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
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on application ISBN-10: 1 84184 643 0 ISBN-13: 978 1 84184 643 9
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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
6. 9781841846439-FM 2/28/08 5:20 PM Page vi
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
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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
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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
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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
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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
18. 9781841846439-FM 2/28/08 5:20 PM Page xviii
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 develop- ments
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 signif- icant. 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 interven- tion 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
thera- pies 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 endovas- cular
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
20. 9781841846439-FM 2/28/08 5:20 PM Page xx
21. SECTION I Introduction 9781841846439-Ch01 2/23/08 6:53 PM
Page 1
22. 9781841846439-Ch01 2/23/08 6:53 PM Page 2
23. Epidemiology Peripheral arterial occlusive disease (PAD) of
atherosclerotic origin has an incidence and prevalence nearly equal
to coro- nary 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 claudica-
tion.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 nei- ther.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 rela- tive 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 pri- mary 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 thrombo- cytes, 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 influ- ence 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 infarc- tion 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 inter- mittent
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 endothe- lium leads to deposition and oxidation
of LDL cholesterol, which triggers the subendothelial migration of
blood mono- cytes, 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 endothe- lial 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 impor- tant
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 forma-
tion. 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 recruit-
ment 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 migra- tion. Recently, lipid-lowering diets and treatment
with statins have been shown to increase plaque regression. The
regression of atherosclerotic lesions has been demonstrated by
angiogra- phy 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 physi- cal 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 athero- sclerotic 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 associ- ated with atherosclerosis in femoropopliteal
and tibial territo- ries.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 sus- ceptibility 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 impair- ment, 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 med- ical 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 asympto- matic and unrecognized
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(part I): diagno- sis, 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
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Artery Study: preva- lence of asymptomatic and symptomatic
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Knoke JD, Ridker PM, Fronek A. Risk factors for progression of
peripheral arterial dis- ease in large and small vessels.
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8019 12. Silbernag I, Lang A. Color Atlas of Pathophysiology.
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JF. Atherosclerosis: current con- cepts. Am J Surg 1981; 141: 638
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15. Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on
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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 angiogen- esis with
vascular endothelial growth factor (VEGF) in peripheral arterial
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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
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Novel risk factors for systemic atherosclerosis. A comparison of
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standard cholesterol screening as predictors of peripheral arterial
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Progression of atheroma: a struggle between death and procreation.
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Zatino MA, Giddens DP, et al. Shear stress regulation of artery
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26. 22. Fry DL. Acute vascular endothelial changes associated
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Khalifa AM, Giddens DP. Characterization and evolution of post-
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Glagow S, Zatine MA, et al. Hypertension sustains plaque
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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.
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al. Aortic wall metabolism in relation to susceptibility and
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27. Introduction Endovascular interventions have enjoyed an
explosive growth over the last decade. As the number of
endovascular proce- dures 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 car-
diologist, or interventional radiologist? Consequently, a mul-
tidisciplinary team should be created to determine the optimal
environment for performing combined surgical and endovas- cular
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 ster-
ile conditions will allow immediate conversion from endovascu- lar
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
out- lets 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 operat- ing 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 require- ments. 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 digi- tal 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, anes- thesia equipment,
and circulators. The room should have con- trolled 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 equip- ment
specifically designed for remote or ambulatory applica- tions
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
environ- ment 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 fluo- roscopy is of great
benefit (Figure 2.5). The video monitors should be able to move
from side to side. In addition many sys- tems 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 pro- vide 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 con- ventional
image-intensifier, which allows improved visualiza- tion of the
vasculature. With improved visualization, contrast agent use can be
reduced by approximately 30%.8 This is par- ticularly important
when imaging patients with existing renal dysfunction. Advancements
in technologies have lead to the implemen- tation 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 archiv- ing 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 angio-
graphic 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 interven- tional
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 tor- tuous 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 steno- sis 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 struc- tures 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 posi- tion
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 fea- tures.
Angiographic runs stored on digital memory can be played back for
immediate review and can be stored in mag- netic 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 demon- strate 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 expo- sure. 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 interven- tional 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 angiog- raphy, 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 radi- ographic 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 radia- tion 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 dig- ital 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
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33. SECTION II Techniques 9781841846439-Ch03 2/25/08 5:37 PM
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34. 9781841846439-Ch03 2/25/08 5:37 PM Page 14
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 complica- tions
involve the initial access to the circulation, this impor- tant
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 bifurca- tion 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 cra- nial 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 bifur- cation 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 com- monly related to either too high or too low arterial
entry. When the puncture is too high, a retroperitoneal hemor-
rhage 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 com- pression 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 lig- ament
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 per- form such high
skin incision for fear of entering the abdomi- nal 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 tech- nique where other
approaches fail. Anatomy Anatomical considerations of the femoral
artery and its rela- tionship 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 fail- ure
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 ante- grade 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 desir- able include angioplasty of internal iliacs
or renal transplant artery stenosis (Figure 3.5). Contraindications
to the con- tralateral 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 obstruc- tive 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 arte- rial access is obtained, a guidewire is
advanced into the abdominal aorta and a catheter is chosen to
access the con- tralateral common iliac artery. Diagnostic
catheters useful in crossing the aortic bifurcations include 5- or
6-French diag- nostic 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