Ebook 900 questions - An interventional cardiology board review: Part 1

900 Questions:
An Interventional Cardiology
Board Review



900 Questions:
An Interventional Cardiology
Board Review
EDITORS
Debabrata Mukherjee, MD
Associate Professor of Medicine
Director, Cardiac Catheterization Laboratories
Gill Foundation Professor of Interventional Cardiology
Gill Heart Institute and Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Leslie Cho, MD
Director, Women’s Cardiovascular Center
Medical Director, Preventive Cardiology and Rehabilitation
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
Cleveland, Ohio

David J. Moliterno, MD
Professor and Vice-Chairman of Medicine
Chief, Cardiovascular Medicine
Jefferson Morris Gill Professor of Cardiology
Gill Heart Institute and Division of Cardiovascular Medicine
University of Kentucky

Lexington, Kentucky

Donna A. Gilbreath
Managing Editor
Gill Heart Institute and Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky


Acquisitions Editor: Frances R. DeStefano
Managing Editor: Nicole Dernoski
Project Manager: Jennifer Harper
Senior Manufacturing Manager: Benjamin Rivera
Marketing Manager: Angela Panetta
Art Director: Risa Clow
Production Services: Laserwords Private Limited, Chennai, India
Printer: Victor Graphics, Inc.
© 2007 by LIPPINCOTT WILLIAMS & WILKINS, a Wolters Kluwer business
530 Walnut Street
Philadelphia, PA 19106 USA
LWW.com
All rights reserved. This book is protected by copyright. No part of this book may be
reproduced in any form or by any means, including photocopying, or utilized by any
information storage and retrieval system without written permission from the copyright
owner, except for brief quotations embodied in critical articles and reviews. Materials
appearing in this book prepared by individuals as part of their official duties as U.S.
government employees are not covered by the above-mentioned copyright.
We appreciate that even with the best of efforts from the authors, editors, and
publishers that some of the questions or answers in this textbook may need refinement.
So, too, while the object was to carefully design each question with a single best answer,

some questions may be more controversial than intended or may have more than one
reasonable response. With these points in mind and with our hopes to continually
improve this book with future editions, comments regarding this first edition are
welcomed and can be sent to Dr. Debabrata Mukherjee () or Dr.
David Moliterno ().
Printed in the USA

Library of Congress Cataloging-in-Publication Data
900 questions : an interventional cardiology board review / editors,
Debabrata Mukherjee ... [et al.].
p. ; cm.
ISBN-13: 978-0-7817-7349-2
ISBN-10: 0-7817-7349-0
1. Heart—Diseases—Treatment—Examinations, questions, etc. 2. Cardiovascular
system—Diseases—Treatment—Examinations, questions, etc. I. Mukherjee, Debabrata.
II. Title: Nine hundred questions.
[DNLM: 1. Cardiovascular Diseases—Examination Questions. 2. Cardiovascular
Diseases—therapy—Examination Questions. WG 18.2 Z9991 2007]
RC683.8.N564 2007
616.1 20076—dc22
2006027893

Care has been taken to confirm the accuracy of the information presented and to
describe generally accepted practices. However, the authors, editors, and publisher are not
responsible for errors or omissions or for any consequences from application of the
information in this book and make no warranty, expressed or implied, with respect to the
currency, completeness, or accuracy of the contents of the publication. Application of this
information in a particular situation remains the professional responsibility of the
practitioner.
The authors, editors, and publisher have exerted every effort to ensure that drug

selection and dosage set forth in this text are in accordance with current recommendations
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Some drugs and medical devices presented in this publication have Food and Drug
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10 9 8 7 6 5 4 3 2 1


‘‘To my parents, for their infinite patience, love, and understanding, who
continue to be my source of inspiration, and to my wonderful wife,
Suchandra, for her love and support’’
Debabrata Mukherjee

‘‘To Nathaniel and Benjamin, my sons and suppliers of life’s important
questions, and to Judith, my wife and partner in finding the answers’’
David J. Moliterno

Preface
Insightful questions have been used through the ages as a
metric to assess one’s knowledge, but when coupled with
carefully delivered answers they can become a powerful
teaching tool. This book of questions and annotated
answers covering the field of interventional cardiology
is meant to serve as a helpful resource for individuals
preparing for the interventional cardiovascular medicine
board examination as well as for clinicians who wish to
perform an in-depth self-assessment on individual topics
or the full spectrum. The book has many key features,
which we believe will make the reader successful in passing
the boards and improving clinical practice.
Of foremost importance, the areas covered are relevant not only to the day-to-day practice of interventional
cardiology, but have also been patterned in scope and
content to the actual board examination. The book begins
with several chapters dedicated to the anatomy and physiology associated with interventional cardiology and the
pathobiology of atherosclerosis and inflammation. This
corresponds to the 15% of the board examination targeting material in basic science. The subsequent chapters
focus on the essential interventional pharmacotherapy of
antiplatelets, anticoagulants, and other commonly used
medications in the catheterization laboratory and outpatient setting for patients with atherosclerosis. These
chapters correspond to the next 15% of the boards centering on pharmacology. A similar-sized 15% of the board
examination is directed toward imaging, and the book
includes specific chapters on radiation safety, catheterization laboratory equipment and technique, contrast agents,
and intravascular ultrasound. The two largest areas of the
examination, each covering 25% of the content, include
case selection–management and procedural techniques.
The review book dedicates 25 chapters to comprehensively
cover these areas. Finally, we have included chapters for

the miscellaneous remaining areas covered by the board
examination, including peripheral vascular disease, ethics,
statistics, and epidemiology, as well as a chapter directed
at improving test-taking skills.
Also essential to the quality and appropriateness of
the questions and annotated answers is the expertise of the
chapter authors. We are fortunate to have assembled the
‘‘who’s who of academic interventional cardiology’’. The
59 contributing authors from leading medical centers
around the world have over 4,600 articles cited in
PubMed. We are greatly indebted to these authors who
are recognized both for their interventional expertise and
for their teaching skills. In the end, the true value of this
textbook is not only the relevance of the questions, the
outstanding quality of the authors, but also the value of
the annotated answers. The text includes 910 questions
and 254 figures and tables. The corresponding answers
have been appropriately detailed to provide relevant facts
and information as well as up-to-date journal citations.
The practice of interventional cardiology is exciting,
rewarding, and a privilege each of us enjoys. Likewise,
it has been our privilege to work with the superb
contributors, our colleagues in interventional cardiology,
as well as the editorial team at the University of Kentucky
and Lippincott Williams and Wilkins. It is our personal
hope that you will enjoy this book and that it will be a
valuable resource to you in passing the board examination
and providing the highest quality care possible to your
patients.

DEBABRATA MUKHERJEE, MD
LESLIE CHO, MD
DAVID J. MOLITERNO, MD

vii



Contributors
Robert J. Applegate, MD
Director, Cardiovascular Training Program
Wake Forest University School of Medicine
Winston-Salem, North Carolina

Joseph Babb, MD
Professor of Medicine
Department of Internal Medicine, Cardiology Division
Brody School of Medicine
East Carolina University;
Director, Cardiac Catheterization Laboratories
Pitt County Memorial Hospital
Greenville, North Carolina

Thomas M. Bashore, MD
Professor of Medicine
Division of Cardiovascular Medicine;
Director, Fellowship Training Program
and Adult Congenital and Valvular Disease Program
Duke University Medical Center
Durham, North Carolina

Matthew C. Becker, MD
Fellow in Cardiovascular Disease
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
Cleveland, Ohio

Deepak L. Bhatt, MD
Associate Professor of Medicine
Staff, Cardiac, Peripheral, and Carotid Intervention
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
Cleveland, Ohio

David C. Booth, MD
Endowed Professor Medicine
Gill Heart Institute and
Division of Cardiovascular Medicine
University of Kentucky;
Chief of Cardiology
Lexington VA Medical Center
Lexington, Kentucky

Sorin J. Brener, MD
Associate Professor of Medicine
Department of Medicine
Case Western Reserve University;
Staff Physician
Department of Cardiovascular Medicine
Cleveland Clinic Foundation

Cleveland, Ohio

Ivan P. Casserly, MD
Assistant Professor of Medicine
Cardiology Division
University of Colorado;
Director of Interventional Cardiology
Denver VA Medical Center
Denver, Colorado

Leslie Cho, MD
Director, Women’s Cardiovascular Center
Medical Director, Preventive Cardiology
and Rehabilitation
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
Cleveland, Ohio

Antonio Colombo, MD
Chief of Invasive Cardiology
Universit`a Vita-Salute
and San Raffaele Scientific Institute
and Columbus Hospitals
Milan, Italy

Harold L. Dauerman, MD
Professor of Medicine
University of Vermont;
Director, Cardiovascular Catheterization Laboratories
Fletcher Allen Health Care

Burlington, Vermont

Steven R. Daugherty, PhD
Assistant Professor of Psychology
Assistant Professor of Preventive Medicine
Rush Medical College
Chicago, Illinois
ix


x

Contributors

Stephen G. Ellis, MD
Professor of Medicine
Department of Cardiovascular Medicine
Cleveland Clinic Lerner College of Medicine
Case Western Reserve University;
Director, Cardiac Catheterization Laboratories
Cleveland Clinic Foundation
Cleveland, Ohio

Nezar Falluji, MD, MPH
Clinical Instructor
Gill Heart Institute
Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Hussam Hamdalla, MD
Assistant Professor of Medicine
Gill Heart Institute and
Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Robert A. Harrington, MD
Professor of Medicine
Director, Cardiovascular Clinical Trials
Co-Director, Cardiovascular Research
Duke Clinical Research Institute
Department of Medicine, Division of Cardiology
Duke University Medical Center
Durham, North Carolina

Howard C. Herrmann, MD
David P. Faxon, MD
Director of Strategic Planning
Department of Medicine
Brigham and Women’s Hospital;
Professor of Medicine
Department of Medicine
Harvard Medical School
Boston, Massachusetts

Joel A. Garcia, MD
Interventional Cardiology and Research Fellow
Department of Cardiology
University of Colorado

Denver, Colorado

Thomas Gehrig, MD
Cardiology Fellow
Division of Cardiovascular Medicine
Duke University Medical Center
Durham, North Carolina

Professor of Medicine
Cardiovascular Division
University of Pennsylvania School of Medicine;
Director, Interventional Cardiology and Cardiac
Catheterization Laboratories
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

L. David Hillis, MD
Professor and Vice Chair
Department of Internal Medicine
University of Texas Southwestern Medical Center
Dallas, Texas

Alice K. Jacobs, MD
Professor of Medicine
Department of Medicine, Section of Cardiology
Boston University School of Medicine;
Director, Cardiac Catheterization Laboratories
and Interventional Cardiology
Boston Medical Center
Boston, Massachusetts

John Lynn Jefferies, MD, MPH
Bernard Gersh, MB, ChB, DPhil
Professor of Medicine
Cardiology Diseases
Mayo Clinic College of Medicine
Rochester, Minnesota

John C. Gurley, MD, MBA
Professor of Medicine
Director, Interventional Cardiology Fellowship
Gill Heart Institute
Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Assistant Professor
Adult and Pediatric Cardiology
Baylor College of Medicine
Divisions of Adult Cardiovascular Diseases
and Pediatric Cardiology
Texas Children’s Hospital
Texas Heart Institute at St. Luke’s Episcopal Hospital
Houston, Texas

Hani Jneid, MD
Division of Cardiology
Massachusetts General Hospital
and Harvard Medical School
Boston, Massachusetts

Contributors

Dominique Joyal, MD
Interventional Cardiology Fellow
Cardiology Division
Loyola University Medical Center
Maywood, Illinois

David E. Kandzari, MD
John B. Simpson Assistant Professor of Interventional
Cardiology and Genomic Sciences
Division of Cardiology
Department of Medicine
Duke University Medical Center
Durham, North Carolina

Samir Kapadia, MD
Associate Professor of Medicine
Cleveland Clinic Lerner College of Medicine
of Case Western Reserve University;
Director, Interventional Cardiology Fellowship
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
Cleveland, Ohio

Juhana Karha, MD
Fellow, Cardiovascular Medicine
Department of Cardiovascular Medicine

Cleveland Clinic Foundation
Cleveland, Ohio

Morton J. Kern, MD
Clinical Professor of Medicine
Associate Chief of Cardiology
Department of Cardiology
University of California Irvine
Orange, California

Richard A. Lange, MD
Professor of Medicine
Chief of Clinical Cardiology
Johns Hopkins University
Baltimore, Maryland

Bruce E. Lewis, MD
Professor of Medicine
Associate Director, Interventional Cardiology
Loyola University Medical Center
Maywood, Illinois;
Chief, Cardiology Division
St. Joseph Hospital
Chicago, Illinois

Ferdinand Leya, MD
Cardiology Department
Loyola University Medical Center
Maywood, Illinois

Andrew O. Maree, MD
Interventional Cardiology Fellow
Division of Cardiology
Massachusetts General Hospital;
Instructor, Department of Medicine
Harvard Medical School
Boston, Massachusetts

J. Jeffery Marshall, MD
Medical Director
Cardiac Catheterization Laboratory
Northeast Georgia Heart Center
Gainesville, Florida

Telly A. Meadows, MD
Cardiology Fellow
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
Cleveland, Ohio

Bernhard Meier, MD
Professor of Medicine
Chairman, Department of Cardiology
University Hospital Bern
Bern, Switzerland

David J. Moliterno, MD
Professor and Vice-Chairman of Medicine
Chief, Cardiovascular Medicine
Jefferson Morris Gill Professor of Cardiology

Gill Heart Institute and
Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Pedro R. Moreno, MD
Director, Interventional Cardiology Research
Mount Sinai Hospital;
Associate Professor
Department of Medicine
Mount Sinai School of Medicine
New York, New York

Douglass A. Morrison, MD
Cardiology Department
University of Arizona
Tucson, Arizona

xi


xii

Contributors

Debabrata Mukherjee, MD
Associate Professor of Medicine
Director, Cardiac Catheterization Laboratories
Gill Foundation Professor of Interventional Cardiology
Gill Heart Institute and

Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Brahmajee K. Nallamothu, MD, MPH
Assistant Professor of Medicine
Interventional Cardiologist
Department of Internal Medicine
University of Michigan Health System
Ann Arbor, Michigan

Craig R. Narins, MD
Assistant Professor of Medicine
Division of Cardiology
University of Rochester School of Medicine
Rochester, New York

Zoran S. Nedeljkovic, MD
Assistant Professor of Medicine
Department of Medicine, Section of Cardiology
Boston University School of Medicine;
Interventional Cardiologist
Boston Medical Center
Boston, Massachusetts

Michael R. Nihill, MBBS
Professor of Clinical Pediatrics
Department of Pediatrics
Baylor College of Medicine;
Associate in Pediatric Cardiology

Department of Cardiology
Texas Children’s Hospital
Houston, Texas

Alan W. Nugent, MBBS
Assistant Professor of Pediatrics
Baylor College of Medicine;
Pediatric Cardiologist
Texas Children’s Heart Center
Texas Children’s Hospital
Houston, Texas

Igor F. Palacios, MD
Physician
Cardiac Unit
Massachusetts General Hospital
Boston, Massachusetts

Karen S. Pieper, MS
Senior Statistician
Duke Clinical Research Institute
Department of Medicine, Division of Cardiology
Duke University Medical Center
Durham, North Carolina

Marco Roffi, MD
Lecturer in Cardiology
Zurich Medical School;
Staff Cardiologist
University Hospital

Zurich, Switzerland

Christopher L. Sarnoski, MD
Cardiology Fellow
Division of Cardiovascular Medicine
University of Vermont
Burlington, Vermont

Paul Sorajja, MD
Assistant Professor of Medicine
Mayo Clinic College of Medicine
Rochester, Minnesota

Amy L. Seidel, MD
Interventional Cardiology Fellow
Division of Cardiovascular Medicine
Emory University School of Medicine
Atlanta, Georgia

Steven R. Steinhubl, MD
Associate Professor of Medicine
Director of CV Education and Clinical Research
Gill Heart Institute and
Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Ann O’Connor, MD
Instructor in Medicine
Section of Cardiology

Department of Medicine
University of Chicago
Chicago, Illnois

Eric J. Topol, MD
Professor of Genetics
Department of Genetics
Case Western Reserve University
Cleveland, Ohio


Contributors

Thomas T. Tsai, MD
Cardiology Fellow
Department of Internal Medicine
University of Michigan
Ann Arbor, Michigan

E. Murat Tuzcu, MD
Professor of Medicine
Department of Cardiovascular Medicine
Cleveland Clinic Lerner College of Medicine
Case Western Reserve University;
Vice Chairman
Department of Cardiovascular Medicine
Cleveland Clinic Foundation
Cleveland, Ohio

Christopher Walters, MD

Cardiology Fellow
Gill Heart Institute
Division of Cardiovascular Medicine
University of Kentucky
Lexington, Kentucky

Peter Wenaweser, MD
Attending Physician
Department of Cardiology
University Hospital Bern
Bern, Switzerland

Christophe A. Wyss, MD
Cardiology Fellow
University Hospital
Zurich, Switzerland

Khaled M. Ziada, MD
Assistant Professor of Medicine
Gill Heart Institute
Division of Cardiovascular Medicine
University of Kentucky;
Director, Cardiac Catheterization Laboratories
Lexington VA Medical Center
Lexington, Kentucky

xiii

Contents
1 Vascular Biology

................................

1

Pedro R. Moreno

. . . . . . . . . . . . 118

Joel A. Garcia and Ivan P. Casserly

2 Anatomy and Physiology

......................

6

Richard A. Lange and L. David Hillis

16 Restenosis and Percutaneous Options . . . . . . . 125
Craig R. Narins

3 Radiation Safety, Equipment, and Basic

17 Atherectomy, Rotablation, and Laser . . . . . . . . 135

Concepts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
John C. Gurley

Robert J. Applegate

18 Stents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142

4 Inflammation and Arterial Injury

...........

25

Christopher L. Sarnoski and Harold L. Dauerman

Thrombolytic Agents

...........................

32

David J. Moliterno

Delivery for the Prevention of
Restenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
Peter Wenaweser and Bernhard Meier

6 Inotropes, Antiarrhythmics, Sedatives,
and Lipid-Lowering Agents

...................

20 Percutaneous Interventions in
41

J. Jeffrey Marshall and David J. Moliterno

Aortocoronary Saphenous Vein Grafts . . . . . . 155
Christophe A. Wyss and Marco Roffi

7 Guiding Catheter Selection for Coronary

21 Closure Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 164

Interventions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49
Bruce E. Lewis and Dominique Joyal

Leslie Cho and Debabrata Mukherjee

22 Management of Intraprocedural and

8 Intravascular Contrast Agents . . . . . . . . . . . . . . . . 57
Thomas T. Tsai and Brahmajee K. Nallamothu

Postprocedural Complications . . . . . . . . . . . . . . . . 170
Ferdinand Leya

9 Elective Coronary Intervention . . . . . . . . . . . . . . . 62

23 Qualitative and Quantitative
Angiography

Douglass A. Morrison

Acute Coronary Syndromes

...................

73

Christopher Walters and Steven R. Steinhubl

25 Intravascular Ultrasound . . . . . . . . . . . . . . . . . . . . . . 192
88

David J. Moliterno, Leslie Cho, and Debabrata
Mukherjee

Hussam Hamdalla and Khaled M. Ziada

26 Approach to Patients with Hemodynamic
Compromise

12 Periprocedural Myocardial Infarction
.........................

24 Interventional Coronary Physiology . . . . . . . . . 185
Morton J. Kern

11 Primary, Rescue, and Facilitated
......................................

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181

Sorin J. Brener

10 Percutaneous Coronary Intervention for

and Emboli Protection

Stephen G. Ellis

19 Drug-Eluting Stents and Local Drug

5 Antiplatelet, Antithrombotic, and

Angioplasty

15 Long Lesions and Diffuse Disease

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202

Zoran S. Nedeljkovic and Alice K. Jacobs

97

Telly A. Meadows and Deepak L. Bhatt

27 Peripheral Interventional Procedures

. . . . . . . 212

Matthew C. Becker and Samir Kapadia

13 Chronic Total Occlusions . . . . . . . . . . . . . . . . . . . . . . 105
David E. Kandzari

28 Cerebrovascular Interventions . . . . . . . . . . . . . . . . 225
Nezar Falluji and Debabrata Mukherjee

14 Ostial and Bifurcation Lesions . . . . . . . . . . . . . . . . 112
Antonio Colombo

xv


xvi

Contents

29 Valvuloplasty and Percutaneous Valve
Replacement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
Thomas Gehrig and Thomas M. Bashore

30 Congenital Heart Disease . . . . . . . . . . . . . . . . . . . . . . 244
John Lynn Jefferies, Michael R. Nihill, and
Alan W. Nugent

31 Patent Foramen Ovale and Atrial Septal
Defect

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254

Howard C. Herrmann

32 Percutaneous Balloon Pericardiotomy for
Patients with Pericardial Effusion and
Tamponade . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262
Andrew O. Maree, Hani Jneid, and Igor F. Palacios

33 Percutaneous Alcohol Septal Ablation for
Hypertrophic Cardiomyopathy . . . . . . . . . . . . . . . 270
Amy L. Seidel and E. Murat Tuzcu

34 Chronic Stable Angina: American College
of Cardiology/American Heart
Association Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . 278
Paul Sorajja and Bernard Gersh

35 Practice Guidelines in Non–
ST-Elevation Acute Coronary Syndromes . . 288
Juhana Karha and Eric J. Topol

36 Percutaneous Coronary Intervention:
American College of
Cardiology/American Heart Association
Guidelines 2005 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299
Leslie Cho

37 ST-Elevation Myocardial Infarction:
American College of
Cardiology/American Heart Association

Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309
Ann O’Connor and David P. Faxon

38 Ethical Issues and Risks Associated
with Catheterization and Interventional
Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
Christopher Walters and David C. Booth

39 Statistics Related to Interventional
Cardiology Procedures

. . . . . . . . . . . . . . . . . . . . . . . . . 339

Robert A. Harrington and Karen S. Pieper

40 Approach to Interventional Boards and
Test-Taking Strategies

. . . . . . . . . . . . . . . . . . . . . . . . . 347

Joseph Babb and Steven R. Daugherty

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357


1
Vascular Biology
Pedro R. Moreno

Questions

1 All of the following statements regarding the American Heart Association (AHA) classification for early
atherosclerosis are true, except:
(A) The type I lesion is proteoglycan rich and prone
to develop atherosclerosis
(B) The type II lesion is characterized by foam cell
infiltration and may regress
(C) The type III lesion is characterized by pools of
intracellular lipid and collagen
(D) Early lesions are flat, asymptomatic, and do not
obstruct the lumen
2 All of the following statements regarding advanced
atherosclerosis are true, except:
(A) Vasa vasorum neovascularization is increased in
ruptured plaques
(B) Thin-cap fibroatheromas are characterized by
cap thickness <65 µm, macrophages, and large
lipid core
(C) Extravasation of red blood cells (RBCs) within
plaques increases lipid core expansion
(D) Plaque rupture is most frequently symptomatic,
leading to acute coronary events
3 All of the following statements regarding advanced
atherosclerosis are true, except:
(A) Coronary calcification is a predictor of future
coronary events
(B) Coronary calcification always reflects advanced
disease by histologic criteria
(C) Plaque erosion is more frequently seen in
smokers
(D) Chronic stable angina lesions are frequently

healed ruptured plaques

(E) Plaque rupture more frequently occurs at the
center of the fibrous cap
4 All of the following statements are true, except:
(A) Nonobstructive lesions are the most frequent
cause of acute myocardial infarction (MI)
(B) Obstructive lesions can evolve into complete
occlusion silently
(C) The individual risk for plaque progression to
complete occlusion is higher in nonobstructive
lesions
(D) Vulnerable plaques are located predominately in
the proximal segments of the coronary arteries
5 All of the following statements are true, except:
(A) Plaque rupture may occur simultaneously in
two different arteries
(B) Plaque healing after rupture is mediated by
smooth muscle cell (SMC) production of collagen III
(C) SMCs are responsible for weakening the fibrous
cap
(D) T lymphocytes increase proteolytic activity and
decrease collagen synthesis
6 All of the following statements are true, except:
(A) Inflammation precipitates plaque rupture and
thrombosis
(B) Collagen is the most thrombogenic substrate
after plaque rupture
(C) Inflammation promotes neovascularization
(D) Macrophages are the main source of metalloproteinases in the plaque

1


2

900 Questions: An Interventional Cardiology Board Review

7 All of the following statements are true, except:
(A) The main source of plaque neovessels is the vasa
vasorum
(B) C-reactive protein (CRP) is produced in the liver
as a proinflammatory response to interleukin-6
(IL-6)
(C) CRP has been found within the plaque at the
lipid core
(D) CRP has intrinsic atherogenic properties stimulating foam cell formation
(E) CRP has been found to be an independent
predictor for events only in univariate analysis
8 All of the following statements about inflammation
are true, except:
(A) Patients with unstable angina and increased
inflammation have a higher risk for subsequent
events
(B) Randomized trials have shown no benefit for
steroids in unstable angina
(C) Leukocytosis is an independent predictor for
future events
(D) The beneficial effects of acetylsalicylic acid
(ASA) in primary prevention are independent

of CRP levels
9 All of the following statements are true, except:
(A) Remodeling preserves the lumen area and protects from heart attacks
(B) Positive remodeling is most frequently seen in
unstable syndromes
(C) Positive remodeled plaques have more macrophages
(D) Plaques can grow up to 40% area stenosis
without significantly obstructing the lumen
10 All of the following statements are true, except:
(A) Coronary thrombosis in unstable angina is
predominately platelet rich
(B) Deep-vein thrombosis in pulmonary embolism
(PE) is predominately fibrin rich
(C) Coronary thrombosis in ST-elevation myocardial infarction (STEMI) is a combination of
platelet-rich and fibrin-rich thrombus
(D) Natural anticoagulants include protein C, protein S, and tissue factor pathway inhibitor (TFPI)
(E) The plasminogen-activator inhibitor-1 (PAI-1)
system is decreased in patients with diabetes
11 Metalloproteinases are relevant for the following,
except:
(A) Positive remodeling, by digesting the internal
elastic lamina

(B) Plaque angiogenesis, by mediating tunnelization
of neovessels
(C) Plaque rupture, by digesting the collagen of the
fibrous cap
(D) Myocardial salvage by preventing expansion and
remodeling
12 Monocyte-derived macrophages are involved in the

following, except:
(A) Foam cell formation
(B) Matrix metalloproteinases (MMPs) expression
(C) Tissue factor expression
(D) Plaque regression
13 Which of the following statements is true regarding
the lipid core?
(A) Is composed of cholesterol crystals and collagen
(B) The predominant cell is the SMC
(C) Can be identified as a green structure on polarized microscopy using the picrosirius red
stain
(D) Is the most potent thrombogenic substrate of
human atherosclerotic plaques
14 Which of the following statements is true regarding
the fibrous cap?
(A) It is composed of collagen and SMCs
(B) It is located at the base of the plaque, in contact
with the internal elastic lamina
(C) It can be easily quantified by intravascular
ultrasound
(D) It is the major source of neovessels in human
atherosclerosis
15 Which of the following statements is false regarding
vulnerable plaques?
(A) They are located predominately in the proximal
segments of coronary arteries
(B) They are mostly lipid rich, with increased
macrophage infiltration
(C) They exhibit positive remodeling
(D) They can be identified by angioscopy, showing

a white surface
16 Which of the following statements is true regarding
plaques undergoing erosion?
(A) They are more frequently seen in hypercholesterolemic, postmenopausal women
(B) They are mostly calcified plaques
(C) They are associated with positive remodeling
(D) They commonly exhibit a thick, SMC-rich fibrous cap


Vascular Biology

17 Which of the following statements is true regarding
atherosclerotic mast cells?
(A) They produce nitric oxide
(B) They are increased in rupture plaques
(C) They are located mostly in the tunica media
(D) They are known as potent thrombogenic cells
18 Which of the following statements is false regarding
plaque rupture?
(A) It occurs more frequently in lipid-rich plaques
(B) It may occur simultaneously in multiple coronary vessels
(C) It may occur more than once in the same plaque
(D) Increased macrophage activity in ruptured
plaques is related to decreased macrophage
apoptosis
19 Which of the following statements is false regarding
diabetes?
(A) It is associated with increased atherosclerotic
burden
(B) Diabetic coronary plaques have increased macrophage infiltration

(C) It is associated with increased thrombogenicity
(D) Macrophage receptor for advanced endglycation products (RAGE) is downregulated
20 Which of the following statements is false regarding
vessel wall inflammation?
(A) T cells are less frequently found when compared
with macrophages
(B) Plaque inflammation is associated with increased neovascularization
(C) Cell-adhesion molecules (vascular cell adhesion molecule [VCAM], intercellular adhesion
molecule [ICAM]) are mostly expressed in
the endothelium and less expressed in plaque
neovessels
(D) It is reduced after lipid-lowering therapy
21 Which of the following is not an independent
predictor of positive remodeling?
(A) Inflammation
(B) Calcification
(C) Medial atrophy
(D) Cigarette smoking
22 Which of the following statements is false regarding
intraplaque hemorrhage?
(A) It is associated with increased neovascularization
(B) It is associated with symptomatic carotid disease
(C) RBC extravasation stimulates lipid core expansion
(D) It downregulates macrophage CD163 receptor

3

(E) It increases the production of reactive oxygen
species
23 Which of the following statements is false regarding

plaque neovascularization?
(A) It is increased in ruptured plaques
(B) It is associated with inflammation
(C) Hypoxic factor-1α triggers plaque angiogenesis
(D) Most neovessels communicate with the vessel
lumen to nurture the base of the plaque
24 Which of the following statements is false regarding
SMC proliferation after stent deployment?
(A) It is increased in diabetic lesions after bare metal
stenting
(B) It is characterized by increased production of
collagen I
(C) It is associated with inflammation
(D) It is reduced after complete endothelialization
(E) It is associated with increased cell apoptosis
25 Which of the following statements is false regarding
coronary thrombosis in unstable angina and non–STelevation myocardial infarction (NSTEMI)?
(A) It is more frequently mediated by plaque rupture
rather than erosion
(B) It is associated with distal embolization, predominately composed of cholesterol crystals and
necrotic debris
(C) Thrombosis reduces embolization and facilitates intervention
(D) It is associated with increased circulating tissue
factor particles and cell apoptosis
26 Which of the following statements is false regarding
plaque regression?
(A) It follows an eccentric pattern, reducing plaque
volume before improving the lumen
(B) It can be obtained by aggressive lipid-lowering
therapy

(C) It improves the lumen and therefore reduces
coronary events
(D) It is associated with reverse lipid transport from
the plaque to the liver
27 Which of the following statements is false regarding
symptomatic, nonculprit plaque progression 1 year
after percutaneous coronary revascularization?
(A) It can be as high as 12% per year in patients with
three-vessel coronary disease
(B) It is higher in patients with diabetes
(C) It is higher in patients younger than 65 years
(D) Most patients present with acute coronary
syndrome (ACS)
(E) Statins are protective


Answers and Explanations
1 Answer C. The AHA classification for early lesions
(Arterioscler Thromb. 1994;14:840–856) defines the
type III lesion as characterized by pools of extracellular lipid and collagen.

11 Answer D. Metalloproteinases do not salvage myocardium. On the contrary, MMPs are associated
with expansion and remodeling of the ventricle after
MI (Circulation. 2002;105:753–758).

2 Answer D. Plaque rupture more frequently is
asymptomatic. Symptomatic plaque rupture is the
exception and not the rule.

12 Answer D. Macrophages are associated

plaque progression, not plaque regression.

3 Answer E. Plaque rupture more frequently occurs
at the shoulders, not the center of the fibrous cap
(Lancet. 1989;2:941–944).
4 Answer C. The individual risk for plaque progression to complete occlusion is lower in nonobstructive
lesions (<5%) when compared with obstructive
lesions (24%) (J Am Coll Cardiol. 1993;22:1141–
1154).

with

13 Answer D. The lipid core is the most potent
thrombogenic substrate of human atherosclerotic
plaques (J Am Coll Cardiol. 1994;23:1562–1569).
14 Answer A.
and SMCs.

The fibrous cap is composed of collagen

15 Answer D. On angioscopy, vulnerable plaques are
associated with a glistening yellow color. Stable
plaques are white (Am Heart J. 1995;130:195–203).

5 Answer C. SMCs are responsible for strengthening, not weakening of the fibrous cap (J Am Coll
Cardiol. 1998;32:283–285).

16 Answer D. Plaque erosion is associated with a
thick, SMC-rich fibrous cap (Circulation. 1996;93:
1354–1363).

6 Answer B. Collagen is not the most potent thrombogenic substrate of the plaque. Lipid core is by far
much more thrombogenic than any other plaque
substrate (J Am Coll Cardiol. 1994;23:1562–1569).

17 Answer B. Mast cells are increased in ruptured
plaques (J Am Coll Cardiol. 1998;32:606–612).

7 Answer E. CRP has been found to be an independent predictor for events in univariate and
multivariate analysis (N Engl J Med. 2005;352:20–28).
8 Answer D. The beneficial effects of ASA in primary
prevention are closely related to CRP levels (N Engl J
Med. 1997;336:973–979). In patients with the lowest
quintile of CRP, ASA does not prevent cardiovascular
events (13% reduction when compared with placebo;
p = not significant). However, in patients with the
highest quintile of CRP, ASA prevents cardiovascular
events (53% reduction when compared with placebo;
p < 0.0001).
9 Answer A. Remodeling preserves the lumen, but
does not protect from heart attacks. It is actually
increased in plaques in patients with acute coronary
events (Circulation. 2000;101:598–603).
10 Answer E. PAI-1 is increased in diabetic plaques
(Circulation. 1998;97:2213–2221).
4

18 Answer D. Macrophage activity in plaque rupture
is mediated by increased apoptosis (J Am Coll Cardiol.
2005;46:937–954).

19 Answer D. Diabetes atherosclerosis is characterized by upregulation of RAGE (Atherosclerosis. 2006;
185:70–77).
20 Answer C. Cell-adhesion molecule expression is
two to three times higher in plaque neovessels than
in the luminal endothelium (J Clin Invest. 1993;92:
945–951).
21 Answer D. The independent predictors of plaque
remodeling include inflammation, calcification, and
medial atrophy (Circulation. 2002;105:297–303).
Cigarette smoking is associated with plaque erosion
but not positive remodeling.
22 Answer D. Intraplaque hemorrhage upregulates
macrophage CD163 receptor, increasing inflammation and foam cell formation (Atherosclerosis.
2002;163:199–201).


Vascular Biology

5

23 Answer D. Most neovessels are derived from adventitial vasa vasorum and do not communicate with the lumen. Only a minority of plaque
neovessels originates from the lumen (Hum Pathol.
1995;26:450–456).

associated with positive remodeling. Most importantly, plaque regression is associated with a significant reduction of new plaque formation, preventing
plaque rupture, and reducing acute coronary events
(J Am Coll Cardiol. 2005;46:937–954).

24 Answer B. SMC proliferation after stent deployment is characterized by increased production of
collagen III, not collagen I.

27 Answer E. Nonculprit plaque progression is a
major cause of recurrent events within the first
year of percutaneous coronary intervention (PCI),
increasing from 4% in single vessel up to 12%
in three-vessel coronary artery disease (CAD).
Independent predictors include diabetes, unstable
syndromes at presentation and age <65 years. Up to
65% present with ACS, and 9% present with total
occlusion. Of note, statins were not protective against
rapid progression within the first year (Circulation.
2005;111:143–149).

25 Answer C. Coronary thrombosis in unstable angina and NSTEMI is mediated by platelet-rich
thrombus (J Am Coll Cardiol. 2005;46:937–954).
Thrombosis activates platelets and may be harmful
in ACS (Circulation. 1994;90:69–77).
26 Answer C. Plaque regression follows an eccentric pattern, initially improving the plaque burden


2
Anatomy and Physiology
Richard A. Lange and L. David Hillis

Questions

mmHg

1 Pressure recordings from the coronary catheter tip
during catheter engagement in the coronary ostium

and withdrawal (see arrow) into the aorta indicate:

100

0

(A) Collateral coronary flow
(B) Obstruction of antegrade coronary flow by the
catheter
(C) Anomalous origin of a coronary artery
(D) Severe aortic stenosis
2 Left ventriculography in the 30 degree right anterior
oblique (RAO) projection shows a ‘‘button’’ projecting from the aortic root (see following figure). This
suggests the patient has:

(A) Occlusion of the proximal right coronary
artery (RCA)
(B) Ulceration in the proximal ascending aorta
(C) Anomalous origin of the left circumflex artery
(D) Focal aortic root dissection
3 Which of the following projections allows the operator to best visualize a proximal left circumflex
stenosis?
(A) 30 degree RAO
(B) 30 degree RAO, 30 degree cranial
(C) 60 degree left anterior oblique (LAO), 30 degree
cranial
(D) 30 degree RAO, 30 degree caudal
4 In what percentage of individuals does the left
circumflex coronary artery provide the blood flow to
the sinoatrial node?

(A) 90%
(B) 60%
(C) 40%
(D) 10%
5 What percentage of individuals with a bicuspid aortic
valve have a left dominant coronary circulation?
(A) 1%
(B) 10%
(C) 30%
(D) 50%
6 In order to obtain a ‘‘spider view’’ to better visualize
the left main, proximal left anterior descending
(LAD) and left circumflex views, the radiographic

6


Anatomy and Physiology

technician should be directed to position the image
intensifier:
(A) 15 degree RAO, 30 degree cranial
(B) 30 degree RAO, 30 degree caudal
(C) 50 degree LAO, 35 degree cranial
(D) 50 degree LAO, 20 degree caudal
7 In clinical practice, the severity of coronary stenosis
is estimated from visual inspection of the coronary
angiogram. Compared with quantitative coronary
angiography, visual estimation of coronary stenosis
usually:

(A)
(B)
(C)
(D)

Underestimates the severity of stenosis by 20%
Underestimates the severity of stenosis by 10%
Overestimates the severity of stenosis by 20%
Provides similar results

8 Impaired vasodilator reserve is first noted when the
coronary luminal diameter narrowing (e.g., stenosis) is:
(A) 50%
(B) 60%
(C) 75%
(D) 90%
9 Coronary angiography demonstrates a mid-right
coronary stenosis in which there is penetration of
contrast material without perfusion. This would be
characterized as:
(A) Thrombolysis in myocardial infarction (TIMI)
0 flow
(B) TIMI 1 flow
(C) TIMI 2 flow
(D) TIMI 3 flow
10 What is a Kugel’s artery?
(A) Anomalous origin of the LAD coronary artery
from the pulmonary artery
(B) Coronary arteriovenous fistula
(C) Conus artery branch

(D) Right-to-right collateral (from proximal to
distal RCA through the atrioventricular (AV)
node branch)
11 A 50% luminal diameter narrowing (e.g., stenosis)
on coronary angiography corresponds to a crosssectional area narrowing of:
(A)
(B)
(C)
(D)

50%
60%
75%
90%

7

12 Endothelial dysfunction can be identified by:
(A) Reduced coronary sinus blood levels of
endothelial-derived relaxing factor (EDRF) and
nitric oxide (NO)
(B) Inability to vasodilate in response to intracoronary nitroprusside
(C) Vasoconstrictor response to intracoronary acetylcholine
(D) Luminal irregularities on coronary angiography
13 All of the following are characteristic of a hemodynamically significant coronary stenosis, except:
(A) A myocardial fractional flow reserve (FFR)
<0.90
(B) An impaired phasic pattern of phasic coronary
flow distal to the stenosis with diastolic to
systolic ratio <1.5

(C) Impaired coronary hyperemic flow (less than
two times basal values)
(D) A translesional pressure gradient >30 mm Hg
14 Flow from which coronary artery or arteries is
represented by great cardiac vein flow?
(A) LAD
(B) Left circumflex
(C) LAD and left circumflex
(D) RCA
15 Which of the following is not true of coronary flow
reserve (CFR)?
(A) It is computed as hyperemic flow velocity
divided by basal mean flow velocity
(B) It can be used to assess the physiologic significance of the stenosis in the epicardial coronary
vessels
(C) Normal CFR is 2.5 to 5
(D) Maximal hyperemia is attained with intracoronary injections of adenosine, papaverine, or
acetylcholine
16 All of the following are true regarding coronary
vascular resistance, except:
(A) In the absence of stenosis, R1 (epicardial vessels)
resistance is trivial
(B) The R2 (prearteriolar) vessels are responsible
for most of the total coronary resistance
(C) The R3 (arteriolar and intramyocardial) vessels
are regulated by neurogenic and local control
(D) Left ventricular (LV) hypertrophy and diabetes
can impair microcirculatory (R3) resistance

8

900 Questions: An Interventional Cardiology Board Review

17 CFR measurements obtained through thermodilution catheter (e.g., Webster catheter) are typically:
(A) Lower than values obtained with Doppler guidewire
(B) Higher than values obtained with Doppler
guidewire
(C) Similar to values obtained with Doppler guidewire
18 The correct formula for determining myocardial oxygen consumption (MVO2 ) from the coronary arterial
or venous flow (Q), arterial oxygen content (AoO2 ),
and coronary sinus oxygen content (CSO2 ) is:
(A) MVO2 = Q/(AoO2 − CSO2 )
(B) MVO2 = Q × (AoO2 − CSO2 )
(C) MVO2 = (AoO2 − CSO2 )/Q
(D) Unable to calculate with the data provided
19 The ‘‘abbreviated’’ form of the Gorlin formula (socalled, Hakki√equation: valve area (cm2 ) = flow (L
per minute)/ peak-to-peak pressure gradient) is often used to estimate valve area in patients with valvular stenosis referred for catheterization. It may be
inaccurate in which of the following circumstances:
(A) Bradycardia (heart rate <60 bpm) or tachycardia (heart rate >60 bpm)
(B) Valve area <1.0 cm2
(C) High cardiac output
(D) Low transvalvular gradient
20 In which of the following circumstances does the use
of an LV–Ao pullback pressure to assess aortic valve
area yield inaccurate results?
(A)
(B)
(C)
(D)

Low (<35 mm Hg) transvalvular gradient
Atrial fibrillation
Postventriculography
All the above

21 Coronary venous oxygen saturation is typically:
(A) 30%
(B) 50%

(C) 65%
(D) 80%
22 Which of the following is not true of corrected TIMI
frame counts (CTFCs)?
(A) TIMI frame counts should be performed on
angiograms obtained at 30 frames per second
(B) The frame rate required for full opacification of
the LAD is 1.7 times longer than the RCA or left
circumflex vessels
(C) In patients successfully treated with thrombolysis, a CTFC of <20 frames per second is
associated with a high risk of adverse events
(D) Prolonged CTFC 4 weeks after myocardial
infarction (MI) is associated with impaired
infarct-related arterial flow at 1 year
23 Which of the following coronary artery anomalies
does not course between the aorta and pulmonary
artery?
(A) Anomalous origin of the LAD artery from the
right cusp
(B) Anomalous origin of the left circumflex artery

from the right cusp
(C) Anomalous origin of the RCA from the left cusp
(D) Anomalous origin of the left main from the right
cusp
24 All of the following are true regarding coronary blood
flow, except:
(A) Coronary α1 -adrenergic receptor stimulation
causes vasodilatation
(B) Stimulation of the parasympathetic nervous
system results in vasoconstriction
(C) Stimulation of B1 receptors in the coronary
arterioles leads to vasodilatation
(D) Stimulation of B2 receptors in the coronary
arterioles leads to vasodilatation


Answers and Explanations
1 Answer B. The pressure recording shows ‘‘ventricularization,’’ in which diastolic pressure is reduced
but systolic pressure is preserved. Normally, the
catheter tip pressure and the sidearm pressure are
similar. If an ostial coronary stenosis is present,
engagement of the catheter may obstruct antegrade blood flow and cause ventricularization of the
catheter pressure waveform (Am Heart J. 1989;118:
1160–1166).
2 Answer C. The most common coronary anomaly
is origin of the left circumflex artery from the
right sinus of Valsalva. This can often be visualized during left ventriculography (30 degree
RAO projection) as a ‘‘dot’’ or ‘‘button’’ projecting
from the aortic root as the left circumflex courses
posterior to the aorta (Circulation 1974;50:768–

773, Ann Thorac Surg. 1997;63:377–381).
3 Answer D. In the 30 degree RAO projection, one
is looking down the AV plane, in which the left
circumflex artery resides. Because the proximal
portion of the vessel is foreshortened in this
view, caudal angulation needs to be applied to
unforeshorten it. In the other angles listed, the
proximal left circumflex is either foreshortened or
overlapped by other vessels.
4 Answer C. The sinus node artery originates from
the left circumflex artery in 40% of individuals and as
a proximal branch from the RCA in 60%, regardless
of whether the patient is right or left dominant.

approximately 20% more severe than that measured
by quantitative coronary angiography (Circulation
1990;82:2231–2234). Therefore, a stenosis that measures 50% is typically called 70%.
8 Answer A. A 50% reduction in lumen diameter
(hence, a 75% reduction in cross-sectional area)
is ‘‘hemodynamically significant’’ in that it reduces the three- to fourfold CFR (N Engl J Med.
1994;330:1782–1788). The ability to increase flow
during vasodilator stimulus is impaired when luminal diameter is reduced 50% and abolished when the
stenosis is >70%.
9 Answer B. As initially defined by the TIMI investigators (N Engl J Med. 1985;312:932–936), TIMI 0
flow represents no perfusion, TIMI 1 flow represents
penetration of contrast material without perfusion
(e.g., contrast material is visualized beyond the area
of obstruction but fails to opacify the entire distal
coronary bed), TIMI 2 flow represents partial perfusion (contrast material visualized in the coronary
distal to the obstruction), and TIMI 3 flow represents

complete perfusion.
10 Answer D. A Kugel’s artery passes from either the
proximal right or left coronary artery down along the
anterior margin of the atrial septum to anastomose
with the AV node branch of the distal RCA to
provide blood supply to the posterior circulation
(Tex Heart Inst. 2004;31:267–270, Am Heart J. 1950;
40:260–270.)

5 Answer C. In the general population, only 10%
of individuals are right dominant (e.g., the posterior
descending artery arises from the distal left circumflex
artery). However, 30% of patients with a bicuspid
valve are left dominant (Am J Cardiol. 1978;42:
57–59).
6 Answer D. The LAO caudal view projects the LAD
upward from the left main in the appearance of a
spider and permits improved visualization of the left
main and the proximal bifurcation.

Kugel’s

RC
V

7 Answer C. Visual estimation of coronary stenosis is subject to significant operator variability
and a systematic form of ‘‘stenosis inflation,’’ in
which the operator’s estimate of diameter stenosis is

A-

P
L

PD

V

9