempt to address the poor quality of the evidence base (Figure 23.10). The issue is also confounded by varying definitions, including what constitutes a hematoma. The common use of a 10-cm threshold underestimates the complication rate8 while a threshold as small as 2 cm tends to overestimate it.11 The most common complication has been minor bleeding and hematoma, and the most serious has been retroperitoneal bleeding, the latter associated with a mortality between 4% and 6%.4,36 Retroperitoneal bleeding occurs in < 1% of interventional cases, though the percentage appears to have increased in the era of glycoprotein IIb/IIIa inhibitors. The use of VCDs increases retroperitoneal hemorrhage risk36,37 by odds ratios as high as 3:1; in the earlier Cleveland Clinic analysis, retroperitoneal hemorrhage after VCD use was 1.2–1.8%37 compared to 0.2% with MC. The phenomenon may be due to two likely causes: first, VCDs are deployed while the patient is fully anticoagulated, whereas MC is only used when the ACT has normalized. This all but guarantees greater bleeding risk with VCD use in patients who have undergone percutaneous intervention, though the effect of rapid resolution of anticoagulation with an agent like bivalirudin may help mitigate this.38
Second, in the setting of high punctures, the transversus abdominis muscle may lie between the skin site of puncture and the external iliac artery, and may prevent the collagen plug, knot, or staple/clip from descending all the way down to the arterial surface (Figure 23.11). The second most morbid complication is infection secondary to VCD use. The incidence appears to be < 0.3%, but the co-morbidities are significant, and a 6% mortality has been reported.39 Mycotic pseudoaneurysm is found in nearly half of cases, positive blood cultures (predominantly S. aureus) in nearly 90%. The median time of occurrence is 8 days, but in our experience, can first present as late as one month. Because VCDs can serve as a wick for bacterial passage to the arteriotomy site, and provide a foreign body focus for abscess formation, surgical intervention is required in half or more of patients and conservative management typically requires prolonged and usually parenteral antibiotic therapy. Several other complications are worth noting. Vascular occlusion occurs in < 0.2% of cases and has several causes: first, direct closure of the vessel by active approximation of the front and back walls, typically by suture or clip/staple devices. Second, and more commonly, insertion of a thrombosing agent into the vessel, usually the Angio-Seal collagen plug, causing acute or subacute thrombosis. Third, the Angio-Seal anchor has resulted in a localized reaction or on occasion has migrated distally and been trapped in a diseased superficial
No. (%) vascular complications All procedures (n = 21,841)
VCD
MC
0.1
1
10
Propensity score adjusted OR (95%CI)
(n = 8,807)
(n = 13,034)
Any VC
120 (1.36)
188 (1.44)
0.87 (0.68-1.13)
Major VC
67 (0.76)
99 (0.76)
0.96 (0.68-1.35)
Minor VC
76 (0.86)
140 (1.07)
0.75 (0.55-1.02)
(n = 3,600)
(n = 9,524)
Any VC
31 (0.86)
118 (1.24)
0.81 (0.54-1.22)
Major VC
18 (0.50)
63 (0.66)
0.94 (0.54-1.62)
Minor VC
19 (0.53)
92 (0.97)
0.64 (0.38-1.06)
(n = 5,207)
(n = 3,510)
Any VC
89 (1.71)
70 (1.99)
0.92 (0.66-1.28)
Major VC
49 (0.94)
36 (1.03)
0.99 (0.63-1.56)
Minor VC
57 (1.09)
48 (1.37)
0.84 (0.56-1.26)
Diagnostic caths (n = 13,124)
PCI's (n = 8,717)
175
VCD protective
VCD harmful
Figure 23.10 Propensity score adjusted analysis of vascular complications in over 20,000 patients undergoing diagnostic or interventional catheterization. Complications were compared for patients receiving VCDs (Angio-Seal, Perclose, or VasoSeal) and those undergoing manual compression. In general the complications straddle the null hypothesis. As with virtually all of this literature, there is an absence of randomized, intention-to-treat data, hence the use of propensity score adjustment to attempt to account for selection bias. MC = manual compression. VCD = vascular closure device. From Applegate et al.32
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Textbook of peripheral vascular interventions I
"high" entry
Inguinal ligament
Usual entry Fascia of Camper Fascia of Scarpa Obliquus externus abdominis Obliquus internus abdominis
Femoral artery
Transversus abdominis
External iliac artery
Deep inferior epigastric artery Tamper
II
Collagen plug Fascia of Camper Fascia of Scarpa Obliquus externus abdominis Femoral artery
Obliquus internus abdominis Transversus abdominis
Deep inferior epigastric artery
External iliac artery
Figure 23.11 The relationship of the external iliac artery site of entry to surrounding structures in the setting of a high stick. Note the interposition of the transversus abdominis muscle between the skin and the arterial puncture site, resulting in interference with deployment of the Angio-Seal collagen plug onto the arterial surface. Presumably as a result, retroperitoneal hemorrhage in the setting of Angio-Seal use has an odds ratio of 2.8:1. From Ellis et al.36
femoral artery, or obstructed the smaller lumens of the popliteal, tibioperoneal trunk, or lower circulation. The latter have typically occurred several days to 2 weeks after device deployment, although progressive claudication has been reported in some cases to take many months to fully develop.40 Neural injury caused by suture or clip/staple entrapment probably occurs, although the evidence base is murky, with only anecdotal reports of surgery to relieve nerve entrapment. Pseudoaneurysms or AV fistulae do not seem to correlate with VCD use.
The importance of femoral angiography The instructions for use for VCDs call for femoral angiography prior to device insertion despite which a significant percentage of operators, particularly outside the US, continue to avoid this practice.6 Femoral angiography provides essential information for safe deployment. Low punctures, particularly into the bifurcation vessels, should dictate avoidance of VCD use.40 A significant percentage of VCD complications, in particular vessel obstruction, result from low puncture40,41 or deployment into atherosclerotic vessel segments. High puncture is associated with up to a 17:1 higher risk of retroperitoneal hemorrhage.36 If femoral angiography through the sheath is performed as soon as access is obtained, and the puncture is seen to be above the origin of the IEA,
prudence dictates avoiding intervention and anticoagulation in that setting.
