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CARDIOLOGY
SECRETS
To Lydia, who inspires me to try to be a better husband, friend, and person.
 SIXTH EDITION

CARDIOLOGY
SECRETS

GLENN N. LEVINE, MD, FACC, FAHA

Professor of Medicine, Baylor College of Medicine
Chief, Cardiology Section
Michael E. DeBakey VA Medical Center
Houston, Texas, USA
Elsevier
1600 John F. Kennedy Blvd.
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CARDIOLOGY SECRETS, SIXTH EDITION ISBN: 978-0-323-82675-4

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 In memory of our most beloved Gabby, the best companion ever.

“You think dogs will not be in heaven? I tell you, they will be there long before any of us”.
–Robert Louis Stevenson
 CONTRIBUTORS

Suhny Abbara, MD Neal Barshes, MD, MPH

Chief, Cardiothoracic Imaging Associate Professor of Surgery
Department of Radiology Michael E. DeBakey Department of Surgery
Professor, Department of Radiology Baylor College of Medicine
UT Southwestern Medical Center Houston, Texas, USA
Dallas, Texas, USA
Luc M. Beauchesne, MD, FRCPC, FACC
Richa Agarwal, MD Cardiologist, Adult Congenital Heart Disease Program
Associate Professor of Medicine University of Ottawa Heart Institute
Division of Cardiology Ottawa, Ontario, Canada
Duke University School of Medicine
Durham, North Carolina, USA Jeffrey S. Berman, MD
Cardiology Fellow
Ali M. Agha, MD Department of Medicine, Division of Cardiology
Department of Cardiology Baylor College of Medicine
Baylor College of Medicine Houston, Texas, USA
Houston, Texas, USA
Sheilah Bernard, MD
David Aguilar, MD, MSc Associate Professor of Medicine
Professor of Medicine Section of Cardiology, Department of Medicine
Division of Cardiovascular Medicine Boston Medical Center
University of Kentucky College of Medicine Boston, Massachusetts, USA
Lexington, Kentucky, USA
Gilad Birnbaum, MD
Rami Akhrass, MD Department of Medicine
Regional Director Section of Cardiology
Department of Thoracic and Cardiovascular Surgery Baylor College of Medicine
Cleveland Clinic Houston, Texas, USA
Cleveland, Ohio, USA
Yochai Birnbaum, MD
Mahmoud Al Rifai, MD, MPH Professor
Cardiology Fellow Department of Medicine
Department of Medicine-Cardiology Section of Cardiology
Baylor College of Medicine Baylor College of Medicine
Houston, Texas, USA Houston, Texas, USA
Eric Awtry, MD Fernando Boccalandro, MD, FACC, FSCAI
Associate Professor of Medicine Pro-Care/Odessa Heart Institute
Section of Cardiology Director, Cardiovascular Laboratory
Boston University School of Medicine; Medical Center Hospital
Associate Chief for Clinical Affairs Department of Cardiology
Section of Cardiology Associated Clinical Professor
Boston Medical Center Texas Tech University Health Science Center
Boston, Massachusetts, USA Department of Internal Medicine
Faisal G. Bakaeen, MD Odessa, Texas
Professor Michael Boone, DO
Department of Thoracic and Cardiovascular Surgery Resident, Department of Family Medicine
Cleveland Clinic Waco Family Health Center
Cleveland, Ohio, USA Waco, Texas, USA
Gary J. Balady, MD Stephen Boone, MD, FACEP
Director, Non Invasive Cardiovascular Laboratories Assistant Professor
Section of Cardiology Department of Emergency Medicine
Boston Medical Center Assistant Professor
Professor of Medicine Department of Internal Medicine
Boston University School of Medicine Baylor College of Medicine
Boston, Massachusetts, USA Houston, Texas, USA

vi
 CONTRIBUTORS vii

Sanket Borgaonkar, MD Kim A. Eagle, MD

Chief Fellow, PGY-VII Albion Walter Hewlett Professor of Internal Medicine
Department of Cardiology Department of Internal Medicine
Baylor College of Medicine University of Michigan
Houston, Texas, USA Ann Arbor, Michigan, USA
Biykem Bozkurt Lothar Faber, MD, FESC, FACC
Professor Professor
Mary and Gordon Cain Chair and Professor of Home Office
Medicine Schuerhornweg 36
Director, Winters Center for Heart Failure Bielefeld, Germany
Research at Baylor College of Medicine Savitri Fedson, MA, MD
Medical Care Line Executive Professor
DeBakey VA Medical Center Center for Medical Ethics and Health Policy
Houston, Texas, USA Baylor College of Medicine;
Arzu Canan, MD Professor
Assistant Professor Department of Medicine
Department of Radiology, Cardiothoracic Imaging Michael E. DeBakey VA Medical Center
UT Southwestern Medical Center Houston, Texas, USA
Dallas, Texas, USA Matthew J. Feinstein, MD, MSc
Kelly N. Casteel, MD Assistant Professor of Medicine
Assistant Professor Division of Cardiology, Department of Medicine
Department of Benign Hematology Northwestern University Feinberg School of Medicine
MD Anderson Cancer Center Chicago, Illinois, USA
Houston, Texas, USA G. Michael Felker, MD, MHS
Professor of Medicine
Tiffany Chen, MD
Division of Cardiology
Assistant Professor of Clinical Medicine
Duke University School of Medicine
Division of Cardiovascular Medicine
Durham, North Carolina, USA
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania, USA James J. Fenton, MD
Clinical Associate Professor
Leslie T. Cooper Jr., MD Pulmonary Medicine
Elizabeth C. Lane, Ph.D. and M. Nadine Zimmerman, National Jewish Health
Ph.D. Professor of Internal Medicine Denver, Colorado, USA
Chair, Cardiovascular Department
Jacksonville, Florida, USA Michael E. Field, MD
Professor of Medicine
Edmond M. Cronin, MB BCh BAO Department of Medicine
Associate Professor Medical University of South Carolina
Department of Medicine Charleston, South Carolina, USA
Temple University
Philadelphia, Pennsylvania, USA Scott D. Flamm, MD, MBA
Professor of Radiology
George D. Dangas, MD, Department of Radiology
Professor of Medicine and Surgery Cleveland Clinic
Director, Cardiovascular Innovation Cleveland, Ohio, USA
Mount Sinai Hospital
Icahn School of Medicine at Mount Sinai Lee A. Fleisher, MD
New York, USA Professor
Department of Anesthesiology and Critical Care
Amish S. Dave, MD, PhD, FACC Perelman School of Medicine at the University
Assistant Professor of Medicine of Pennsylvania
Department of Cardiology Philadelphia, Pennsylvania, USA
Houston Methodist Hospital
Laura Flink
Houston, Texas, USA
The permanente medical group
Ali E. Denktas, MD California, USA
Professor of Medicine Marat Fudim, MD
Department of Cardiology Assistant Professor of Medicine
Baylor College of Medicine Division of Cardiology
Houston, Texas, USA Duke University School of Medicine
Durham, North Carolina, USA
 viii CONTRIBUTORS

Sanjay Ganapathi, MD, DM Brian D. Hoit, MD

Professor Professor of Medicine and Physiology and Biophysics
Department of Cardiology Department of Medicine
Sree Chitra Tirunal Institute for Medical Sciences and Case Western Reserve University;
Technology Director of Echocardiography
Trivandrum, India University Hospitals Cleveland Medical Center
Cleveland, Ohio, USA
Kathryn A. Gayle, MD
Fellow Geoffrey D. Huntley, MD
Department of Cardiovascular Medicine Fellow
Vanderbilt University Medical Center Department of Cardiovascular Medicine
Nashville, Tennessee, USA Mayo Clinic
Rochester, Minnesota, USA
Marie Gerhard-Herman, MD
Associate Professor Aliza Hussain, MD
Department of Medicine Fellow Physician
Mass General Brigham Department of Medicine, Section of Cardiology
Boston, Massachusetts, USA Baylor College of Medicine
Houston, Texas, USA
Casey Graziani, MD
Fellow Scott E. Janus, MD
Departments of Pulmonary and Critical Care Medicine Physician
Baylor College of Medicine Department of Cardiology
Houston, Texas, USA University Hospitals of Cleveland
Cleveland, Ohio, USA
Cindy Grines, MD
Chief Scientific Officer Xiaoming Jia, MD
Cardiovascular Institute Fellow, Department of Medicine
Northside Hospital Baylor College of Medicine
Atlanta, Georgia, USA Houston, Texas, USA

Aakriti Gupta, MD Hani Jneid, MD, FACC, FAHA, FSCAI

Cardiologist Associate Professor of Medicine
Department of Cardiology Department of Cardiology
Columbia University Irving Medical Center Baylor College of Medicine
New York, New York, USA Houston, Texas, USA

Gabriel B. Habib Sr., MD, FACC, FCCP, FAHA Jose A. Joglar, MD

Professor of Medicine Professor of Internal Medicine
Department of Medicine Department of Internal Medicine
Baylor College of Medicine UT Southwestern Medical Center
Houston, Texas, USA Dallas, Texas, USA

Ihab Hamzeh, MD Thomas A. Kent, MD

Associate Professor of Medicine Robert Welch Chair Professor
Department of Medicine Center for Genomic and Precision Medicine
Baylor College of Medicine Institute of Biosciences and Technology
Houston, Texas, USA Texas A&M Health Science Center-Houston
Adjunct Professor
Sivadasanpillai Harikrishnan, MD, DM, DNB Stanley H. Appel Department of Neurology
Professor Houston Methodist Hospital
Department of Cardiology Houston, Texas, USA
Sree Chitra Tirunal Institute for Medical Sciences and
Umair Khalid, MD, FACC
Technology
Assistant Professor of Medicine – Cardiology
Trivandrum, India
Baylor College of Medicine
Gustavo A. Heresi, MD, MS Houston, Texas, USA
Director, Pulmonary Vascular and CTEPH Program
Sarah Kohnstamm, MD
Department of Pulmonary and Critical Care Medicine
Clinical Assistant Professor
Cleveland Clinic
Department of Cardiovascular Medicine
Cleveland, Ohio, USA
Michigan Medicine
Tomoya T. Hinohara, MD Ann Arbor, Michigan, USA
Fellow, Department of Cardiology Nitin Kondamudi, MD
Houston Methodist Hospital House Staff
Houston, Texas, USA Division of Cardiology, Department of Internal Medicine
University of Texas Southwestern Medical Center
Dallas, Texas, USA
 CONTRIBUTORS ix

Chayakrit Krittanawong, MD Sharyl R. Martini

House Staff Medical Director
Section of Cardiology VA National Telestroke Program
Baylor College of Medicine Department of Veterans Affairs
Houston, Texas, USA Assistant Professor
Department of Neurology
Michael H. Kroll, MD Baylor College of Medicine
Professor Houston, Texas, USA
Department of Benign Hematology
UT MD Anderson Cancer Center Jim McCord, MD
Houston, Texas, USA Professor of Medicine, Wayne State Medical School
Heart and Vascular Institute
Richard A. Lange, MD, MBA Cardiology Director Observation Unit
President Henry Ford Hospital
Texas Tech University Health Sciences Center El Paso Detroit, Michigan, USA
Dean, Paul L. Foster School of Medicine
El Paso, Texas, USA Roxana Mehran, MD, FACC, FAHA, MSCAI
Mount Sinai Professor in Cardiovascular Clinical
Glenn N. Levine, MD, FACC, FAHA Research and Outcomes
Professor of Medicine Professor of Medicine (Cardiology), and Population
Baylor College of Medicine Health Science and Policy
Chief, Cardiology Section Director, the Center for Interventional Cardiovascular
Michael E. DeBakey VA Medical Center Research and Outcomes
Houston, Texas, USA Icahn School of Medicine at Mount Sinai
Paul Litvak, MD New York, New York, USA
Assistant Professor Lisa A. Mendes, MD
Department of Neurology Professor of Medicine
Baylor College of Medicine Department of Cardiovascular Medicine
Houston, Texas, USA Vanderbilt University Medical Center
Jing Liu, MD Nashville, Tennessee, USA
Cardiology Fellow Geno J. Merli, MD, MACP, FHM, FSVM
Department of Internal Medicine-Cardiology Professor of Medicine and Surgery
Baylor College of Medicine Department of Surgery
Houston, Texas, USA Sydney Kimmel Medical College at Thomas Jefferson
Melissa A. Lyle, MD University
Assistant Professor of Medicine Co-Director
Cardiologist, Department of Cardiovascular Medicine Jefferson Vascular Center
Mayo Clinic Thomas Jefferson University
Jacksonville, Florida, USA Senior Vice President & Associate CMO
Thomas Jefferson University Hospital
Thomas Maddox, MD, MSc Philadelphia, Pennsylvania, USA
Professor
Division of Cardiology Hassan Mir, MD, FRCPC
Washington University School of Medicine Cardiologist and Clinician Investigator
St. Louis, Missouri, USA Cardiology
University of Ottawa Heart Institute;
Jamal H. Mahar, MD, MEd Assistant Professor
Cardiology Fellow Department of Medicine
Department of Cardiology University of Ottawa
Baylor College of Medicine Ottawa, Ontario, Canada
Houston, Texas, USA
Arunima Misra, MD
Salvatore Mangione, MD Associate Professor
Associate Professor of Medicine Department of Internal Medicine
SKMC of Thomas Jefferson University Baylor College of Medicine
Philadelphia, Pennsylvania, USA Houston, Texas, USA
Rita Marr, BS, MD Ajith Nair, MD
Staff Cardiologist Assistant Professor of Medicine
Department of Cardiology Department of Medicine
Michael E. DeBakey VA Medical Center Baylor College of Medicine
Houston, Texas, USA Houston, Texas, USA
 x CONTRIBUTORS

Vijay Nambi, MD, PhD Lawrence Phillips, MD

Staff Cardiologist Director, Nuclear Cardiology
Department of Medicine Division of Cardiology, Department of Medicine
Michael E DeBakey Veterans Affairs Hospital; NYU Langone Health
Associate Professor New York, New York, USA
Division of Atherosclerosis and Vascular Medicine, June K. Pickett, MD
Section of Cardiovascular Research Fellow
Department of Medicine Department of Cardiology/Internal Medicine
Baylor College of Medicine Baylor College of Medicine
Houston, Texas, USA
Houston, Texas, USA
G. Titus Ngeno, MBCHB, MSc Andrew Pipe, BA, MD, LLD(Hon), DSc(Hon), FRCPSC(Hon)
Assistant Professor Professor
Department of Medicine Faculty of Medicine, University of Ottawa;
Duke University Division of Cardiac Prevention and Rehabilitation
Durham, North Carolina, USA University of Ottawa Heart Institute
Vuyisile T. Nkomo, MD, MPH Ottawa, Ontario, Canada
Professor of Medicine Stuart B. Prenner, MD
Director, Valvular Heart Disease Clinic Assistant Professor of Clinical Medicine
Department of Cardiovascular Medicine Section of Advanced Heart Failure and Cardiac Transplant
Mayo Clinic University of Pennsylvania
Rochester, Minnesota, USA Philadelphia, Pennsylvania, USA
E. Magnus Ohman, MD, FRCPI, FESC, FACC Prabhakar Rajiah, MBBS, MD,FRCR
Professor Professor of Radiology
Department of Medicine Department of Radiology, Mayo Clinic
Duke University School of Medicine Rochester, Minnesota, USA
Durham, North Carolina, USA
Pattara Rattanawong, MD
Nicolas L. Palaskas, MD Fellow in Cardiovascular Medicine
Assistant Professor Assistant Professor of Medicine
Department of Cardiology Department of Cardiovascular Diseases
UT MD Anderson Cancer Center Mayo Clinic
Houston, Texas, USA Phoenix, Arizona, USA
Ambarish Pandey, MD, MSCS Heidi Reich, MD
Assistant Professor Cardiothoracic Surgeon
Division of Cardiology, Department of Medicine Department of Surgery
University of Texas Southwestern Medical Center Central California Heart and Lung Surgery
Dallas, Texas, USA Fresno, California, USA
Shivda Pandey, MBBS Eric E. Roselli, MD, FACS
Assistant Professor of Medicine Chief, Adult Cardiac Surgery
Section of Cardiology Surgical Director, Aorta Center
Boston University School of Medicine Department of Thoracic and Cardiovascular Surgery
Boston, Massachusetts, USA Heart Vascular and Thoracic Institute, Cleveland Clinic
Cleveland, Ohio, USA
Lavannya M. Pandit, MD, MS
Associate Professor of Medicine Smita Scholtz
Department of Pulmonary, Critical Care, and Sleep Clinic for General and Interventional Cardiology/Angiology
Medicine Herz- und Diabeteszentrum NRW, Ruhr University Bochum
Baylor College of Medicine/Michael E. DeBakey Bad Oeynhausen, Germany
VA Medical Center Paul Schurmann, MD
Houston, Texas, USA Associate Professor
Maria A. Parekh, MD Department of Cardiology
Chief Resident Houston Methodist Hospital
Department of Neurology Houston, Texas, USA
Baylor College of Medicine Nagendra Boopathy Senguttuvan, MD, DM, FACC, FSCAI
Houston, Texas, USA Associate Professor of Cardiology & Senior Consultant
W. Frank Peacock, MD, FACEP, FACC Interventional Cardiologist
Vice Chair for Research Sri Ramachandra Institute of Higher Education
Department of Emergency Medicine and Research
Baylor College of Medicine Adjunct Faculty, Indian Institute of Technology-Madras
Houston, Texas, USA Chennai, Tamil Nadu, India
 CONTRIBUTORS xi

Hirak Shah, MD John M. Suffredini, DO

Department of Cardiology Cardiology Fellow
Duke University Section of Cardiology
Durham, North Carolina, USA Baylor College of Medicine
Houston, Texas, USA
Nishant R. Shah, MD, MPH
Assistant Professor Luis A. Tamara, MD
Department of Medicine, Division of Cardiology Chief of Nuclear Medicine/PET-CT
Alpert Medical School of Brown University Department of Nuclear Medicine
Providence, Rhode Island, USA MEDVAMC
Houston, Texas, USA
Sanjiv J. Shah, MD
Stone Professor of Medicine Jeremy J. Thaden, MD
Department of Medicine/Cardiology Assistant Professor
Northwestern University Department of Cardiovascular Medicine
Chicago, Illinois, USA Mayo Clinic
Rochester, Minnesota, USA
Tina Shah, MD
Staff Cardiologist Paaladinesh Thavendiranathan, MD, MSc
Kaiser Permanente Cardiologist, Associate Professor of Medicine
Seattle, Washington, USA Division of Cardiology and Joint Division of Medical Imaging
Peter Munk Cardiac Center,
Fidaa Shaib, MD TGH, UHN, University of Toronto
Associate Professor Toronto, Ontario, Canada
Departments of Pulmonary, Critical Care, and Sleep Medicine
Baylor College of Medicine Kara A. Thompson, MD, FACC
Houston, Texas, USA Associate Professor, Department of Cardiology
MD Anderson
Win K. Shen, MD Houston, Texas, USA
Professor and Consultant
Department of Cardiovascular Diseases Miguel Valderrábano, MD
Mayo Clinic Arizona Lois and Carl Davis Centennial Chair, Methodist DeBakey
Phoenix, Arizona, USA Heart and Vascular Center
Associate Professor of Medicine, Weill College of Medicine,
Katherine Shreyder, MD, PhD Cornell University
Cardiology Fellow Director, Division of Cardiac Electrophysiology
Department of Cardiovascular Medicine Department of Cardiology
Lahey Hospital and Medical Center Houston Methodist Hospital
Tufts University School of Medicine
Burlington, Massachusetts, USA Patrick R. Vargo, MD
Associate Staff
Mohita Singh, MD Department of Thoracic and Cardiovascular Surgery
Cardiology Fellow Cleveland Clinic
Department of Internal Medicine Cleveland, Ohio, USA
UT Southwestern
Dallas, Texas, USA Mahesh K. Vidula, MD
Fellow in Cardiovascular Medicine
Gulmohar Singh-Kucukarslan, MD, MS Department of Medicine, Division of Cardiovascular Medicine
Department of Internal Medicine University of Pennsylvania
Henry Ford Hospital Philadelphia, Pennsylvania, USA
Detroit, Michigan, USA
Shilpa Vijayakumar, MD
Audrey E. Spelde, MD Cardiology Fellow
Clinical Instructor Department of Medicine, Division of Cardiology
Department of Anesthesiology and Critical Care Alpert Medical School of Brown University
The University of Pennsylvania Providence, Rhode Island, USA
Philadelphia, Pennsylvania, USA
Salim S. Virani, MD, PhD
Sarah A. Spinler, BS Pharm, PharmD Professor
Professor and Chair Sections of Cardiovascular Research, Department of Medicine
Department of Pharmacy Practice Baylor College of Medicine
Binghamton University School of Pharmacy Houston, Texas, USA
and Pharmaceutical Sciences
Johnson City, New York, USA Birgit Vogel, MD
Cardiovascular Imaging Fellow
Deepthi Sudhakar, MD, MS Mount Sinai Morningside Hospital
Fellow Icahn School of Medicine at Mount Sinai
Department of Cardiology
New York, New York, USA
Baylor College of Medicine
Houston, Texas, USA
 PREFACE

This is now the sixth edition of Cardiology Secrets and the fourth edition I have edited. Among the 16 books I have
authored or edited, this series of books is the most satisfying and rewarding; from the feedback that we receive, it is
clear that we, to at least some extent, achieve our objectives of trying to educate readers and disseminate knowledge
on the optimal evaluation and management of patients of cardiovascular disease, and do so in a concise, digestible,
and entertaining manner. As always, we have updated all chapters to bring readers the most up-to-date information
and recommendations to the extent that a format such as this allows.
I am again deeply indebted to the hundreds of national and international experts and thought leaders in cardio-
vascular disease who over the years have taken time from their many academic and clinical responsibilities, as well
as family time, to contribute to the Cardiology Secrets series of books. I am similarly appreciative to the many persons
at Elsevier who I have worked with to bring this book in both hardcopy and electronic format to fruition.
It is my hope that you find this edition of the book both educational and enjoyable and that it in some small
way serves to improve the care of the patients that entrust their health and wellbeing to us. As always, I welcome
comments and suggestions from readers; my email is glevine@bcm.tmc.edu.
Glenn N. Levine, MD, FACC, FAHA

xii
CONTENTS

Top 100 Secrets xvii

Glenn N. Levine

I  Diagnostic Examinations and Procedures

CHAPTER 1 CARDIOVASCULAR PHYSICAL EXAMINATION 3
Glenn N. Levine, Salvatore Mangione

CHAPTER 2 HEART MURMURS AND SOUNDS 10

Glenn N. Levine, Salvatore Mangione

CHAPTER 3 ELECTROCARDIOGRAPHY 19
Gilad Birnbaum, Glenn N. Levine, Yochai Birnbaum

CHAPTER 4 CHEST X-RAY 27

James J. Fenton, Glenn N. Levine

CHAPTER 5 EXERCISE STRESS TESTING 35

Fernando Boccalandro, Katherine Shreyder

CHAPTER 6 AMBULATORY ECG MONITORS 42

Chayakrit Krittanawong, Glenn N. Levine

CHAPTER 7 ECHOCARDIOGRAPHY 49
Xiaoming Jia, Arunima Misra

CHAPTER 8 NUCLEAR CARDIOLOGY 63

Laura Flink, Lawrence Phillips

CHAPTER 9 CARDIAC POSITRON EMISSION TOMOGRAPHY 71

Luis A. Tamara

CHAPTER 10 CARDIAC MAGNETIC RESONANCE IMAGING 77

Paaladinesh Thavendiranathan, Scott D. Flamm

CHAPTER 11 CARDIAC COMPUTED TOMOGRAPHY 85

Arzu Canan, Prabhakar Rajiah, Suhny Abbara

CHAPTER 12 BEDSIDE HEMODYNAMIC MONITORING 97

Ajith Nair

CHAPTER 13 CARDIAC CATHETERIZATION: CORONARY ANGIOGRAM, INTRACORONARY IMAGING,

AND PHYSIOLOGY 105
Umair Khalid

II Chest Pains, Coronary Artery Disease,

and Acute Coronary Syndromes
CHAPTER 14 CHEST PAINS AND ANGINA 117
Glenn N. Levine

CHAPTER 15 CHRONIC STABLE ANGINA 126

Mahmoud Al Rifai, Glenn N. Levine, Richard A. Lange

CHAPTER 16 NON–ST-ELEVATION ACUTE CORONARY SYNDROME 133

John M. Suffredini, Glenn N. Levine

xiii
 xiv contents

CHAPTER 17 ST-ELEVATION MYOCARDIAL INFARCTION 141

Jing Liu, Glenn N. Levine

CHAPTER 18 CARDIOGENIC SHOCK 151

Deepthi Sudhakar, Sanket Borgaonkar, Hani Jneid

CHAPTER 19 PERCUTANEOUS CORONARY INTERVENTION 158

Ali E. Denktas, Cindy Grines

CHAPTER 20 CORONARY ARTERY BYPASS SURGERY 168

Rami Akhrass, Faisal G. Bakaeen

III Heart Failure and Cardiomyopathies

CHAPTER 21 MYOCARDITIS 177
Melissa A. Lyle, Leslie T. Cooper Jr

CHAPTER 22 LV DYSFUNCTION AND DILATED CARDIOMYOPATHY: ETIOLOGIES AND EVALUATION 186

Hirak Shah, Richa Agarwal

CHAPTER 23 HEART FAILURE WITH PRESERVED EJECTION FRACTION 193

Nitin Kondamudi, Ambarish Pandey

CHAPTER 24 HYPERTROPHIC CARDIOMYOPATHY 199

Lothar Faber, Smita Scholtz

CHAPTER 25 RESTRICTIVE CARDIOMYOPATHY 208

Stuart B. Prenner, Sanjiv J. Shah

CHAPTER 26 ACUTE DECOMPENSATED HEART FAILURE 217

G. Michael Felker, Marat Fudim

CHAPTER 27 HEART FAILURE: LONG-TERM MANAGEMENT 224

Savitri Fedson, Glenn N. Levine, Biykem Bozkurt

CHAPTER 28 HEART TRANSPLANTATION 235

Savitri Fedson

IV Valvular Heart Disease

CHAPTER 29 AORTIC STENOSIS 249
Geoffrey D. Huntley, Jeremy J. Thaden, Vuyisile T. Nkomo

CHAPTER 30 AORTIC REGURGITATION 260

Kathryn A. Gayle, Lisa A. Mendes

CHAPTER 31 MITRAL REGURGITATION 267

Mahesh K. Vidula, Tiffany Chen

CHAPTER 32 MITRAL STENOSIS 279

Sivadasanpillai Harikrishnan, Sanjay Ganapathi

CHAPTER 33 TRANSCATHETER AORTIC VALVE REPLACEMENT 285

Nagendra Boopathy Senguttuvan, George D. Dangas

CHAPTER 34 ENDOCARDITIS AND ENDOCARDITIS PROPHYLAXIS 296

June K. Pickett, Tina Shah, Rita Marr

V Arrhythmias
CHAPTER 35 ATRIAL FIBRILLATION 307
Michael E. Field

CHAPTER 36 SUPRAVENTRICULAR TACHYCARDIA 313

Mohita Singh, Jose A. Joglar
 contents xv

CHAPTER 37 VENTRICULAR ARRHYTHMIAS 319

Edmond M. Cronin

CHAPTER 38 CARDIAC PACING FOR BRADYCARDIA, CONDUCTION ABNORMALITIES, AND HEART

FAILURE 327
Paul Schurmann, Miguel Valderrábano

CHAPTER 39 IMPLANTABLE CARDIOVERTER DEFIBRILLATORS 336

Paul Schurmann, Amish S. Dave

CHAPTER 40 CARDIAC ARREST AND RESUSCITATION 345

Jeffrey S. Berman, Glenn N. Levine

VI Primary and Secondary Prevention

CHAPTER 41 HYPERTENSION 353
Gabriel B. Habib Sr

CHAPTER 42 HYPERLIPIDEMIA 362

Aliza Hussain, Salim S. Virani, Vijay Nambi

CHAPTER 43 DIABETES AND CARDIOVASCULAR DISEASE 371

David Aguilar

CHAPTER 44 SMOKING CESSATION 377

Hassan Mir, Andrew Pipe

CHAPTER 45 PHYSICAL ACTIVITY, EXERCISE, AND THE HEART 382

Shivda Pandey, Eric Awtry, Gary J. Balady

VII  The Heart in Specific Populations and Conditions

CHAPTER 46 CARDIAC MANIFESTATIONS OF HIV 391
Matthew J. Feinstein

CHAPTER 47 CARDIAC MANIFESTATIONS OF RHEUMATOLOGIC DISORDERS 397

Shilpa Vijayakumar, Nishant R. Shah

CHAPTER 48 CARDIO-ONCOLOGY 402

Kara A. Thompson

CHAPTER 49 COCAINE AND THE HEART 409

Gulmohar Singh-Kucukarslan, Jim McCord

CHAPTER 50 CARDIOVASCULAR SEQUELAE OF COVID-19 415

Aakriti Gupta, Thomas Maddox

CHAPTER 51 HEART DISEASE IN THE ELDERLY 420

G. Titus Ngeno, Tomoya T. Hinohara, E. Magnus Ohman

CHAPTER 52 HEART DISEASE IN PREGNANCY 430

Sheilah Bernard

CHAPTER 53 HEART DISEASE IN WOMEN 438

Birgit Vogel, Roxana Mehran

CHAPTER 54 SLEEP APNEA AND THE HEART 444

Ihab Hamzeh, Fidaa Shaib

VIII Peripheral Vascular and Cerebrovascular Disease

CHAPTER 55 PERIPHERAL ARTERIAL DISEASE 451
Marie Gerhard-Herman

CHAPTER 56 AORTIC ANEURYSMS 459

Heidi Reich, Patrick R. Vargo, Faisal G. Bakaeen, Eric E. Roselli
 xvi contents

CHAPTER 57 AORTIC DISSECTION 468

Sarah Kohnstamm, Kim A. Eagle

CHAPTER 58 CAROTID ARTERY DISEASE 475

Ali M. Agha, Vijay Nambi, Neal Barshes

CHAPTER 59 ISCHEMIC STROKE 482

Maria A. Parekh, Paul Litvak, Sharyl R. Martini, Thomas A. Kent

CHAPTER 60 HEMORRHAGIC STROKE AND CEREBRAL VENOUS SINUS THROMBOSIS 493

Maria A. Parekh, Paul Litvak, Sharyl R. Martini, Thomas A. Kent

IX Venous Thromboembolic Disease

CHAPTER 61 DEEP VEIN THROMBOSIS 499
Geno J. Merli

CHAPTER 62 PULMONARY EMBOLISM 508

Jamal H. Mahar, Gustavo A. Heresi

CHAPTER 63 HYPERCOAGULABLE STATES 520

Kelly N. Casteel, Michael H. Kroll

X Additional Topics in Cardiology

CHAPTER 64 ADULT CONGENITAL HEART DISEASE 529
Luc M. Beauchesne

CHAPTER 65 CARDIAC TUMORS 537

Nicolas L. Palaskas, Glenn N. Levine

CHAPTER 66 HYPERTENSIVE CRISIS 542

Stephen Boone, Michael Boone, W. Frank Peacock

CHAPTER 67 ORAL ANTICOAGULATION THERAPY 548

Sarah A. Spinler

CHAPTER 68 PERICARDITIS, PERICARDIAL CONSTRICTION, AND PERICARDIAL TAMPONADE 563

Scott E. Janus, Brian D. Hoit

CHAPTER 69 PREOPERATIVE CARDIAC EVALUATION 569

Audrey E. Spelde, Lee A. Fleisher

CHAPTER 70 PULMONARY HYPERTENSION 577

Casey Graziani, Lavannya M. Pandit

CHAPTER 71 SYNCOPE 586

Pattara Rattanawong, Glenn N. Levine, Win K. Shen

CHAPTER 72 TRAUMATIC HEART DISEASE 597

Fernando Boccalandro, Katherine Shreyder

INDEX 604
TOP 100 SECRETS

1. The four conditions identified as having the highest risk of adverse outcome from endocarditis for which
prophylaxis with dental procedures is still recommended by the American Heart Association are prosthetic cardiac
valve, previous infective endocarditis, certain cases of congenital heart disease, and cardiac transplantation
recipients who develop cardiac valvulopathy.
2. Causes of ST-segment elevation include acute myocardial infarction (MI) as a result of thrombotic occlusion of a
coronary artery, Prinzmetal’s angina, cocaine-induced myocardial infarction, pericarditis, left ventricular aneurysm,
left bundle branch block (LBBB), left ventricular hypertrophy with repolarization abnormalities, J point elevation,
and severe hyperkalemia.
3. During pregnancy, maternal heart rate (HR) increases throughout the 40 weeks, mediated partially by increased
sympathetic tone and heat production. Hormonal changes cause an increase in both plasma volume (from water
and sodium retention) and red blood cell volume (from erythrocytosis) during a normal pregnancy. Stroke volume
subsequently continues to increase until the third trimester, when inferior vena cava (IVC) return may be
compromised by the gravid uterus. Maternal cardiac output (CO) increases by 30% to 50% during a normal
pregnancy. Systolic blood pressure drops during the first half of pregnancy and returns to normal levels by
delivery.
4. The major risk factors for coronary artery disease (CAD) are family history of premature coronary artery disease
(father, mother, brother, or sister who first developed clinical CAD at age younger than 45–55 for males and at age
younger than 55–60 for females), hypercholesterolemia, hypertension, cigarette smoking, and diabetes mellitus.
5. Coronary flow reserve (the increase in coronary blood flow in response to agents that lead to microvascular
dilation) begins to decrease when a coronary artery stenosis is 50% or more luminal diameter. However, basal
coronary flow does not begin to decrease until the lesion is 80% to 90% luminal diameter.
6. Important causes of chest pain not related to atherosclerotic coronary artery disease include aortic dissection,
pneumothorax, pulmonary embolism, pneumonia, hypertensive crisis, Prinzmetal’s angina, cardiac syndrome X,
anomalous origin of the coronary artery, pericarditis, esophageal spasm or esophageal rupture (Boerhaave’s
syndrome), and shingles.
7. Sinus node dysfunction, commonly referred to as sick sinus syndrome, refers to a broad array of abnormalities of
the sinus node ranging from atrial impulse formation through propagation of the depolarization impulse. Sick
sinus syndrome can manifest as sinus bradycardia, paroxysmal sinus arrest, sinus node exit block or chronotropic
insufficiency. Tachycardia-bradycardia (“tachy-brady”) syndrome is a common appearance of sick sinus syndrome
in patients with an atrial fibrillation or atrial flutter.
8. Other causes of elevated cardiac troponin besides acute coronary syndrome and myocardial infarction that should
be considered in patients with chest pains include pulmonary embolism, aortic dissection, myopericarditis, severe
aortic stenosis, and severe chronic kidney disease.
9. Causes of pericarditis include infectious (viral, bacterial, fungal, mycobacterial, human immunodeficiency virus
[HIV] associated), neoplastic (usually metastatic from lung or breast; melanoma, lymphoma, or acute leukemia),
myocardial infarction, injury (postpericardiotomy, traumatic), radiation, metabolic (myxedema, uremia), and
connective tissue disease. In the developed world, the most common cause remains viral etiologies, whereas
tuberculosis is the most frequent cause in developing countries.
10. Prinzmetal’s angina, also called variant angina, is an unusual cause of angina caused by coronary vasospasm.
Patients with Prinzmetal’s angina are typically younger and often female. Treatment is based primarily on the use
of calcium channel blockers and nitrates.
11. Microvascular angina appears to play a major role in the underlying mechanisms of ischemia with nonobstructive
coronary arteries (INOCA) and is defined as the occurrence of chest pain based on abnormal coronary flow
reserve due to coronary microvascular dysfunction in the absence of obstructive coronary artery disease. This
condition was prior referred to as “syndrome X.” Microvascular angina is more common in women and likely
underdiagnosed. Abnormal coronary flow reserve is diagnosed as a coronary flow reserve of less than 2.5, which
requires measurement using invasive (flow wire) or noninvasive (positron emission tomography, echo Doppler, or
cardiac magnetic resonance imaging) techniques. Standardized criteria for diagnosis of microvascular angina
have been proposed. However, many uncertainties about the underlying pathophysiological mechanisms of
microvascular angina persist, and further studies are needed to develop the evidence base for diagnosis and
especially for the treatment of this condition. For now, potential therapies include beta-blockers, short-acting
nitrates, calcium antagonists, and angiotensin-converting enzyme inhibitors for symptom relief.
12. The three main types of ASDs are secundum (80%), primum (15%), and sinus venosus (5%). The secundum ASD
is a defect involving the floor of the fossa ovalis of the atrial septum. It usually presents as an isolated anomaly.
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The primum ASD is a defect at the base of the atrial septum adjacent to the atrioventricular valves. It is invariably
part of an atrioventricular septal defect (endocardial cushion defect), and a cleft mitral valve is almost always
present. The sinus venosus ASD is a defect of the posterior part of the septum, usually located in the superior
part. In the majority of cases, a sinus venosus ASD is associated with anomalous connections or drainage of the
right-sided pulmonary veins
13. Numerous cardiovascular medications are associated with drug-induced lupus erythematosus. Those with a
definitive causative relationship include procainamide, hydralazine, diltiazem, quinidine, and methyldopa. Those
with a probable causative relationship include beta-blockers, captopril, hydrochlorothiazide, amiodarone, and
ticlopidine.
14. Subarachnoid hemorrhage due to aneurysm rupture classically presents with the worst headache of one’s life;
loss of consciousness, nausea/vomiting, nuchal rigidity, and focal neurologic signs are also common. Although
large amounts of subarachnoid blood are readily apparent on CT, even small amounts of subarachnoid blood can
provoke symptoms. Detection of these small “sentinel bleeds” is vital, as they herald aneurysm rupture.
15. Findings that suggest a heart murmur is pathologic and requires further evaluation include the presence of
symptoms, extra heart sounds, thrills, abnormal ECG or chest radiography, diminished or absent S2, holosystolic
(or late systolic) murmur, any diastolic murmur, and all continuous murmurs.
16. In the early- and pre-ART eras (early 2000s and prior), common CVD manifestations of HIV/AIDS included
pericardial effusion/tamponade, dilated cardiomyopathy and severe systolic dysfunction, myocarditis, marantic
(thrombotic) or infectious endocarditis, cardiac tumors (Kaposi’s sarcoma, lymphoma), pulmonary arterial
hypertension, and sudden cardiac death. These complications may still occur in the present era, especially in the
setting of poor HIV control, although now common CVD complications tend to be more subacute and chronic,
including coronary artery disease and MI, heart failure with preserved and reduced ejection fraction, and sudden
cardiac death
17. The major categories of ischemic stroke are large vessel atherosclerosis (including embolization from carotid to
cerebral arteries), small vessel vasculopathy or lacunar type, and cardioembolic. Hemorrhagic strokes are
classified by their location: subcortical (associated with uncontrolled hypertension in 60% of cases) versus cortical
(more concerning for underlying mass, arteriovenous malformation, or amyloidosis).
18. Acute MI remains the leading cause of cardiogenic shock in the United States. In fact, despite the decline in its
incidence with progressive use of timely primary PCI, cardiogenic shock still occurs in 5% to 8% of hospitalized
patients with ST-segment elevation myocardial infarction (STEMI). Unlike what is commonly believed, cardiogenic
shock may also occur in up to 2% to 3% of patients with non–ST-segment-elevation myocardial infarction
(NSTEMI). Overall, 40,000 to 50,000 cases of cardiogenic shock occur annually in the United States. Chronic
congestive heart failure may decompensate into cardiogenic shock and is the second most common etiology for
cardiogenic shock after acute MI. Ventricular septal rupture and papillary muscle rupture, both usually occurring
within days of a transmural MI, are less common causes.
19. Cardiomyopathy in COVID-19 may occur as a result of direct viral damage, myocarditis, microvasculature
dysfunction secondary to endothelial cell damage or systemic inflammatory response syndrome in response to
SARS-CoV-2 infection. Other potential etiologies include thrombotic myocardial infarction or severe myocardial
ischemia in patients with preexisting coronary artery disease, stress-mediated myocardial dysfunction,
tachycardia-induced cardiomyopathy, and myocardial stunning after resuscitation or prolonged hypotension. The
mainstay of management of COVID-19–related cardiomyopathy is supportive care.
20. Findings that should raise the suspicion for endocarditis include bacteremia/sepsis of unknown cause, fever,
constitutional symptoms, hematuria/glomerulonephritis/suspected renal infarction, embolic event of unknown
origin, new heart murmurs, unexplained new atrioventricular (AV) nodal conduction abnormality, multifocal or rapid
changing pulmonic infiltrates, peripheral abscesses, certain cutaneous lesions (Osler’s nodes, Janeway’s lesions),
and specific ophthalmic manifestations (Roth’s spots).
21. Common radiographic signs of congestive heart failure include enlarged cardiac silhouette, left atrial enlargement,
hilar fullness, vascular redistribution, linear interstitial opacities (Kerley’s lines), bilateral alveolar infiltrates, and
pleural effusions (right . left).
22. Classic ECG criteria for the diagnosis of ST-segment elevation myocardial infarction (STEMI), warranting
thrombolytic therapy, are ST-segment elevation greater than 0.1 mV in at least two contiguous leads (e.g., leads III
and aVF or leads V2 and V3) or new or presumably new left bundle branch block (LBBB).
23. Perioperative cardiac morbidity occurs most commonly during the first 3 postoperative days and includes
perioperative myocardial infarction (PMI), unstable angina, congestive heart failure, cardiac death, and nonfatal
cardiac arrests. Studies suggest a peak incidence of PMI within the first 48 hours or earlier. Among patients with
known ischemic heart disease, incidence of PMI is approximately 5%, with incidence decreasing to 2% to 4%
among patients with risk factors but no history of ischemic heart disease and decreasing still among patients with
no risk factors. Additionally, mortality from PMI has decreased from previous rates of 30% to 50% to
approximately 12%. A more recently described but separate syndrome from PMI is myocardial injury after
noncardiac surgery (MINS). MINS is defined by elevated troponin in the perioperative period due to cardiac
ischemia that does not meet criteria for MI set by the Fourth Universal Definition of Myocardial Infarction. While
seemingly more benign, MINS is independently associated with risk of death and cardiovascular complications in
the year following surgery.
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24. In patients receiving anthracycline therapy for cancer, cardiac function should be reassessed before therapy, at 3,
6, and 9 months during treatment, and at 12 and 18 months after initiation of treatment. If the ejection fraction
decreases to less than 40%, the anthracycline should be discontinued. Lifelong cardiac monitoring of cardiac
function is recommended, as the incidence of cardiac toxicity increases with length of time since treatment, with
LVEF assessment every 1 to 5 years, depending on the total dose of anthracycline administered. More frequent
monitoring is recommended in patients who received radiation therapy in addition to anthracyclines.
25. The triad of findings suggestive of right ventricular infarction is hypotension, distended neck veins, and clear
lungs.
26. Cessation of cerebral blood flow for as short a period as 6 to 8 seconds can precipitate syncope.
27. The most common causes of syncope in pediatric and young patients are neurally mediated syncope (up to 75%
of cases), conversion reactions (psychiatric causes), and primary arrhythmic causes (e.g., long-QT syndrome,
Wolff-Parkinson-White syndrome, catecholaminergic polymorphic ventricular tachycardia [CPVT], arrhythmogenic
right ventricular dysplasia/cardiomyopathy [ARVC/D], or Brugada syndrome), obstructive structural heart diseases
(hypertrophic cardiomyopathy [HCM], aortic stenosis, pulmonary hypertension), and myocardial dysfunction
(myocarditis, cardiomyopathy, congenital coronary anomaly, or post-Kawasaki disease). Smoking cessation is the
most important of the modifiable risk factors for cardiovascular disease. The products of tobacco smoke
contribute directly, and distinctly, to the development of atherosclerosis and the adverse consequences that follow.
With smoking cessation, a rapid and sustained reduction in the likelihood of incident cardiac disease. In those
with established cardiac disease, there similarly is a dramatic reduction in future or recurrent cardiovascular
adverse event. In both instances, the benefits of smoking cessation accrue rapidly and reflect the elimination,
rather than the ongoing management, of a major risk factor. Smoking cessation should be accorded a priority in
those with cardiac disease in every professional setting; to do otherwise can be seen as reflective of substandard
care.
28. Preexisting renal disease and diabetes are the two major risk factors for the development of contrast nephropathy.
Preprocedure and postprocedure hydration is the most established method of reducing the risk of contrast
nephropathy.
29. Very high-risk congenital heart disease lesions in pregnancy associated with particularly poor outcome include
Eisenmenger’s syndrome, severe symptomatic aortic stenosis, severe mitral stenosis, Marfan’s syndrome with a
dilated aortic root (.45 mm), bicuspid valve with ascending aorta greater than 50 mm, Mechanical valve
prosthesis, significant systemic ventricular dysfunction (EF #30%), and history of Fontan’s procedure with an
associated complication. These patients should be counseled accordingly about the significant maternal risks and
poor fetal outcomes that are associated with pregnancy.
30. All adults aged 20 years or older should undergo dyslipidemia screening with either a fasting or nonfasting
lipoprotein profile to document baseline low-density lipoprotein cholesterol (LDL-C) and evaluate atherosclerotic
cardiovascular disease (ASCVD) risk (class IB). Testing should include total cholesterol, LDL-C, high-density
lipoprotein cholesterol (HDL-C), and triglycerides. To assess response to lifestyle changes or lipid-lowering
medications, a repeat fasting lipid panel is still recommended 4 to 12 weeks after starting or changing therapy.
The most common secondary causes of dyslipidemia include hypothyroidism, overt proteinuria (such as in chronic
renal failure and nephrotic syndrome), excessive alcohol intake, uncontrolled diabetes mellitus, obstructive liver
disease, weight gain/obesity, pregnancy, and drugs (e.g., progestins, anabolic steroids, corticosteroids).
31. The four main patient management groups in whom lipid-lowering therapy should be considered based on the
2018 ACC/AHA cholesterol guidelines are as follows:
32. Established ASCVD: Individuals with clinical ASCVD (i.e., acute coronary syndromes, or a history of MI, stable or
unstable angina, coronary or other arterial revascularization, stroke, transient ischemic attack, or peripheral artery
disease, including aortic aneurysm presumed to be of atherosclerotic origin).
33. Primary severe hypercholesterolemia: Individuals with primary elevations of LDL-C (defined as LDL-C 190 mg/dL;
i.e., familial hypercholesterolemia [FH]).
34. Diabetes mellitus (DM): Individuals 40 to 75 years of age with diabetes and LDL-C 70 to 189 mg/dL.
35. Underlying ASCVD risk: Individuals without clinical ASCVD or LDL-C $190 mg/dL or diabetes who are 40 to
75 years of age with LDL-C 70 to 189 mg/dL and an estimated 10-year ASCVD risk of 7.5% or higher.
36. Components of high-quality CPR include (1) chest compressions at a rate between 100 and 120 times per minute;
(2) chest compressions for adults at least 2 inches but not more than 2.4 inches (6 cm), for children compressions of
2 inches (5 cm), and for infants compressions of 1.5 inches (4 cm); (3) allowing for complete chest recoil after each
compression; (4) minimizing interruptions in chest compressions; and (5) avoiding excessive ventilation.
37. D-Dimer is highly sensitive but not specific for the diagnosis of PE (sensitivity 99%, specificity 41% using a cutoff
of 599 mg/L). It should be used in conjunction with other clinical prediction rules and can be elevated in states
associated with inflammation such as infection, malignancy, recent surgery, and renal insufficiency. D-dimer levels
can also increase with age, and adjusted D-dimer cutoffs can be estimated as age 3 10.
38. Up to 5% of all hypertension cases are secondary, meaning that a specific cause can be identified. