Table of Contents

Cover

Title Page

Contributors

Preface

Chapter 1: Epidemiology of Peripheral Artery Disease

Definitions
PAD Clinical Syndromes
Prevalence and Incidence
Risk Factors for Development of PAD
Awareness of PAD in the Community
Progression, Natural History, and Outcomes of PAD
Summary
References

Chapter 2: Office Evaluation of Peripheral Artery Disease – History and Physical Examination Strategies

Introduction
Identifying At-Risk Individuals
Regional Symptom Analysis
Physical Examination
References

Chapter 3: Vascular Laboratory Evaluation of Peripheral Artery Disease

Introduction
Physiological Testing
Duplex Scanning
Vascular Laboratory Accreditation
References

Chapter 4: Magnetic Resonance, Computed Tomographic, and Angiographic Imaging of Peripheral Artery Disease

Introduction
Computed Tomography Angiography
Magnetic Resonance Angiography
Conventional Angiography
Intravascular Ultrasonography
Results
Conclusion
References

Chapter 5: Non-atherosclerotic Peripheral Artery Disease

Introduction – Presentation of Peripheral Artery Disease
When Should Non-atherosclerotic Causes of PAD Be Suspected?
Entities that Make up Non-atherosclerotic PAD
Diagnostic Evaluation of Patients with Leg Pain with Exertion
Treatment Considerations
Conclusions
References

Chapter 6: Medical Therapy of Peripheral Artery Disease

Introduction
Atherosclerotic Risk Factor Management
Management of Claudication
Exercise Therapy
Claudication Management Strategies: A Comparison
Lower Extremity Wound Care
Summary
References

Chapter 7: Endovascular Treatment of Peripheral Artery Disease

Introduction
Clinical Background
Background for Endovascular Therapy
Clinical Evidence for Peripheral Intervention
Post-procedural Care
Conclusion
References

Chapter 8: Surgical Management of Peripheral Artery Disease

When to Refer Patients with Claudication
When to Refer Patients with CLI
Revascularization Options and Results
Complications of Revascularization
Preoperative Evaluation and Management
Conclusion
References

Index

End User License Agreement

List of Illustrations

Chapter 1: Epidemiology of Peripheral Artery Disease

Figure 1.1 Prevalence of peripheral artery disease by age in men and women in high-income countries (HICs) and low- to middle-income countries (LMICs).
Figure 1.2 Comparison of the global and US prevalence of peripheral artery disease (PAD) and two other common cardiovascular diseases (congestive heart failure [CHF] and atrial fibrillation [AF]).
Figure 1.3 Ethnic-specific prevalence of peripheral arterial disease: (a) men; (b) women. AA, African American; AI, American Indian; AS, Asian American; HS, Hispanic; NHW, non-Hispanic white.
Figure 1.4 Mean prevalence of claudication in large population studies.
Figure 1.5 Odds ratios (ORs) of major peripheral artery disease risk factors in high-income countries (HICs) and low- to middle-income countries (LMICs). CVD, cerebrovascular disease; CRP, C-reactive protein; HDL, high-density lipoprotein; BMI, body mass index.
Figure 1.6 (a) Comparison of disease prevalence and the relative awareness of the general US population. (b) Perceived consequences of peripheral artery disease (PAD) among “PAD aware” individuals.
Figure 1.7 Adjusted odds of a cardiovascular event by ankle–brachial index (ABI). Data from the placebo arm of the Appropriate Blood Pressure Control in Diabetes study. CV, cardiovascular; MI, myocardial infarction.
Figure 1.8 Typical overlap in vascular disease affecting different territories. Based on Reduction of Atherothrombosis for Continued Health (REACH) registry data. PAD, peripheral artery disease.
Figure 1.9 Survival of patients with peripheral arterial disease compared with healthy controls. IC, intermittent claudication; CLI, critical limb ischemia.
Figure 1.10 The natural history of peripheral artery disease (PAD). CV, cerebrovascular; MI, myocardial infarction; CLI, critical limb ischemia.

Chapter 2: Office Evaluation of Peripheral Artery Disease – History and Physical Examination Strategies

Figure 2.1 Posterior versus anterior stroke symptom. ACI, anterior circulation infarction; PCI, posterior circulation infarction.
Figure 2.2 Walking distance questionnaire.