Issues for peripheral vascular interventions VCDs have specific advantages and drawbacks in the setting of peripheral vascular interventions. Early ambulation can be particularly helpful for patients with peripheral vascular disease, since early discharge, one of the potential benefits of VCD use, is more likely to occur after peripheral than after coronary interventions. MC or compression devices used upstream from ipsilateral access is undesirable, inasmuch as they result in prolonged blood stasis at the fresh angioplasty or stent site downstream from the puncture. Although potentially more hazardous, device closure, in particular Perclose, has been effective in anecdotal series,42 including one randomized trial comparing Perclose to MC in the setting of peripheral vascular disease.43 VCD closure of antegrade femoral punctures has been reported with both Perclose and Angio-Seal.44,45 Similarly, compression upstream or over a synthetic graft may cause stasis and thrombosis, and some interventionalists have advocated off-label Perclose use in this setting. Finally, VCDs have been utilized for a variety of non-femoral access sites,46 though the evidence base is thin and care should be taken to avoid infection risk if the arteriotomy is close to the skin surface.
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Cost considerations
Conclusion
Vascular closure devices are expensive. Without a clear evidence base to show superior outcomes or lower complication rates, their use remains a question of preference and economics. The argument has been made that costs can be offset by earlier ambulation with less requirement for post-procedure nursing care and potentially earlier discharge from the hospital.47 These considerations do not apply in many parts of the world, and resistance to adoption of VCDs remains high in those areas.
VCDs substantially increase the comfort and convenience of patients and allow earlier ambulation. These benefits come at a price of a possibly higher rate of complications and the cost of the devices themselves. Until a more substantial evidence base is developed, or the economic arguments become more compelling, the use of VCDs will remain largely an issue of physician and patient preference. A new generation of VCDs may provide for a more compelling risk/benefit/cost ratio to mandate use of these devices.
REFERENCES 1. 2. 3.
4.
5.
6. 7. 8. 9.
10. 11.
12.
13.
14.
15.
16. 17.
Seldinger SI. Catheter replacement of the needle in percutaneous arteriography; a new technique. Acta Radiol 1952; 39: 368–76 Barry WH, Levin DC, Green LH et al. Left heart catheterization and angiography via the percutaneous femoral approach using an arterial sheath. Cathet Cardiovasc Diagn 1979: 5: 401–9 Schnyder G, Sawhney N, Whisenant B et al. Common femoral artery anatomy is influenced by demographics and comorbidity: implications for cardiac and peripheral invasive studies. Catheter Cardiovasc Interv 2001; 53: 289–95 Farouque HM, Tremmel JA, Raissi SF et al. Risk factors for the development of retroperitoneal hematoma after percutaneous coronary intervention in the era of glycoprotein IIb/IIIa inhibitors and vascular closure devices. J Am Coll Cardiol 2005; 45: 363–8 Sherev DA, Shaw RE, Brent BN. Angiographic predictors of femoral access site complications: implication for planned percutaneous coronary intervention. Catheter Cardiovasc Interv 2005; 65: 196–202 Turi ZG. Optimizing vascular access: routine femoral angiography keeps the vascular complication away. Catheter Cardiovasc Interv 2005; 65: 203–4 Grier D, Hartnell G. Percutaneous femoral artery puncture: practice and anatomy. Br J Radiol 1990; 63: 602–4 Chandrasekar B, Doucet S, Bilodeau L et al. Complications of cardiac catheterization in the current era: A single-center experience. Catheter Cardiovasc Interv 2001; 52(3): 289–95 Gowda S, Bollis AM, Haikal M et al. Incidence of new focal pulmonary emboli after routine cardiac catheterization comparing the brachial to the femoral approach. Cathet Cardiovasc Diagn 1984; 10: 157–61 Jackson A, Beards SC, Gillespie JE. Possible hazard associated with the use of the “FemoStop” groin compression device. Br J Radiol 1993; 66: 748 Pracyk JB, Wall TC, Longabaugh JP et al. A randomized trial of vascular hemostasis techniques to reduce femoral vascular complications after coronary intervention. Am J Cardiol 1998; 81: 970–6 Juergens CP, Leung DY, Crozier JA et al. Patient tolerance and resource utilization associated with an arterial closure versus an external compression device after percutaneous coronary intervention. Catheter Cardiovasc Interv 2004; 63: 166–70 Amin FR, Yousufuddin M, Stables R et al. Femoral haemostasis after transcatheter therapeutic intervention: a prospective randomised study of the angio-seal device vs. the femostop device. Int J Cardiol 2000; 76: 235–40 Chamberlin JR, Lardi AB, McKeever LS et al. Use of vascular sealing devices (VasoSeal and Perclose) versus assisted manual compression (Femostop) in transcatheter coronary interventions requiring abciximab (ReoPro). Catheter Cardiovasc Interv 1999; 47: 143–7 Benson LM, Wunderly D, Perry B et al. Determining best practice: comparison of three methods of femoral sheath removal after cardiac interventional procedures. Heart Lung 2005; 34: 115–21 Vistnes LM, Goodwin DA, Tenery JH et al. Control of capillary bleeding by topical application of microcrystalline collagen. Surgery 1974; 76: 291–4 Kuhn C, Sumpelmann D, Geiger B et al. [Early hemostasis after coronary therapeutic interventions by using a collagen plug]. Z Kardiol 1993; 82: 515–20
18. 19.
20.
21. 22. 23.
24.
25.
26. 27. 28.
29. 30.
31. 32.
33.
34.
Farndale RW, Sixma JJ, Barnes MJ et al. The role of collagen in thrombosis and hemostasis. J Thromb Haemost 2004; 2: 561–73 Kahn ZM, Kumar M, Hollander G et al. Safety and efficacy of the Perclose suture-mediated closure device after diagnostic and interventional catheterizations in a large consecutive population. Catheter Cardiovasc Interv 2002; 55: 8–13 Nikolsky E, Mehran R, Halkin A et al. Vascular complications associated with arteriotomy closure devices in patients undergoing percutaneous coronary procedures: a meta-analysis. J Am Coll Cardiol 2004; 44: 1200–9 Tavris DR, Dey S, Albrecht-Gallauresi B et al. Risk of local adverse events following cardiac catheterization by hemostasis device use – phase II. J Invasive Cardiol 2005; 17: 644–50 Blankenship JC, Balog C, Sapp SK et al. Reduction of vascular access site bleeding in sequential abciximab coronary intervention trials. Catheter Cardiovasc Interv 2002; 57: 476–83 Warren BS, Warren SG, Miller SD. Predictors of complications and learning curve using the Angio- Seal closure device following interventional and diagnostic catheterization. Catheter Cardiovasc Interv 1999; 48: 162–6 Balzer JO, Scheinert D, Diebold T et al. Postinterventional transcutaneous suture of femoral artery access sites in patients with peripheral arterial occlusive disease: a study of 930 patients. Catheter Cardiovasc Interv 2001; 53: 174–81 Katsouras CS, Michalis LK, Leontaridis I et al. Treatment of acute lower limb ischemia following the use of the Duett sealing device: Report of three cases and review of the literature. Cardiovasc Intervent Radiol 2004; 27: 268–70 Doyle BJ, Godfrey MJ, Lennon RJ et al. Initial experience with the cardiva Boomerangtrade mark vascular closure device in diagnostic catheterization. Catheter Cardiovasc Interv 2006; 69: 203–8 Applegate RJ, Sacrinty M, Kutcher MA et al. Vascular complications with newer generations of angioseal vascular closure devices. J Interv Cardiol 2006; 19: 67–74 Applegate RJ, Grabarczyk MA, Little WC et al. Vascular closure devices in patients treated with anticoagulation and IIb/IIIa receptor inhibitors during percutaneous revascularization. J Am Coll Cardiol 2002; 40: 78–83 Quinn SF, Kim J. Percutaneous femoral closure following stentgraft placement: use of the Perclose device. Cardiovasc Intervent Radiol 2004; 27: 231–6 Mahadevan VS, Jimeno SS, Benson LN et al. Pre-closure of femoral venous access sites used for large sized sheath insertion with the PercloseTM device in adults undergoing cardiac intervention. Heart; 2006; Published online 3 November 2006 Schnyder G, Turi ZG. Complications of vascular closure devices— not yet evidence based. J Am Coll Cardiol 2002; 39: 1705–6 Applegate RJ, Sacrinty MT, Kutcher MA et al. Propensity score analysis of vascular complications after diagnostic cardiac catheterization and percutaneous coronary intervention 1998–2003. Catheter Cardiovasc Interv 2006; 67: 556–62 Koreny M, Riedmuller E, Nikfardjam M et al. Arterial puncture closing devices compared with standard manual compression after cardiac catheterization: systematic review and meta-analysis. JAMA 2004; 291: 350–57 Dangas G, Mehran R, Kokolis S et al. Vascular complications after percutaneous coronary interventions following hemostasis with manual compression versus arteriotomy closure devices. J Am Coll Cardiol 2001; 38: 638–41
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36. 37.
38.
39. 40.
41.
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Textbook of peripheral vascular interventions Arora N, Matheny ME, Sepke C et al. A propensity analysis of the risk of vascular complications after cardiac catheterization procedures with the use of vascular closure devices. Am Heart J 2007; 153: 606–11 Ellis SG, Bhatt D, Kapadia S et al. Correlates and outcomes of retroperitoneal hemorrhage complicating percuta-neous coronary intervention. Catheter Cardiovasc Interv 2006; 67: 541–5 Cura FA, Kapadia SR, L’Allier PL et al. Safety of femoral closure devices after percutaneous coronary interventions in the era of glycoprotein IIb/IIIa platelet blockade. Am J Cardiol 2000; 86: 780–2 Lincoff AM, Bittl JA, Harrington RA et al. Bivalirudin and provisional glycoprotein IIb/IIIa blockade compared with heparin and planned glycoprotein IIb/IIIa blockade during percutaneous coronary intervention: REPLACE-2 randomized trial. JAMA 2003; 289: 853–63 Sohail MR, Khan AH, Holmes DR, Jr. et al. Infectious complications of percutaneous vascular closure devices. Mayo Clin Proc 2005; 80: 1011–15 Dregelid E, Jensen G, Daryapeyma A. Complications associated with the Angio-Seal arterial puncture closing device: intra-arterial deployment and occlusion by dissected plaque. J Vasc Surg 2006; 44:1357–59 Jang JJ, Kim M, Gray B et al. Claudication secondary to Perclose use after percutaneous procedures. Catheter Cardiovasc Interv 2006; 67: 687–95
42.
43.
44.
45. 46.
47.
48.
Mackrell PJ, Kalbaugh CA, Langan EM, III et al. Can the Perclose suture-mediated closure system be used safely in patients undergoing diagnostic and therapeutic angiography to treat chronic lower extremity ischemia? J Vasc Surg 2003; 38: 1305–8 Starnes BW, O’Donnell SD, Gillespie DL et al. Percutaneous arterial closure in peripheral vascular disease: a prospective randomized evaluation of the Perclose device. J Vasc Surg 2003; 38: 263–71 Biondi-Zoccai GG, Fusaro M, Tashani A et al. Angioseal use after antegrade femoral arteriotomy in patients undergoing percutaneous revascularization for critical limb ischemia: A case series. Int J Cardiol; 2006 Mukhopadhyay K, Puckett MA, Roobottom CA. Efficacy and complications of Angioseal in antegrade puncture. Eur J Radiol 2005; 56: 409–12 Bilecen D, Bongartz G, Ostheim-Dzerowycz W. Off-label use of Angio-Seal vascular closure device for brachial artery puncture closure-deployment modification and initial results after transbrachial PTA. Eur J Vasc Endovasc Surg 2006; 31: 431–3 Resnic FS, Arora N, Matheny M et al. A cost-minimization analysis of the angio-seal vascular closure device following percutaneous coronary intervention. Am J Cardiol 2007; 99: 766–70 Turi ZG. Overview of vascular closure. Endovasc Today 2007; 6: 93–9
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Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis JA Silva and JS Jenkins
Percutaneous retrieval of foreign bodies
available including the loop-snare retrieval systems, biopsy forceps, baskets, and others.
The use of indwelling catheters as well as the application of percutaneous diagnostic and revascularization procedures has grown exponentially over the past decade. As a result, endovascular therapists are sometimes confronted with the problem of misplacement or migration of some of these devices into unintended and potentially dangerous anatomical locations. The rate of serious complications associated with foreign body embolism has been reported to be as high as 71% with a mortality rate ranging from 24 to 60%.1 Consequently, non-surgical removal of misplaced intravascular foreign bodies is desirable. In the last few years, there have been several reports regarding the successful percutaneous retrieval of these devices. Some of these experiences are discussed in the present section. The first report of successful percutaneous retrieval of an intravascular foreign body was published in 1964.2 Following that case report, Dotter et al.3 published their multi-center experience on endovascular retrieval of foreign bodies and described successful percutaneous removal of intravascular foreign bodies in 29 cases. In 1978, Bloomfield conducted an international survey and published the results of 180 cases of non-surgical retrieval of intracardiac foreign bodies, suggesting that percutaneous retrieval yielded a very high success rate.4 Since then several case reports or small case series have described the successful non-surgical extraction of intravascular foreign bodies.5–7 In 1986, Uflacker and coworkers7 described their experience on the successful extraction of 19 of 20 intravascular foreign bodies. In this experience, 70% of the fragments were the sheared-off tips of through-the-needle venous catheters. Compared to that early experience3–7 which included the extraction of catheter fragments in the majority of the cases, metal stents, embolization coils, and vena cava filters encompass the majority of foreign bodies removed in more contemporary clinical practice. In addition, technologic innovations and the introduction of new retrieval devices available for extraction of intravascular foreign bodies have enhanced the intravascular recovery rate. Many retrieval tools are currently
Loop-snare retrieval systems Loop-snare devices are frequently among the first choice when attempting percutaneous removal of a foreign body because they are safe and easy to use.8 One loop-snare retrieval system described in the literature is the Welter retrieval loop catheter (Cook, Letchworth, UK), which consists of a wire snare operated from the proximal handle. This device has radio-opaque markers at the catheter tip and the origin of the loop, which facilitates visualization during manipulation and retrieval (Figure 24.1). The Retriever snare (Target Therapeutics, Fremont, CA) consists of an adjustable platinum loop that can be visualized during fluoroscopy and allows retrieval of different-sized objects. It has a low profile (6-French guiding catheters), which allows access to distal and tortuous vessels (Figure 24.2). More recently, the Amplatz gooseneck snare (Microvena Corp, White Bear Lake, MN), which has a nitinol 90° snare loop to shaft orientation has been shown to be of great utility in percutaneous retrieval of foreign bodies (Figure 24.3).9 Compared to other loop-snare techniques in which parallel-opening, self-made, or early wire snares limit foreign body capture,10 the nitinol gooseneck micro-snare has a rightangle design which maximizes engagement and capture of the foreign body. Cekirge et al.,11 described the successful retrieval of intravascular foreign bodies in 13 patients (11 venous, 2 arterial: 10 catheter fragments, 1 stent, 1 coil, 1 guidewire) using nitinol gooseneck snares. Egglin and his colleagues12 attempted removal of 35 intravascular foreign bodies (30 venous and 5 arterial: 16 catheter fragments, 6 embolization coils, 5 metal stents, 4 guidewires, 2 vena cava filters, 1 balloon catheter fragment) in 32 patients. The retrieval devices included nitinol gooseneck snares (n = 28), flexible grasping forceps (n = 5), pigtail catheters (n = 4), and tip-deflecting wires (n = 2) with more than one retrieval system required in 25% of the cases. The retrieval success rate was 97% in this series. In a report of 45 patients using nitinol gooseneck snares in 78% of the cases, retrieval of foreign bodies (12 endovascular stents, 14 catheter fragments, 11 embolization coils, 4 guidewire fragments, 179
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Figure 24.3 permission.
Figure 24.1 permission.
The Welter retrieval loop. Reproduced with
The Amplatz gooseneck snare. Reproduced with
It is important to understand that the free end of the foreign body must be present if loop-snare retrieval is to be attempted. Different techniques have been reported to obtain free end of entrapped foreign bodies. A double-curve catheter or a pigtail may be used to dislodge the target object in a remote vessel or may be used to pull or rotate them exposing an adequate profile or free end for entrapment by a snare.15
3 vena cava filters, and 1 cardiac valve fragment) was successful in 91%.13 More recently, Koseoglu et al.14 reported retrieval of 15 intravascular foreign bodies in 15 patients using nitinol gooseneck snares, with a procedural success rate of 100% and no complications. Interestingly, the authors were capable of successfully retrieving foreign bodies in potentially dangerous locations such as the carotid and middle cerebral arteries.
Retrieval baskets Several baskets for retrieval of foreign bodies have been described in the literature: the Dotter retrieval catheter,16,17 the mini-basket, and the Dormia stone catheter or other stone basket retrieval catheters (Figure 24.4).18–20 These consist of an outer sheath enclosing movable parallel metal wires which can be opened or closed by a sliding cone in and out of a coronary catheter. In a
Figure 24.2
Figure 24.4 permission.
The Retriever snare. Reproduced with permission.
The Cook retrieval forceps. Reproduced with
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Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis report on retrieval attempt of 12 intravascular foreign bodies,19 10 were successfully removed with the stone basket retrieval catheter (Bard Inc., US). Eight of the 10 cases were from major veins. In a recent series of 26 patients with intravascular foreign bodies (8 stents, 4 embolization coils, 9 guidewires, 1 pacemaker lead, and 4 catheter fragments), retrieval was successful in 25 patients (96%) using the Dormia basket without in-hospital or long-term procedural complications.20 Retrieval basket devices appear to be of particular importance for the removal of relatively large objects from the great veins, intracardiac chambers, and the arterial circulation when the objects have reached large arteries or the aorta.21 Biotope and grasping forceps Different types of forceps have been utilized for the retrieval of intravascular foreign bodies.13,22–24 The Cook retrieval forceps is a 3-French profile device operated from a proximal handle and includes a distal spring coil to minimize vascular trauma. The Cordis biopsy forceps (Cordis Corp., Miami, FL), although used to obtain myocardial biopsies, have also been used to remove intravascular foreign bodies. This catheter is relatively large and rigid which enhances the likelihood of vascular trauma and procedural complications. Miscellaneous techniques A variety of improvised retrieval techniques have been utilized to retrieve lost foreign bodies from the vasculature. Doubling an exchange-length wire at its mid-section and inserting it into a 4-French probing catheter can create snares. Alternatively, looping the distal 5 cm of a standard-length wire or tying together the flexible ends of two 0.014-inch wires may build a snare.25,26 The probing catheter is then passed through the guide catheter and positioned just proximal to the retained fragment. The loop is front-loaded through the probing catheter and then passed over the object. Once the object is trapped, the wire ends are pulled firmly to secure the object against the catheter tip and removed through the femoral sheath. Inflated or deflated balloon catheters may be used to drag fragments physically from the vessel into the guide catheter in the coronary circulation.27,28 There are also reports on the use of pigtail catheters to snare and retrieve catheter fragments.29,30 These last techniques have the potential of causing vascular damage necessitating operator care if attempted.
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Coil embolization The delivery of embolization coils has the purpose of inducing selective and “controlled” thrombosis, leading to interruption of vascular flow in a specific target vessel. This endovascular technique has been shown to have important clinical applicability for the treatment of many vascular territories and conditions. It is beyond the scope of this discussion to address the use of embolization coils in every clinical scenario, but instead to provide a general view of their potential applications. Embolization coils are useful for the treatment of patients with patent ductus arteriosus (PDA), systemic-topulmonary artery shunts, and pulmonary arteriovenous (AV) malformations. In addition, coil embolization therapy has become an important treatment modality for intracranial aneurysms, mesenteric aneurysmal disease, gastrointestinal bleeding, iatrogenic vascular perforation in the coronary and peripheral circulation, and others (see below). Most coils consist of preshaped, stainless steel or platinum wire covered with Dacron fiber that are advanced through standard angiographic catheters or microcatheters and delivered to the vessel to be occluded. They are available in different lengths, diameters, and configurations, including straight, helical, or conical shapes (Figure 24.5). The coils are delivered into the target vessel by pushing them through the catheter with an introducer, guidewire, or saline flush and detaching them from an introducing wire after they are placed in the target vessel. The nominal coil diameter is determined by the effective diameter of the extended coil, and range from 0.018to 0.052-inch size. Nester coils are soft, long, platinum-fiber coils which are excellent for packing large vessels or arteriovenous connections and are available in 0.018- and 0.035-inch diameters. Therapeutic embolization of unwanted thoracic vessels was first reported in 1974.31 Vascular occlusion techniques using coil embolization for the treatment of patients with PDA is an attractive and an effective therapeutic modality. Approximately 95% of PDAs smaller than 2.5–3.0 mm can be completely occluded with a single coil. Larger PDAs can also be occluded but require multiple coils.32–35 Coil embolization therapy has also been successfully utilized for the closure of aortopulmonary collaterals, arteriovenous malformations, Blalock–Taussig shunts, venous collaterals, venae cavae, and coronary artery fistulas.36–39
Embolization therapy: coils and occlusive agents There are clinical conditions in which selective interruption of blood flow by inducing thrombosis of the vessel is desirable or necessary to decrease the patient’s morbidity and mortality. These include vascular malformations, arteriovenous fistulas, aneurysms, and spontaneous or iatrogenic bleeding. Endovascular catheter-based therapy with selective embolization of coils, occlusive agents, and sclerotherapy appears to be very useful for the treatment of many of these conditions.
Figure 24.5 permission.
Different embolization coils. Reproduced with
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Over the past 15 years the use of embolization coils has dramatically changed treatment of intracranial aneurysms. The development of the Guglielmi detachable coil led in 1995 to the approval of this technique by the Food and Drug Administration for the treatment of intracranial aneurysms.40 Many prospective and retrospective studies have now confirmed that coil embolization is a feasible alternative treatment to surgery, which carries 5–10% morbidity, negligible mortality and the achievement of complete or near-complete occlusion of > 90% of patients with unruptured intracranial aneurysms.41–43 Likewise coil embolization has been shown to be a feasible alternative to surgery for the treatment of aneurysms in other anatomical locations, such as the renal, mesenteric, coronary, and peripheral circulation in selected patients.44–50 Pseudoaneurysms in the coronary and noncoronary circulation or those that result as a complication of arterial vascular access have also been successfully treated with coil embolization therapy.51–53 Severe gastrointestinal bleeding, retroperitoneal hemorrhage, and iatrogenic complications of percutaneous interventions can be treated with coil embolization after the source of bleeding has been identified.54–56 Occlusive agents Occlusive agents that induce thrombosis and interruption of blood flow are divided into embolization agents such as polyvinyl alcohol foam and gel foam; sclerosing agents such as ethanol, tetradecyl ethanolamine, polydocanol, doxycycline, and others which produce irritation, endothelial damage and thrombosis of the vessel; and more recently, natural procoagulants such as thrombin.57 These occlusive agents are used for treating arteriovenous malformations, arteriovenous fistulas, hemangiomas, venous and lymphatic malformations,57–60 and acquired or iatrogenic bleeding complications after percutaneous coronary and peripheral vascular interventions (Figure 24.6).61–64 In the treatment of arteriovenous malformations the results are mixed and patients often require
several treatment sessions due to recurrence of the condition. Treatment of bleeding and iatrogenic complications is limited to case reports. When treating these conditions the operator must keep in mind potential complications such as tissue necrosis, nerve injuries, and thrombosis of non-targeted vessels, pulmonary embolism, and others.57
Angiogenesis Symptomatic patients with significant peripheral vascular disease should be considered for percutaneous or surgical revascularization therapy. A proportion of these individuals are not suitable for either revascularization strategy due to poor target vessels, inability to cross chronic total occlusions, or other comorbidities, and often require amputation. Angiogenesis is the process of new blood vessel development (neovascularization) from pre-existing vasculature. Vasculogenesis refers to blood vessel formation from endothelial progenitors that differentiate in situ. Until recently, angiogenesis was considered the only means of adult neovascularization and vasculogenesis was thought to be limited to embryologic development. The existence of bone marrow-resident and/or circulating endothelial progenitor cells (EPCs) has provided evidence that postnatal vasculogenesis also occurs in adults. Based on promising preclinical studies and the abundant information of their biological properties, the potential of EPCs to regulate angiogenesis as a therapeutic modality for saving tissue from ischemic damage has been suggested.65,66 Based on this recent research, investigators have explored therapies aimed at promoting the development of new vessels in the coronary and peripheral circulation as a way to enhance perfusion to the ischemic tissue with promising results.67–70 In a murine model of limb ischemia, successful induction of angiogenesis was accomplished by transplantation of peripheral blood mononuclear cells and platelets.70 In patients with critical lower-extremity ischemia, the pioneer work of
Figure 24.6 Retroperitoneal bleeding caused by laceration of the inferior epigastric artery, successfully treated with balloon catheter-delivery of thrombin. Reproduced with permission from Silva JA et al. Catheter Cardiovasc Interv 2004; 62: 230–3.
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Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis Tateishi-Yuyama et al.71 showed that transferring bone marrow-derived mononuclear cells (BM-MNCs) into ischemic limbs dramatically decreased ischemic symptoms, increased ankle–brachial index (ABI), enhanced the transcutaneous oxygen pressure, and prolonged exercise tolerance. The safety, feasibility, and clinical benefits of
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this form of therapy have recently been confirmed by other investigators.72–74 Angiogenesis appears to be a promising revascularization strategy in patients who are poor candidates for conventional surgical or percutaneous revascularization, and is at present undergoing intense research.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.
17. 18. 19. 20.
21. 22.
Richardson JD, Grover FL, Trinkle JK. Intravenous catheter emboli experience with 20 cases and collective review. Am J Surg 1974; 128: 722–8 Thomas J, Sinclair SB, Bloomfield D et al. Nonsurgical retrieval of a broken segment of steel spring guide from right atrium and inferior vena cava. Circulation 1964; 30: 106–8 Dotter CT, Roesch J, Bilbao MK. Transluminal extraction of catheter and guide fragments from the heart and great vessels: 29 collected cases. AJR Am J Roentgenol 1971; 111: 467–72 Bloomfield DA. The non-surgical retrieval of intracardiac foreign bodies: an international survey. Cathet Cardiovasc Diagn 1978; 4: 1–14 Zollikofer C, Nath PH, Castaneda-Zuniga WR et al. Non-surgical removal of intravascular foreign bodies. ROFO 1979; 130: 590–3 Rubinstein ZJ, Morag B, Itzchak Y. Percutaneous removal of intravascular foreign bodies. Cardiovasc Intervent Radiol 1982; 5: 64–8 Uflacker R, Lima S, Melichar AC. Intravascular foreign bodies: percutaneous retrieval. Radiology 1986: 160: 731–5 Furui S, Yamauchi T, Makita K, et al. Intravascular foreign bodies: loop snare retrieval system with a three-lumen catheter. Radiology 1992; 182: 283–4 Nazarian GK, Myers TV, Bjarnason H, et al. Applications of the Amplatz snare device during interventional radiologic procedures. AJR Am J Roentgenol 1995; 165: 673–8 Savander SJ, Brodkin J, Osterman FA. In-situ formation of a loop snare for retrieval of a foreign body without a free end. Cardiovasc Intervent Radiol 1996; 19: 298–301 Cekirge S, Weiss JP, Foister RG et al. Percutaneous retrieval of foreign bodies: experience with the nitinol goose neck snare. J Vasc Interv Radiol 1993; 4: 805–10 Egglin TKP, Dickey KW, Rosenblatt M et al. Retrieval of intravascular foreign bodies: experience in 32 cases. AJR Am J Roentgenol 1995; 164: 1259–64 Gabelmann A, Kramer S, Gorich J. Percutaneous retrieval of lost or misplaced intravascular objects. AJR Am J Roentgenol 2001; 176: 1509–13 Koseoglu K, Parildar M, Oran I et al. Retrieval of intravascular foreign bodies using the goose neck snare. Eur J Radiol 2004; 49: 281–5 Seong KC, Kim JK, Chung JW et al. Tubular foreign body or stent: safe retrieval or repositioning using the coaxialsnare technique. Korean J Radiol 2002; 3: 30–7 Steele PM, Holmes DR, Mankin HT et al. Intravascular retrieval of broken guidewire from the ascending aorta after percutaneous transluminal coronary angioplasty. Cathet Cardiovasc Diagn 1985; 11: 623–8 Bellamy CM, Roberts DH, Ramsdale DR. Ventriculo-atrial shunt causing tricuspid endocarditis: its percutaneous removal. Int J Cardiol 1990; 28: 260–2 Lassers BW, Pickering D. Removal of an iatrogenic foreign body from aorta by means of uretric stone catheter. Am Heart J 1967; 73: 375–8 Yang FS, Ohta I, Chiang HJ et al. Non-surgical retrieval of intravascular foreign body: experience of 12 cases. Eur J Radiol 1994; 18: 1–5 Sheth R, Someshwar V, Warawdekar G. Percutaneous retrieval of misplaced intravascular foreign objects with the Dormia basket: an effective solution. Cardiovasc Intervent Radiol (2007; 30: 48–53; published on line) Grech ED, Ramsdale DR. Percutaneous removal of retained foreign bodies. In: Grech ED, Ramsdale DR, eds. Practical Interventional Cardiology, second edition. London: Martin Dunitz, 2002, 425–40 Foster-Smith KW, Garratt KN, Higano ST et al. Retrieval techniques for managing for managing flexible intracoronary stent misplacement. Cathet Cardiovasc Diagn 1993; 30: 63–8
23. 24. 25. 26. 27. 28.
29. 30.
31. 32. 33. 34. 35. 36. 37. 38. 39. 40.
41. 42. 43. 44.
Eeckout E, Stauffer J, Goy J. Retrieval of a migrated coronary stent by means of an alligator forceps catheter. Cathet Cardiovasc Diagn 1993; 30: 166–8 Roberts DH, Bellamy CM, Ramsdale DR. Removal of a fractured temporary pacemaker electrode using endomyocardial biopsy forceps. PACE 1989; 12: 1835–6 Bogart DB, Earnest JB, Miller JT. Foreign body retrieval using simple snare device. Cathet Cardiovasc Diagn 1990; 19: 248–50 Tatsumi T, Howland WJ. Retrieval of a ventriculoatrial shunt catheter from the heart by a venous technique. J Neurosurg 1970; 32: 593–6 Krone RJ. Successful percutaneous removal of retained broken coronary angioplasty guidewire. Cathet Cardiovasc Diagn 1986; 12: 409–10 Feldman RL, Trice WA, Henneman WW et al. Retrieval of a fractured USCI probe tip from a diseased coronary artery using another fixed-wire balloon catheter, the Cordis Orion. Cathet Cardiovasc Diagn 1990; 19: 257–63 Auge JM, Orial A, Serr C et al. The use of pigtail catheters for retrieval of foreign bodies in the vcardiovascular system. Cathet Cardiovasc Diagn 1984; 10: 2635–638 Bessoud B, de Baere T, Kuoch V et al. Experience at a single institution with endovascular treatment of mechanical complications caused by implanted central venous access devices in pediatric and adult patients. AJR Am J Roentgenol 2003; 180: 527–32 Zuberbuhler JR, Dankner E, Zoltum R et al. Tissue adhesive closure of aorto-pulmonary communications. Am Heart J 1974; 88: 41–46 Moore JW, Cambier PA. Transcatheter occlusion of patent ductus arteriosus. J Intervent Cardiol 1995; 18: 517–31 Cambier PA, Kirby WC, Wortham DC et al. Percutaneous closure of small (< 2.5 mm) patent ductus arteriosus using coil embolization. Am J Cardiol 1992; 69: 815–6 Lloyd TR, Raymond F, Mendelsohn AM et al. Transcatheter occlusion of patent ductus arteriosus with Gianturco coils. Circulation 1993; 88: 1412–20 Akagi T, Iemura M, Tananari Y, et al. Simultaneous double or triple coil technique for closure of moderate sized (> or = 3.0 mm) patent ductus arteriosus. J Interv Cardiol 2001; 14: 91–6 Perry SB, Radtke W, Fellows KE, et al. Coil embolization to occlude aortopulmonary collateral vessels and shunts in patients with congenital heart disease. J Am Coll Cardiol 1989; 13: 100–8 Perry SB, Rome J, Keane JF et al. Transcatheter closure of coronary artery fistulas. J Am Coll Cardiol 1992; 20: 205–9 Okamoto M, Makita Y, Fujii Y et al. Successful coil embolization with assistance of coronary stenting in an adult patient with a huge coronary arterial-right atrial fistula. Intern Med 2006; 45: 865–70 Guo H, You B, Lee JD. Dilated cardiomyopathy caused by a coronary-pulmonary fistula treated successfully with coil embolization. Circ J 2006; 70: 1223–5 Vinuela F, Duckwiler G, Mawad M, MASH Study Group. Guglielmi detachable coil embolization of acute intracranial aneurysm: preoperative anatomical and clinical outcome in 403 patients. J Neurosurg 1997; 86: 475–82 Pouratian N, Oskouian RJ Jr, Jensen ME et al. Endovascular management of unruptured intracranial aneurysms. J Neurol Neurosurg Psychiatry 2006; 77: 572–8 Koebbe CJ, Veznedaroglu E, Jabbour P et al. Endovascular management of intracranial aneurysms: current experience and future advances. Neurosurgery 2006; 59: S93–S102 van Rooji WJ, Sluzewski M. Procedural morbidity and mortality of elective coil treatment of intracranial aneurysm. AJNR Am J Neuroradiol 2006; 27: 1678–80 Nosher JL, Chung J, Brevetti LS et al. Visceral and renal artery aneurysms: a pictorial essay on endovascular therapy. Radiographics 2006; 26: 1687–704
9781841846439-Ch24
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46. 47.
48. 49. 50.
51. 52. 53. 54.
55.
56. 57. 58. 59.
2/25/08
5:54 PM
Page 184
Textbook of peripheral vascular interventions Sachdev U, Baril DT, Ellozy SH et al. Management of aneurysms involving branches of the celiac and the superior mesenteric arteries: a comparison of surgical and endovascular therapy. J Vasc Surg 2006; 44: 718–24 Kereiakes DJ, Long DE, Ivey TD. Coil embolization of a circumflex coronary aneurysm at the time of percutaneous coronary stenting. Cathet Cardiovasc Interv 2006; 67: 607–10 Bachthaler M, Lenhart M, Paetzel C et al. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Catheter Cardiovasc Interv 2004; 62: 380–4 Heve S. Preoperative internal iliac artery coil embolization for aneurysms involving the iliac bifurcation. Acta Chir Belg 2006; 106: 144–8 Boules TN, Selzer F, Stanziale SF et al. Endovascular management of isolated iliac artery aneurysms. J Vasc Surg 2006; 44: 29–37 Kuzuya A, Fujimoto K, Iyomasa S, et al. Transluminal coil embolization of an inferior gluteal artery aneurysm by ultrasoundguided direct puncture of the target vessel. Eur J Vasc Endovasc Surg 2005; 30: 130–2 Maroo A, Rasmussen PA, Masaryk TJ et al. Stent-assisted detachable coil embolization of pseudoaneurysms in the coronary circulation. Catheter Cardiovasc Interv 2006; 68: 409–15 Yamakado K, Nakatsuka A, Tanaka N et al. Transcatheter arterial embolization of ruptured pseudoaneurysms with coils and n-butyl cyanoacrylate. J Vasc Interv Radiol 2000; 11: 66–72 Kobeiter H, Lapeyre M, Becquemin JP et al. Percutaneous coil embolization of postcatheterization arterial femoral pseudoaneurysms. J Vasc Surg 2002; 36: 127–31 Ledermann HP, Schoch E, Jost R et al. Superselective coil embolization in acute gastrointestinal hemorrhage; personal experience in 10 patients and review of the literature. J Vasc Interv Radiol 1998; 9: 753–60 Sharafuddin MJ, Andresen KJ, Sun S et al. Spontaneous extraperitoneal hemorrhage with hemodynamic collapse in patients undergoing anticoagulation: management with selective arterial embolization. J Vasc Interv Radiol 2001; 12: 1231–4 Gaxiola E, Browne KF. Coronary artery perforation repair using microcoil embolization. Cathet Cardiovasc Diagn 1998; 43: 474–6 Burrows PE. Endovascular treatment of vascular anomalies. In: Rutherford RB, ed. Vascular Surgery, sixth edition. Philadelphia: Elsevier Saunders, 2005, 1650–64 Gomes AS. Embolization therapy of congenital arteriovenous malformations: use of alternate approaches. Radiology 1994; 190: 191–98 Suh J, Shin K, Na J et al. Venous malformations: sclerotherapy with a mixture of ethanol and lipiodol. Cardiovasc Interv Radiol 1997; 20: 268
60. 61.
62. 63.
64.
65. 66. 67. 68. 69. 70. 71.
72. 73.
74.
Hammer FD, Boon LM, Mathurin P et al. Ethanol slerotherapy of venous malformations: evaluation of systemic ethanol contamination. J Vasc Interv Radiol 2001; 12: 595–600 Yoo BS, Yoon J, Lee SH, Kim JY, Lee HH, Ko JY, Lee BK, Hwang SO, Choe KH. Guidewire-induced coronary artery perforation treated with transcatheter injection of polyvinyl alcohol form. Cathet Cardiovasc Intervent 2001; 52: 231–4 Dixon SR, Webster MWI, Ormiston JA, Wattie WJ, Hammett CJK. Gelfoam embolization of a distal coronary artery guidewire perforation. Cathet Cardiovasc Intervent 2000; 49: 214–7 Fischell TA, Korban EH, Lauer MA. Successful treatment of distal coronary guidewire-induced perforation with balloon catheter delivery of intracoronary thrombin. Cathet Cardiovasc Intervent 2003; 53: 370–4 Silva JA, Stant J, Ramee SR. Endovascular treatment of a massive retroperitoneal bleeding. Successful balloon catheter-delivery of intra-arterial thrombin. Cathet Cardiovasc Intervent 2005; 64: 218–22 Elsheikh P et al. Only a specific subset of human peripheral-blood monocytes has endothelial-like functional capacity. Blood 2005; 106: 2347–55 Zambides ET. Blood-forming endothelium in human ontogeny: lessons from in utero development and embryonic stem cell culture. Trend Cardiovasc Med 2006; 16: 95–101 Isner JM, Vale PR, Symes JF et al. Assessment of risks associated with cardiovascular gene therapy in human subjects. Circ Res 2001; 89: 389–400 Ferrara N, Alitalo K. Clinical application of angiogenic growth factors and their inhibitors. Nat Med 1999; 5: 1359–64 Urbanek K, Torella D, Sheikh F et al. Myocardial regeneration by activation of multipotent cardiac stem cells in ischemic heart failure. Proc Natl Acad Sci USA 2005; 102: 8692–7 Iba O, Matsubara H, Nozawa Y, et al. Angiogenesis by implantation of peripheral blood mononuclear cells and platelets into ischemic limbs. Circulation 2002; 106: 2019–25 Tateishi-Yuyama E, Matsubara H, Murohara T et al. Therapeutic angiogenesis for patients with limb ischaemia by autologous transplantation of bone-marrow cells: a pilot study and a randomized controlled trial. Lancet 2002; 360: 427–35 Higashi Y, Kimura M, Hara K et al. Autologous bone-marrow mononuclear cell implantation improves endothelium-dependent vasodilation in patients with limb ischemia. Circulation 2004; 109: 1215–8 Saigawa T, Kato K, Ozawa T et al. Clinical application of bone marrow implantation in patients with arteriosclerosis obliterans, and the association between efficacy and the number of implanted bone marrow cells. Circ J 2004; 68: 1189–93 Huang P, Li S, Han M et al. Autologous transplantation of granulocyte colony-stimulating factor-mobilized peripheral blood mononuclear cells improves critical limb ischemia in diabetics. Diabetes Care 2005; 29: 2155–60
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SECTION III Neurovascular
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Epidemiology and pathophysiology of neurovascular disease C Klonaris, A Papapetrou, and A Katsargyris
Historical background The great importance of carotid artery in cerebral blood perfusion was recognized by the ancient Greeks. The name “carotid” comes from the ancient Greek word “caroun” (‘καρου´ν’), which means “to plunge into deep sleep,” or “to stupefy,” because compression of these arteries is said to produce carus or stupor. The correlation of carotid artery disease and cerebral ischemia was first described in 1856, when Savory found carotid artery occlusion at postmortem examination1 of a patient with neurological symptoms. Later, Chiari1a described cerebral emboli arising from an ipsilateral carotid lesion; Hunt suggested that cerebrovascular ischemic symptoms were similar to claudication symptoms in the lower extremities and that both manifestations were due to reduced blood flow.2 In 1927, Moniz2a developed the technique of cerebral angiography for assessment of carotid circulation and visualized four cases of carotid thrombus associated with ipsilateral cerebral infarction. The first attempt to restore blood flow to the ischemic brain was made by Carrea and his colleagues in 1951, but their work was not reported until 1955.3 They excised the proximal part of a diseased internal carotid artery (ICA) and performed an end-to-end anastomosis of the external carotid artery (ECA) to the distal part of the ICA. A different carotid bifurcation reconstruction had been performed
