textbook of peripheral_vascular_interventions__second_edition

1. Textbook of Peripheral Vascular Interventions 9781841846439-FM 2/28/08 5:20 PM Page i

2. 9781841846439-FM 2/28/08 5:20 PM Page ii

3. 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 9781841846439-FM 2/28/08 5:20 PM Page iii

4. 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. 9781841846439-FM 2/28/08 5:20 PM Page iv

5. 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 Herv. 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 9781841846439-FM 2/28/08 5:20 PM Page v

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7. vii Contents List of Contributors xiii Preface xix Color plates SECTION I: INTRODUCTION 1 1. Epidemiology and pathophysiology of peripheral arterial disease (PAD) 3 GI Pandele and C Dima-Cozma 2. The endovascular suite and equipment 7 K Dougherty and Z Krajcer SECTION II: TECHNIQUES 13 3. Arterial access for endovascular interventions: vascular access 15 JS Jenkins 4. Arterial access for endovascular interventions: radial and brachial arterial access 21 PW McMullan Jr and JS Jenkins 5. Arterial access for endovascular interventions: transradial approach 26 I Henry, M Henry, and M Hugel 6. Arterial access for endovascular interventions: popliteal access to peripheral procedures 29 M Henry, I Henry, and M Hugel 7. Introducer sheaths, catheters, guiding catheters, and guidewires 34 K Dougherty and Z Krajcer 8. Percutaneous transluminal angioplasty 39 T Collins and PW McMullan Jr 9. Cutting balloon angioplasty 45 S Tyagi 10. SilverHawk atherectomy device 50 RS Gammon and JR Nelson 11. Percutaneous peripheral atherectomy using the Rotablator 59 I Henry, M Henry, and M Hugel 12. A new rotational thrombectomy and atherectomy catheter: the Rotarex system 69 I Henry, M Henry, and M Hugel 13. Orbital atherectomy system: a novel means of peripheral vascular rotational atherectomy 79 DT Cragen and RR Heuser 14. Subintimal angioplasty 83 G Markose and A Bolia 15. Recanalization devices for chronic total occlusions (including optical coherent reflectometry) 92 G Baweja and RR Heuser 16. Catheter-directed intra-arterial thrombolytic therapy 99 NN Khanna and RR Kasliwal 17. Thromboaspiration and thrombectomy in peripheral vessels 111 NN Khanna 18. The future of thrombolysis 118 T McNamara 9781841846439-FM 2/28/08 5:20 PM Page vii

8. viii Contents 19. Endovascular treatment for acute and chronic lower extremity deep vein thrombosis 119 PE Thorpe and FJ Osse 20. Stents 132 RR Heuser, KL Waters, CW Hatler, and LM Kelly 21. Role of covered stents in peripheral arterial diseases 140 M Henry, I Henry, and M Hugel 22. Embolic protection devices 156 M Henry, I Henry, A Polydorou, and M Hugel 23. Vascular closure devices 168 ZG Turi 24. Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis 179 JA Silva and JS Jenkins SECTION III: NEUROVASCULAR 185 25. Epidemiology and pathophysiology of neurovascular disease 187 C Klonaris, A Papapetrou, and A Katsargyris 26. Neuroradiological anatomy 192 MH Wholey and WS Wu 27. Doppler ultrasound and carotid angioplasty: carotid ultrasonography and transcranial Doppler 199 S Kownator and F Luizy 28. The value of transcranial Doppler ultrasonography before, during, and after surgery for carotid occlusive disease 207 NM Bornstein and AY Gur 29. Carotid plaque characterization using ultrasound 211 AN Nicolaides, M Griffin, S Kakkos, G Geroulakos, E Kyriacou, and N Georgiou 30. Cerebral perfusion imaging 229 W-J Jiang 31. Stent-assisted angioplasty for symptomatic atherosclerotic intracranial stenosis 238 W-J Jiang 32. Intracranial stenting for cerebrovascular pathology 247 EI Levy, AS Boulos, BR Bendok, SH Kim, AI Qureshi, LR Guterman, and LN Hopkins 33. The stroke unit 255 P Lylyk and JF Vila 34. Interventional treatment of acute ischemic stroke: past, present, and future 288 CS Eddleman, ZA Hage, DL Surdell, EI Levy, RM Samuelson, YA Mikhaeil, and BR Bendok 35. Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations 300 M Henry, A Polydorou, I Henry, Ad Polydorou, and M Hugel 36. Complications of internal carotid artery stenting and their management 336 DL Surdell, ZA Hage, CS Eddleman, S Das, E Duckworth, MK Eskandari, IA Awad, HH Batjer, and BR Bendok 37. Which patients should be referred for surgical endarterectomy and not have carotid stenting 345 FJ Criado and C Gallagher 38. Common carotid artery: PTA stenting 348 J Franke, G Robertson, and H Sievert 39. Percutaneous transluminal angioplasty of the subclavian arteries 353 M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel 9781841846439-FM 2/28/08 5:20 PM Page viii

9. Contents ix 40. Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis 371 V Polydorou, I Henry, A Polydorou, M Henry, Ad Polydorou, J Stephanides, M Hugel, and S Anagnostopoulou 41. Elective endovascular revascularization of the intracranial cerebral arteries 382 HC Schumacher, PM Meyers, B Bateman, and RT Higashida SECTION IV: UPPER EXTREMITY ARTERIAL DISEASES 399 42. Upper extremity arterial diseases 401 J Laredo and BB Lee 43. Compression syndromes of the superior thoracic aperture 408 JE Molina SECTION V: THORACIC AORTA 415 44. Thoracic aorta: epidemiology and pathophysiology 417 EB Diethrich 45. Radiology and anatomy of the thoracic aorta 422 AR Owen, GH Roditi, and AW Reid 46. Thoracic aorta: thoracic aortic aneurysms 432 EB Diethrich 47. Thoracic aortic dissection 439 J May, GH White, and JP Harris SECTION VI: ABDOMINAL AORTA 447 48. Abdominal aortic aneurysm treatment by endoluminal exclusion: a historical perspective 449 JC Parodi, CJ Schnholz, and RR Heuser 49. Role of Doppler ultrasound in the assessment of peripheral vascular disease 456 K Irshad, M Ali, AW Reid, A Sinha, and DB Reid 50. Abdominal aortic dissections 461 OC Morcos, JC Pereda, and ML Marin 51. Endovascular treatment of abdominal aortic occlusive disease 467 C Klonaris and A Katsargyris SECTION VII: THORACOABDOMINAL ANEURYSMS AND DISSECTIONS 473 52. Thoracoabdominal aneurysms and dissections: current indications and management 475 JF Dowdall, Q Lu, and RK Greenberg SECTION VIII: ATHEROSCLEROTIC RENAL ARTERY STENOSIS 485 53. Atherosclerotic renal artery stenosis: epidemiology and pathophysiology 487 KI Paraskevas, DP Mikhailidis, and G Hamilton 54. Radiological assessment of the renal arteries 494 A Al-Kutoubi 55. Endovascular treatment of a renal artery stenosis: techniques, indications, and results 502 M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel 56. Renal angioplasty and stenting under protection devices 525 M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel 9781841846439-FM 2/28/08 5:20 PM Page ix

10. 57. Renal artery stenosis: when to refer to surgery? 539 C Klonaris, A Katsargyris, and A Giannopoulos 58. Non-atherosclerotic renovascular disease 544 JM Garasic and K Rosenfield SECTION IX: CELIAC AND MESENTERIC ARTERIES 551 59. Etiology, natural history, and pathophysiology of mesenteric ischemia 553 JA Silva 60. Assessment of mesenteric ischemia 557 JA Silva 61. Conventional angiography, CTA, and MRA of the mesenteric arteries 562 Y-W Chi and JA Silva 62. Duplex ultrasound of the mesenteric arteries 570 Y-W Chi and JA Silva 63. Endovascular therapy for mesenteric ischemia 574 JA Silva 64. Mesenteric ischemia: surgical revascularization and indications for surgery 581 JA Silva and DE Allie SECTION X: LOWER EXTREMITY 587 65. Epidemiology and pathophysiology of peripheral arterial disease of the lower extremities 589 C Klonaris, A Papapetrou, and A Giannopoulos 66. Lower extremity arterial disease assessment 593 KF Murphy, K Irshad, A Sinha, and DB Reid 67. Lower extremity: other techniques 601 ML Brennan and L Cho 68. Iliac occlusive diseases 606 DT Cragen and RR Heuser 69. Procedures for the hypogastric artery 614 J Cynamon and P Prabhaker 70. Femoropopliteal disease 625 E Calabrese and F Camerano 71. When to refer to surgery for femoropopliteal disease 630 N Morrissey 72. Infrapopliteal arterial diseases: angioplasty and stenting 633 E Calabrese 73. Critical limb ischemia 639 DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola 74. Acute limb ischemia 648 DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola 75. Endovascular treatment for infrainguinal failing graft 656 A de Carvalho Lobato and DF Colli Jr 76. Thromboangiitis obliterans (Buergers disease) 661 A Pokrovsky and AV Chupin 77. Percutaneous endovascular treatment of peripheral aneurysms 670 M Henry, I Henry, and M Hugel x Contents 9781841846439-FM 2/28/08 5:20 PM Page x

11. Contents xi SECTION XI: OTHER LOCALIZATIONS 681 78. Embolization in peripheral territory 683 CJ Schnholz, E Mendaro, and K Ehrens 79. Uterine artery embolization for fibroids 692 J Pisco and M Duarte 80. Hemodialysis access intervention 699 E Calabrese and B Yasin 81. Endovascular surgery in treatment of some congenital heart defects 703 BG Alekyan, VP Podzolkov, VA Garibyan, MG Pursanov, KE Kardenas, and E Yu Danilov 82. Endovascular treatment of some congenital diseases: hemangiomas and vascular malformations 712 BB Lee, J Laredo, DH Deaton, and RF Neville SECTION XII: UNUSUAL VASCULAR DISEASES OF THE EXTREMITIES 723 83. Endovascular management of Budd-Chiari syndrome suprahepatic inferior vena cava occlusive disease 725 BB Lee, J Laredo, DH Deaton, and RF Neville 84. Unusual vascular conditions of the extremities 732 DH Deaton, RF Neville, J Laredo, and BB Lee 85. Interventions in inflammatory arterial disease 736 S Rajagopal and L Gopalakrishnan 86. Vascular involvement in Behets disease 743 TW Kwon SECTION XIII: MULTIVASCULAR DISEASE 749 87. Potential of endovascular surgery in the treatment of patients with ischemic heart disease associated with other arterial pools pathology 751 LB Bockeria, BG Alekyan, Yu I Buziashvili, EZ Golukhova, TG Niritina NP Mironov, AV Ter-Akopyan, NV Zakarian, and AV Staferov SECTION XIV: TREATMENTS FOR RESTENOSIS 761 88. Pathophysiology of restenosis 763 E Kedhi, J-F Tanguay, and L Bilodeau 89. Interventional therapy: new approaches 770 E Kedhi and L Bilodeau 90. Update on peripheral vascular brachytherapy 776 R Waksman 91. Gene-based and angiogenesis therapy in cardiovascular diseases 782 R Baffour, S Fuchs, and R Kornowski SECTION XV: PTA/STENTING COMPLICATIONS 789 92. Complications of peripheral interventions 791 DT Cragen and RR Heuser 93. Contrast-induced nephropathy 799 G Marenzi and AL Bartorelli 9781841846439-FM 2/28/08 5:20 PM Page xi

12. xii Contents SECTION XVI: PHARMACOLOGICAL TREATMENTS AND RISK FACTOR MANAGEMENT 809 94. Pharmacological treatment in peripheral arterial disease 811 GI Pandele and C Dima-Cozma 95. Risk factors in peripheral arterial disease 822 GI Pandele and C Dima-Cozma SECTION XVII: VENOUS DISEASE 827 96. The anatomy, epidemiology, and pathophysiology of venous disease 829 JI Greenberg, N Angle, and J Bergan 97. Diagnostic evaluation of venous disease 835 B Abai and N Labropoulos 98. Contrast imaging studies of the lower extremity 841 GE Pineda and D Mukherjee 99. Interventional therapy for pulmonary embolism 849 S Faintuch, FB Collares, and GM Martinez Salazar 100. Superior and inferior vena cava thrombosis 858 J Pisco and M Duarte 101. Varicose veins 864 CK Shortell and J Bergan 102. Endovenous laser therapy for varicose veins 870 NN Khanna 103. Vena caval filters 873 NN Khanna 104. Foam treatment of varicose veins 879 JI Greenberg, N Angle, and J Bergan Index 889 9781841846439-FM 2/28/08 5:20 PM Page xii

13. Contributors B Abai MD Department of Surgery, Robert Wood Johnson Medical School, Cooper University Hospital, Camden, NJ, USA. BG Alekyan MD PhD Interventional Cardiology and Angiology Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. M Ali MD Department of Radiology, King Edward Medical University, Lahore, Pakistan. A Al-Kutoubi MD FRCR DMRD Department of Diagnostic Radiology, The American University of Beirut Medical Center, Beirut, Lebanon. DE Allie MD Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA. S Anagnostopoulou MD PhD Anatomy Department, University of Athens, Greece. N Angle MD FACS Section of Vascular Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA. IA Awad BS MSC MD DABNS FACS FICS Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. R Baffour PhD The Cardiovascular Research Institute, Washington Hospital Center, Washington, DC, USA. AL Bartorelli MD Interventional Cardiology, Centro Cardiologico Monzino, IRCCS, Institute of Cardiology of the University of Milan, Milan, Italy. B Bateman MD College of Physicians and Surgeons, Columbia University Medical Center, New York, NY, USA. HH Batjer MD FACS Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. G Baweja MD Sarver Heart Center, University of Arizona, Tucson, AZ, USA. BR Bendok MD Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. J Bergan MD Department of Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA. L Bilodeau MD Montreal Heart Institute, Montreal, Quebec, Canada. LB Bockeria MD PhD Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. A Bolia MBChB DMRD FRCR Department of Radiology, Leicester Royal Infirmary, Leicester, UK. NM Bornstein MD Stroke Unit, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. AS Boulos MD Section of Endovascular Surgery, The Neuroscience Institute; Division of Neurosurgery, Albany Medical Center, Albany, NY, USA. ML Brennan PhD Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA. Yu I Buziashvili MD PhD Clinical and Diagnostic Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. E Calabrese MD National Center for Limb Salvage Clinical Institute Citt di Pavia, Pavia, Italy. F Camerano National Center for Limb Salvage, Clinical Institute Citt di Pavia, Pavia, Italy. Y-W Chi DO RVT RPVI FSVMA Vascular Lab Cardiology, Heart and Vascular Institute, Metairie, LA, USA. L Cho MD FACC Womens Cardiovascular Center, The Cleveland Clinic Foundation, Cleveland, OH, USA. AV Chupin, AV Vishnevsky Institute of Surgery, Moscow, Russia. FB Collares MD Vascular and Interventional Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. DF Colli Jr MD Angiography Unit, Hospital Samaritano-SP, So Paulo, Brazil. TJ Collins MD FACC Department of Cardiovascular Diseases, Ochsner Medical Center, New Orleans, LA, USA. DT Cragen MD Department of Cardiology, St. Luke's Hospital and Medical Center, Phoenix, AZ, USA. Frank J Criado MD FACS FSVM Vascular Surgery and Endovascular Intervention, Union Memorial Hospital-MedStar Health, Baltimore, MD, USA. J Cynamon MD Division of Vascular Interventional Radiology, Montefiore Medical Center, Bronx, NY, USA. E Yu Danilov PhD Department of Psychology and Center for Neuroscience, University of Wisconsin-Madison, Madison, WI, USA. S Das MD PhD Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. A de Carvalho Lobato PhD Vascular & Endovascular Surgery Institute, Beneficncia Portuguesa de So Paulo Hospital, So Paulo, Brazil. DH Deaton MD FACS Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA. EB Diethrich MD Department of Cardiovascular Surgery, Arizona Heart Institute and Hospital, Phoenix, AZ, USA. xiii 9781841846439-FM 2/28/08 5:20 PM Page xiii

14. C Dima-Cozma Department of Internal Medicine, 6th Medical Clinic, Iasi University of Medicine and Pharmacie, Gr. T. Popa, Iasi, Romania. K Dougherty CRTT SICP Peripheral Vascular Interventional Research, St. Lukes Episcopal Hospital and the Texas Heart Institute, Houston, TX, USA. JF Dowdall MD Cleveland Clinic Foundation, Cleveland, OH, USA. M Duarte MD Hospital Pulido Valente, Lisbon, Portugal. 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. Josephs Hospital and Medical Center, Phoenix, AZ, USA. M K Eskandari MD Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. S Faintuch MD Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. J Franke MD Cardiovascular Center Frankfurt, Seckbacher Landstrasse, Frankfurt, Germany. S Fuchs MD 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 Physicians Association, Austin, TX, USA. JM Garasic MD Department of Medicine, Brigham and Womens Hospital, Harvard Medical School, Boston, MA, USA. VA Garibyan MD Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. N Georgiou RN 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 MD Department of Surgery, Athens University Medical School, Athens, Greece. EZ Golukhova MD PhD Non-Invasive Arrhythmology Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. L Gopalakrishnan MD Department of Cardiology, Institute for Cardiac Treatment and Research, Southern Railway Headquarters Hospital, Perambur, Chennai, India. JI Greenberg MD FRCS Department of Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA. RK Greenberg MD Department of Endovascular Research, Cleveland Clinic Foundation, Cleveland, OH, USA. M. Griffin MSc PhD The Vascular Noninvasive Screening and Diagnostic Centre, London, UK. AY Gur MD PhD Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. LR Guterman PhD MD Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo State, University of New York, Buffalo, NY, USA. ZA Hage MD Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University Chicago, IL, USA. 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 PhD RN Phoenix Heart Center, St. Josephs Hospital and Medical Center, Phoenix, AZ, USA. CJ Hebert RT-R RCIS Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA I Henry MD Polyclinique Bois Bernard, Bois Bernard, France. M Henry MD Cabinet de Cardiologie, Nancy, France; Global Research Institute, Apollo Clinic, Hyderabad, India. RR Heuser MD FACC FACP FESC Department of Cardiology, St. Luke's Medical Center; University of Arizona College of Medicine, Phoenix, AZ, USA. RT Higashida MD Department of Radiology, University of California, San Francisco Medical Center, San Francisco, CA, USA. LN Hopkins MD Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Buffalo, NY, USA. M Hugel RN Cabinet de Cardiologie, Nancy, France. K Irshad FRCS King Edward Medical University, Lahore, Pakistan. JS Jenkins 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, Peoples Republic of China. S Kakkos MD PhD DIC Division of Vascular Surgery, Imperial College, London, UK. KE Kardenas MD PhD Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. xiv Contributors 9781841846439-FM 2/28/08 5:20 PM Page xiv

15. RR Kasliwal Indraprastha Apollo Hospitals, New Delhi, India. A Katsargyris MD 1st Department of Surgery, Vascular Division, Athens University Medical School, Athens, Greece. E Kedhi MD Medisch Centrum Rijnmond Zuid (MCRZ) - Hospital Rotterdam, Rotterdam, The Netherlands. LM Kelly RN MBA Phoenix Heart Center, St. Josephs Hospital and Medical Center, Phoenix, AZ, USA. 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 MD Athens University Medical School, Athens, Greece. R Kornowski MD Cardiac Catheterization Unit, Department of Cardiology, Rabin Medical Center, Petah Tikva, Israel. S Kownator MD Cabinet de cardiologie, Thionville, France. Z Krajcer MD Baylor College of Medicine, University of Texas Health Science Center, Houston, TX, USA. TW Kwon MD PhD Department of Surgery, University of Ulsan College of Medicine and Asan Medical Center, Songpa-gu, Seoul, South Korea. E Kyriacou PhD Department of Computer Science and Engineering, Frederick University Cyprus, Palouriotisa, Nicosia, Cyprus. N Labropoulos BSc (Med) PhD DIC RVT Department of Surgery, Stony Brook University Medical Center, Stony Brook, NY, USA. J Laredo MD PhD RVT Division of Vascular Surgery, Georgetown University Hospital, Washington, DC, USA. BB Lee MD PhD Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA. EI Levy MD Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Millard Fillmore Gates Circle Hospital, NY, USA. Q Lu MD 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 MD Coronary Care Unit, Centro Cardiologico Monzino, IRCCS, Institute of Cardiology of the University of Milan, Milan, Italy. ML Marin MD Department of Surgery, Mount Sinai School of Medicine, New York, NY, USA. G Markose 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 Department of Interventional Cardiology, Ochsner Medical Center, New Orleans, LA, USA. T McNamara MD Section of Interventional Radiology, University of California School of Medicine, Los Angeles, CA, USA. E Mendaro MD Department of Vascular Interventional Radiology, Phoenix Heart Center, St. Josephs 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 MD Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. 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 MD Volynskaya Hospital, Moscow, Russia. EV Mitran MD PhD Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA. JE Molina MD Cardiothoracic Surgery, Minneapolis, MN, USA. OC Morcos MD Division of Vascular Surgery, University of Illinois at Chicago, Chicago, IL, USA. N Morrissey MD FACS Division of Vascular Surgery, New York-Presbyterian Hospital, Weill Medical College, Cornell University, New York, NY, USA. D Mukherjee MD Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA. KF Murphy MRCS Vascular & Endovascular Institute, Wishaw Hospital, Scotland. JR Nelson BS Austin Heart Physicians Association, Austin, TX, USA. RF Neville MD 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. Contributors xv 9781841846439-FM 2/28/08 5:20 PM Page xv

16. TG Niritina MD PhD Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. FJ Osse MD Endovascular Surgery, Sanmaritano Hospital, So Paulo, Brazil. AR Owen BSc MRCP FRCR Department of Radiology, Glasgow Royal Infirmary, Glasgow, UK. GI Pandele MD PhD Department of Internal Medicine, 6th Medical Clinic, Iasi University of Medicine and Pharmacie, Gr. T. Popa, Iasi, Romania. A Papapetrou MD FEBVS Department of Vascular Surgery, Athens University School of Medicine, Athens, Greece. 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 MD Department of Vascular Surgery, Phoenix Heart Center, St. Josephs Hospital and Medical Center, Phoenix, AZ, USA. RR Patlola MD Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA. JC Pereda MD South Miami Hospital, Miami, FL, USA. GE Pineda MD Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA. J Pisco MD New University of Lisbon, Lisbon, Portugal. VP Podzolkov MD PhD Congenital Heart Disease Surgery Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. A Pokrovsky MD AV Vishnevsky Institute of Surgery, Moscow, Russia. 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 MD PhD Department of Interventional Cardiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. AI Qureshi MD Department of Neurology and Neurosciences, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA. S Rajagopal MD Department of Cardiology, Institute for Cardiac Treatment and Research, Southern Railway Headquarters Hospital, Perambur, Chennai, India. AW Reid MD FRCR FRCP Glasgow Royal Infirmary, Glasgow, Scotland. DB Reid MD FRCS Vascular & Endovascular Institute, Wishaw Hospital, Scotland. G Robertson MD Emory University Heart and Vascular Center, Atlanta, GA, USA. GH Roditi FRCP FRCR Department of Radiology, Glasgow Royal Infirmary, Glasgow, UK. K Rosenfield MD 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 Schnholz MD Department of Radiology, Phoenix Heart Center, St. Josephs Hospital and Medical Center, Phoenix, AZ, USA. CK Shortell MD 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 Tchefuncte Cardiovascular Associates and TCA Research, Covington, LA, USA. A Sinha FRCS 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 MD Department of Surgery, Veterans Hospital, Athens, Greece. DL Surdell MD Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. J-F Tanguay MD Montreal Heart Institute, Montreal, Quebec, Canada. AV Ter-Akopyan MD PhD Hospital Volynskaya, Moscow, Russia. PE Thorpe MA MD FSIR Endovascular Surgery & Interventional Radiology, Arizona Heart Hospital, Phoenix, AZ, USA. ZG Turi MD 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. xvi Contributors 9781841846439-FM 2/28/08 5:20 PM Page xvi

17. CM Walker MD Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA. KL Waters FNP-C Phoenix Heart Center, St. Josephs 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 Citt di Pavia, Pavia, Italy. NV Zakarian MD PhD Department of Interventional Cardiology and Angiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. Contributors xvii 9781841846439-FM 2/28/08 5:20 PM Page xvii

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19. xix 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, 200000 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 Valrie Davot whose help in coordinating our con- tributing 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 9781841846439-FM 2/28/08 5:20 PM Page xix

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21. SECTION I Introduction 9781841846439-Ch01 2/23/08 6:53 PM Page 1

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23. 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 anklebrachial index resting and during exercise, which is normally greater than 0.90. PAD is still underdiagnosed because only 1030% 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 anklebrachial 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 coun- tries. 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 inacti- vates 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 byApo 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 pro- gressively 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 Epidemiology and pathophysiology of peripheral arterial disease (PAD) GI Pandele and C Dima-Cozma 1 9781841846439-Ch01 2/23/08 6:53 PM Page 3

24. 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 9095% 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: Marfans, Ehlers-Danlos or Gsell- Erdheim syndrome; infection: lues, mycosis in immune-deficient patients. One of the complications of aneurysms is rupturing, accompa- nied 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 regurgi- tation, 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 thromboem- bolism, 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 cardiomy- opathy, or from cardiac valves, which can occur in aortic stenosis, endocarditis, from prosthetic valves, or by paradoxi- cal 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,reproduc- ing 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 hyperho- mocysteinemia. 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 hypercoagu- lable state and abnormalities in platelet biology.17 In observational studies, elevated homocysteine levels are associated with PAD. Among other atherothrombotic bio- markers, 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 allow- ing platelet adhesion to the damaged endothelium. Platelet activation will determine structural and biochemical modifi- cation 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 modifi- cation. Intimal thickening may represent the adaptive response of increased wall stress as has been observed in infants and intrauterine life and was demonstrated experi- mentally 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 4 Textbook of peripheral vascular interventions 9781841846439-Ch01 2/23/08 6:53 PM Page 4

25. Epidemiology and pathophysiology of peripheral arterial disease (PAD) 5 experimental animal models, but associated with hyper- lipemia, 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 atherosclerotic plaques, thrombosis, ulcerations, and aneurysms. The blood flow in the infrarenal aorta is condi- tioned 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 con- tributing 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 oxida- tive stress, and accumulation of somatic mitochondrial DNA mutations) compatible with anacquired metabolic myopathy that manifests clinically as muscle weakness, functional impairment, and walking limitation.29 REFERENCES 1. Gardner AW, Poehlman ET. Exercise rehabilitation programs for the treatment of claudication pain. A meta-analysis. JAMA 1995; 274: 97580 2. Almahameed A. Peripheral arterial disease: recognition and medical management. Cleve Clin J Med 2006; 73 (7): 6216 3. McDermott MM, Greenland P, Liu K, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA 2001; 286: 1599606 4. Criqui MH. Peripheral arterial disease: epidemiological aspects. Vasc Med 2001; 6 (Suppl. 1): 37 5. Kannel WB, McGee DL. Update on some epidemiologic features of intermittent claudication: The Framingham Study. J Am Geriatr Soc 1985; 33: 1318 6. Stoffers HE, Rinkens PE, Kester AD. The prevalence of asymptomatic and unrecognized peripheral arterial occlusive disease. Int J Epidemiol 1996; 25: 282290. 7. Higgins JP, Higgins JA. Peripheral arterial disease (part I): diagnosis, epidemiology and risk factors. J Okla State Med Assoc 2002; 95 (12): 76571 8. 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): 12691 9. 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: 384392 10. 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): 26239 11. Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 1993; 362: 8019 12. Silbernag I, Lang A. Color Atlas of Pathophysiology. Stuttgart: Thieme, 2000: 23641 13. Kinlough-Rathbone RL, Mustard JF. Atherosclerosis: current concepts. Am J Surg 1981; 141: 638 14. Meru AV, Mittra S, Thyagarajan B, Chugh A. Intermittent claudication: an overview. Atherosclerosis 2006; 187 (2): 22137 15. 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: 147279 16. 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: 193338 17. Steinberg HO, Baron AD. Vascular function, insulin resistance and fatty acids. Diabetologia 2002; 45: 62334 18. 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): 7008 19. 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): 248185 20. Geng YJ, Libby P. Progression of atheroma: a struggle between death and procreation. Arterioscler Thromb Vasc Biol 2002; 22: 137080 21. Zarins CK, Zatino MA, Giddens DP, et al. Shear stress regulation of artery lumen diameter in experimental atherogenesis. J Vasc Surg 1987; 5: 413 9781841846439-Ch01 2/23/08 6:53 PM Page 5

26. 22. Fry DL. Acute vascular endothelial changes associated with increased blood velocity gradients. Circ Res 1968; 22: 165 23. Khalifa AM, Giddens DP. Characterization and evolution of post- stenotic flow disturbances. J Biomech 1981; 14: 279 24. Xu CP, Glagow S, Zatine MA, et al. Hypertension sustains plaque progression despite reduction of hypercholesterolemia. Hypertension 1991; 18 (2): 123 25. Olin JW. Hypertension and peripheral arterial disease. Vasc Med 2005; 10: 2416 26. 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: 75761 27. 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 28. Gordon T, Kannel WB. Predisposition to atherosclerosis in the head, heart and legs: The Framingham Study. JAMA 1972; 221: 6616 29. Brass EP, Hiatt WR. Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease. Vasc Med 2000; 5: 559 6 Textbook of peripheral vascular interventions 9781841846439-Ch01 2/23/08 6:53 PM Page 6

27. 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 mul- tidisciplinary 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 catheter- based 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 in- room 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 shat- terproof lighting that allows low, medium, and ultra-bright capabilities. Individual xenon headlamps are also necessary for hybrid procedures. Vascular instrumentation and instru- ment 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.13 Digital imaging has made large steps since its introduction in the 1980s. 7 The endovascular suite and equipment K Dougherty and Z Krajcer 2 9781841846439-Ch02 2/28/08 12:03 PM Page 7

28. 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).57 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 insuffi- ciency 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 bi- plane 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 8 Textbook of peripheral vascular interventions Figure 2.1 A large room is necessary when accommodating endovascular, hybrid, and robotic equipment, and the support staff needed to perform those procedures. 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. 9781841846439-Ch02 2/28/08 12:03 PM Page 8

29. The endovascular suite and equipment 9 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. 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.) (a) (b) 9781841846439-Ch02 2/28/08 12:03 PM Page 9

30. 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 510 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 three- dimensional 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 processing offers results in immediate image availability. Fixed systems also allow image-review functions to be directly acces- sible 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 15 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 10 Textbook of peripheral vascular interventions 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. Figure 2.7 (a) Digitally subtracted and; (b) 3D reconstructed angiography of a carotid pseudoaneurysm. 9781841846439-Ch02 2/28/08 12:03 PM Page 10

31. The endovascular suite and equipment 11 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 endo- graft 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 measure- ment 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 con- cern 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 intes- tinal. 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 elonga- tion or distortion of the structures occurs at the edges of the field, known as parallax. This type of artifact is also exagger- ated 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 dra- matically 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. 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 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.913 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 walls913 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 (0.0140.018 inches, 180300 cm in length); balloons (340 mm in diameter and 2060 mm in length); inflation device with gauge; stents and covered stents. 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. 9781841846439-Ch02 2/28/08 12:03 PM Page 11

32. 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 alterna- tives. 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. 12 Textbook of peripheral vascular interventions REFERENCES 1. 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: 2545 2. 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: 15 3. 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: 516 4. Kotter E, Langer M. Digital radiography with large-area flat-panel detector. Eur Radiol 2002; 12: 256270 5. Spahn M, Strotzer M,Vlk M, et al. Digital radiography with a large- area, amorphous-silicon, flat-panel x-ray detector system. Invest Radiol 2000; 35: 2606 6. Neitzel U, Bhm 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: 21623 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: 17049 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: 5627 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 inter- operability 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: 2216 13. Bush WH, Jones D, Brannen GE. Radiation dose to personnel during percutaneous renal calculus removal. Am J Radiol 1985; 145: 12614 9781841846439-Ch02 2/28/08 12:03 PM Page 12

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35. 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 surgi- cally 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 con- sider 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 morpholog- ical 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 femoralpopliteal 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 12 cm cranial to the level of the center of the femoral head. The needle is directed through an oblique downward course while palpat- ing 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 Arterial access for endovascular interventions: vascular access JS Jenkins 3 9781841846439-Ch03 2/25/08 5:37 PM Page 15

36. 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.68 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. Contralateral iliofemoral artery access Introduction The acquisition and maintenance of vessel access from arterial puncture until sheath removal plays a major role in determining whether peripheral intervention is a success or failure.610 Retrograde common femoral artery access remains by far the most commonly used site and the easiest arterial access method. Peripheral interventionalists should be well familiar- ized 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 12 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 dis- eased 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 suit- able 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 16 Textbook of peripheral vascular interventions Anterior superior Iliac spine Inguinal skin crease Inguinal ligament Common femoral artery Superficial femoral artery Profunda femoral artery Femoral head 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. 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. < 90 9781841846439-Ch03 2/25/08 5:37 PM Page 16

37. Arterial access for endovascular interventions: vascular access 17 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 tech- nically 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 pushabil- ity 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 non- segmented Palmaz stents longer than 30 mm are to be used then 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 Figure 3.3 A 6-French internal mammary artery (IMA) or Judkins right 4 catheter will direct the guidewire to the contralateral iliac artery. Figure 3.4 The proximity of these lesions to the common femoral artery puncture site precludes antegrade femoral artery access. 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. Guidewire 6-French IMA diagnostic catheter Sheath Guide Guidewire Guidewire Crossover guide Sheath 9781841846439-Ch03 2/25/08 5:37 PM Page 17

38. 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 superi

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