Chapter 3: Vascular Laboratory Evaluation of Peripheral Artery Disease

Figure 3.1 (a) Normal Doppler signal showing triphasic flow. (b) Monophasic Doppler signal obtained distal to a hemodynamically significant arterial lesion. The wave is dampened and delayed. Note the absence of forward flow in late diastole.
Figure 3.2 A series of pulse-volume recording cuffs placed at multiple levels of the limb(s).
Figure 3.3 (a) Normal pulse-volume recording (PVR) waveform. The “notch” in the down-slope (dicrotic notch) results from the reflected pulse wave during diastole. (b) PVR obtained distal to a hemodynamically significant arterial lesion. The amplitude is reduced and the contour has changed.
Figure 3.4 The ankle–brachial pressure index (ABI) for a limb is obtained by dividing the ankle pressure (using the higher of the dorsalis pedis or posterior tibial pressure) by the arm pressure (the higher obtained from either arm).
Figure 3.5 Exercise study in patient with left lower limb peripheral artery disease (PAD). In normal limbs (right), both the arm and leg pressure rise with exercise. In limbs with PAD (left) the arm pressure rises but the ankle pressure falls. The exercise capacity, post-exercise pressure fall, and pressure recovery time reflect the severity of the PAD.
Figure 3.6 Transcutaneous oximetry electrodes are placed over points of interest and sealed to the skin with air-tight tape.
Figure 3.7 Grayscale image of femoral artery. Note the irregular lumen with areas of narrowing.
Figure 3.8 (a) Normal color flow duplex scan. The peak pulse-wave Doppler velocities are between 60 and 80 cm/s. (b) Color flow duplex scan of stenotic artery. The peak pulsed-wave velocities across the stenotic lesion are greater than 400 cm/s.

Chapter 4: Magnetic Resonance, Computed Tomographic, and Angiographic Imaging of Peripheral Artery Disease

Figure 4.1 Computed tomography angiography (CTA) of the lower extremities. (a) Axial CTA slice of the proximal thighs shows normal superficial femoral (straight arrow) and profunda femoris (curved arrows) arteries bilaterally. (b) Lower extremity CTA maximum-intensity projection (MIP) demonstrates mild calcific atherosclerotic disease of the distal aorta (arrow), but normal patent vessels distally. (c) Three-dimensional (3D) volume rendering of the same patient without bone. (d) 3D volume rendering with bone. (e) Axial CT in patient with left prosthetic hip (arrow) shows streak artifact, which can make vascular evaluation difficult.
Figure 4.2 Magnetic resonance angiography (MRA) of peripheral arterial disease. (a) MRA maximum-intensity projection (MIP) image of the distal aorta and pelvis shows normal vascular anatomy and patent vessels without significant stenosis or occlusion. (b) T1-weighted axial magnetic resonance image demonstrates artifact (arrow) related to right hip prosthesis. (c) MRA of the same patient shows difficulty in evaluating the right common femoral artery related to the artifact from the hip replacement.
Figure 4.3 Digital subtraction angiogram (DSA). (a) DSA of the left hip shows patient distal common femoral, superficial femoral, and profunda femoris arteries with mild atherosclerotic disease. The profunda femoris branches are incompletely filled due to the timing of the image. (b) Unsubtracted angiogram of the same study shows the adjacent bone. (c) Carbon dioxide DSA of the right hip shows severe stenosis of the origin of the right superficial femoral artery (arrow), along with multifocal stenosis of the superficial femoral artery (curved arrow). There are also several areas of stenosis in the profunda femoris artery and its branches. (d) DSA of the distal thigh and knee shows motion artifact limiting (arrow) vascular evaluation.
Figure 4.4 Intravascular ultrasonography (IVUS) of the lower extremity. (a) Normal IVUS image of the superficial femoral artery showing a normal echogenic intima (arrow) and hypoechoic media (arrowhead). (b) IVUS image shows eccentric intimal plaque (arrowheads) in the superficial femoral artery.

Chapter 5: Non-atherosclerotic Peripheral Artery Disease

Figure 5.1 Necrotic ulcer on the lateral aspect of the second toe of the right foot (“kissing toe ulcer”) in a patient with peripheral artery disease and critical limb ischemia.
Figure 5.2 Left superficial femoral artery occlusion as demonstrated by various imaging modalities. (a) Segmental pressure measurements demonstrating reduced pressures in both the upper and lower thigh cuffs compared with the right lower extremity and brachial pressure cuffs. Pulse volume recordings revealing moderate disease at the thigh level. (b) Computed tomography three-dimensional reconstruction demonstrating total occlusion of the superficial femoral artery on the left near its origin (arrow). (c) Digital subtraction angiography demonstrating total occlusion of the superficial femoral artery on the left near its origin (arrow).
Figure 5.3 Appearance of common femoral artery plaque in two imaging modalities. (a) Magnetic resonance angiography demonstrating two discrete, calcific stenoses in the common femoral artery (arrows). (b) Digital subtraction angiography demonstrating common femoral artery stenoses corresponding to the findings in (a) (arrows).
Figure 5.4 Computed tomography demonstrating total occlusion of the right popliteal artery in a patient with longstanding untreated popliteal artery entrapment syndrome.
Figure 5.5 Digital subtraction angiography of the iliac arteries showing the characteristic “string of beads” appearance of medial fibroplasias fibromuscular dysplasia bilaterally, more evident on the right.
Figure 5.6 Computed tomography demonstrating a cyst compressing the right popliteal artery (arrow) in a patient with cystic adventitial disease.
Figure 5.7 Takayasu's arteritis. (a) Duplex image of a common carotid artery demonstrating long segment wall thickening (asterisks) and an incidental finding of internal jugular vein thrombosis (arrow). (b) A thickened aortic wall (arrow) as seen on computed tomographic angiography. (c) Left subclavian artery occlusion and collateral flow (arrow) as seen on digital subtraction angiography.
Figure 5.8 Diagnostic approach to patients presenting with lower extremity intermittent claudication. *Refer to Table 5.1 for more details. NAPAD, non-atherosclerotic peripheral artery disease; CAD, cystic adventitial disease; PAD, peripheral artery disease; MRA, magnetic resonance arteriography; ABI, ankle–brachial index; PVR, pulse volume recording.

Chapter 7: Endovascular Treatment of Peripheral Artery Disease

Figure 7.1 Aorto-iliac angiography in a patient with right common iliac artery and left common and external iliac artery occlusions. The inferior mesenteric artery and lumbar collaterals reconstitute vessels distal to the occlusions.
Figure 7.2 Right lower extremity angiogram in a patient with superficial femoral artery occlusion. The above-knee popliteal artery is reconstituted via collaterals from the profunda femoral artery.
Figure 7.3 Aortography in a patient with an infrarenal aortic occlusion involving a prior aorto-bifemoral graft. The infrainguinal vessels are reconstituted via the superior mesenteric artery.
Figure 7.4 Left below-knee angiography in a patient with occlusions of the posterior tibial, anterior tibial, and peroneal arteries. Unnamed collaterals formed via arteriogenesis to supply conduits for pedal perfusion.
Figure 7.5 (a) Selective left anterior tibial angiogram showing anterior communicating artery reconstituting an occluded peroneal artery. (b) A guidewire and microcatheter have traversed the anterior tibial artery and anterior communicating artery to access the peroneal artery retrograde. (c) Interventional wire at proximal cap of peroneal occlusion.
Figure 7.6 Depiction of the vascular angiosomes of the foot and lower leg.
Figure 7.7 Demonstration of the plantar arch. An interventional guidewire and microcatheter have traversed the anterior tibial artery and dorsalis pedis artery into the lateral plantar artery (plantar arch) to facilitate true lumen re-entry of the wire in the distal posterior tibial artery.
Figure 7.8 Left lower extremity angiography in a patient with congenital anomaly of peroneal artery supplying the dorsalis pedis artery. Note the interventional wire in the dorsalis pedis artery following successful peroneal reconstruction.
Figure 7.9 (a, b) Left below-knee angiogram in a patient with a wound on the lateral foot following transmetatarsal amputation. (c) Access needle and wire in the left posterior tibial artery. (d) Final angiogram following posterior tibial artery reconstruction.
Figure 7.10 (a) Aorto-iliac angiogram showing left external iliac artery occlusion. (b) Retrograde balloon inflation to facilitate the antegrade wire entry into the true lumen distal to the occlusion. (c) Final angiography following left external iliac artery revascularization.

Chapter 8: Surgical Management of Peripheral Artery Disease

Figure 8.1 Trans-Atlantic Society Consensus (TASC) classification of the distribution of aorto-iliac occlusive disease. EIA, external iliac artery; CIA, common iliac artery; CFA, common femoral artery; AAA, abdominal aortic aneurysm. Source: adapted with permission from TASC paper [9].
Figure 8.2 Aortobifemoral bypass.
Figure 8.3 (a) Axillobifemoral bypass; (b) femoral-femoral crossover bypass.
Figure 8.4 Bypasses from the common femoral artery to: (a) above-knee popliteal artery; (b) posterior tibial artery.
Figure 8.5 Trans-Atlantic Society Consensus (TASC) classification of the distribution of femoropopliteal occlusive disease. CFA, common femoral artery; SFA, superficial femoral artery. Source: adapted with permission from TASC paper [9].

List of Tables

Chapter 1: Epidemiology of Peripheral Artery Disease

Table 1.1 Age- and sex-specific incidence rates of peripheral artery disease measured by claudication and ankle–brachial index (ABI).
Table 1.2 Comparison of prevalence of claudication with prevalence of peripheral artery disease, with diagnosis based on ankle–brachial index (ABI).

Chapter 2: Office Evaluation of Peripheral Artery Disease – History and Physical Examination Strategies

Table 2.1 Classification of peripheral arterial disease: Fontaine's stages and Rutherford's categories.
Table 2.2 Characteristics of common foot and leg ulcers.

Chapter 5: Non-atherosclerotic Peripheral Artery Disease

Table 5.1 Comparison of atherosclerosis and non-atherosclerotic peripheral artery disease (NAPAD).
Table 5.2 Treatment of non-atherosclerotic peripheral artery disease (NAPAD).

Chapter 7: Endovascular Treatment of Peripheral Artery Disease

Table 7.1 Classification of claudication and critical limb ischemia.
Table 7.2 Updated American College of Cardiology Foundation and American Heart Association (ACCF/AHA) Guidelines on endovascular treatment for patients with critical limb ischemia (CLI) [12]
Table 7.3 Important collateral pathways in peripheral artery disease.
Table 7.4 Recommended arterial access sites, depending on lesion location.
Table 7.5 Re-entry devices for endovascular intervention.
Table 7.6 TransAtlantic Inter-Society Consensus (TASC II) morphologic stratification of iliac lesions.
Table 7.7 TransAtlantic Inter-Society Consensus Working Group II (TASC II) classification for femoropopliteal peripheral artery disease.
Table 7.8 Available atherectomy devices for peripheral arterial interventions.

Chapter 8: Surgical Management of Peripheral Artery Disease

Table 8.1 Fontaine classification of vascular disease [1]
Table 8.2 Rutherford classification of acute limb ischemia. Physical examination findings at the time of presentation correlate with the viability of the limb and help to dictate management [11].
Table 8.3 Trans-Atlantic Inter-Society Consensus (TASC II) classification of femoropopliteal disease [9]/

Peripheral Artery Disease

Edited by

Emile R. Mohler, MD, MSVM, FACC, FAHA

University of Pennsylvania, Philadelphia, PA, USA

Michael R. Jaff, DO, FACP, FACC, FAHA, MSVM

Newton-Wellesley Hospital, Newton, MA, USA

Second Edition

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, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.

The right of Emile R. Mohler and Michael R. Jaff to be identified as the author of the editorial material in this work has been asserted in accordance with law.

John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

For details of our global editorial offices, customer services, and more information about Wiley products visit us at www.wiley.com.

Wiley also publishes its books in a variety of electronic formats and by print-on-demand. Some content that appears in standard print versions of this book may not be available in other formats.

The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.

Description: Second edition. | Hoboken, NJ, USA ; Chichester, West Sussex : John Wiley & Sons, Inc., 2017. | Preceded by: Peripheral arterial disease / edited by Emile R. Mohler III, Michael R. Jaff. Philadelphia : American College of Physicians, c2008. | Includes bibliographical references and index. |

Identifiers: LCCN 2017014491 (print) | LCCN 2017015849 (ebook) | ISBN 9781118776070 (pdf) | ISBN 9781118776087 (epub) | ISBN 9781118776094 (cloth)

Subjects: | MESH: Peripheral Arterial Disease-diagnosis | Peripheral Arterial Disease-therapy

Classification: LCC RC694 (ebook) | LCC RC694 (print) | NLM WG 550 | DDC 616.1/31-dc23

Contributors

Wobo Bekwelem, MD MPH
Lillehei Heart Institute and Cardiovascular DivisionUniversity of Minnesota Medical SchoolMinneapolisMN, USA

Scott M. Damrauer, MD
Hospital of the University of Pennsylvania; and Corporal Michael Crescent VA Medical CenterPhiladelphiaPA, USA

Robert S. Dieter, MD RVT
Associate Professor of MedicineLoyola University Medical CenterMaywoodIL, USA

Jay Giri, MD
Interventional Cardiology & Vascular MedicineCardiovascular Medicine DivisionUniversity of PennsylvaniaPA, USA

Julia Glaser, MD
Hospital of the University of PennsylvaniaPhiladelphiaPA, USA

Alan T. Hirsch, MD
Director, Vascular Medicine, Quality Outcomes, and Population HealthProfessor of Medicine, Epidemiology and Community HealthLillehei Heart Institute and Cardiovascular DivisionUniversity of Minnesota Medical SchoolMinneapolisMN, USA

Masahiro Horikawa, MD
Instructor, Dotter Interventional Institute/Oregon Health & Science UniversityPortlandOR, USA

Lee Joseph, MD MS
Division of Cardiovascular DiseasesDepartment of Internal MedicineUniversity of IowaIowa CityIA, USA

Esther S.H. Kim, MD MPH
Cardiovascular Division
Vanderbilt University Medical Center
NashvilleTN, USA

John A. Kaufman, MD MS
Frederick S. Keller Professor of Interventional RadiologyDirector of the Institute, Dotter Interventional Institute/Oregon Health & Science UniversityPortlandOR, USA

Thomas Le, MD MS
Assistant Professor, Department of Radiological SciencesDavid Geffen School of Medicine at UCLA Los Angeles; and Staff Interventional RadiologistSection of Vascular and Interventional RadiologyDepartment of RadiologyOlive View-UCLA Medical CenterSylmarCA, USA

Maen Nusair, MD
PeaceHealth Southwest Heart and Vascular CenterVancouverWA, USA

Vikram Prasanna, MD
Interventional Cardiology & Vascular MedicineCardiovascular Medicine DivisionUniversity of PennsylvaniaPhiladelphiaPA, USA

R. Kevin Rogers, MD MSc
Section of Vascular Medicine and InterventionDivision of CardiologyUniversity of ColoradoAuroraCO, USA

Thomas Rooke, MD BS RVT
Krehbiel Professor of Vascular MedicineMayo ClinicRochesterMN, USA

Ido Weinberg, MD FSVM
Vascular Medicine SectionCardiology DivisionMassachusetts General HospitalBostonMA, USA

Mitchell D. Weinberg, MD FACC
System Director of Peripheral Vascular InterventionNorthwell Health SystemDivision of Cardiology; andAssistant Professor, Hofstra Northwell School of MedicineLong IslandNY, USA

Preface

Peripheral artery disease (PAD) is unfortunately infrequently recognized. The treatment of PAD continues to evolve but is fundamentally focused on control of risk factors in order to prevent the associated risk of heart attack, stroke, and premature cardiovascular death as well as improvement in exercise performance and limb preservation. The pathophysiology of progressive atherosclerotic plaque in the extremities is thought to involve plaque hemorrhage and rupture, but few data support this presumption. Clinical research is needed to develop agents designed to halt progression of atherosclerotic disease in the peripheral arterial system. Despite these current limitations in understanding and treating PAD, new lipid modifying agents and new antiplatelet treatment of risk factors and strategies to improve pain-free walking distance have emerged, including the use of emerging endovascular strategies. In addition, with the rapid evolution of technology to improve arterial perfusion with minimally invasive catheter-based strategies, options for revascularization of patients with advanced symptoms and signs of PAD are improving.

The primary objective of Peripheral Artery Disease is to provide the reader with the most current information on diagnosis and treatment of PAD.

We hope that this reference provides an easy-to-use resource for the practicing clinician, ultimately resulting in better care for our patients. In addition, we would like to dedicate this entire book to Alan T. Hirsch, MD, who died suddenly and unexpectedly in April 2017. It minimizes his impact on the field and all vascular specialists to discuss his publications, presentations, and advocacy. Alan was a tireless voice for patients around the World who suffered from PAD. It was through his efforts that exercise and guidelines-based medical therapies have become primary in the management of these patients. We will forever miss his enthusiasm, humor, expertise and care, but most importantly, the World is a bit smaller with his passing.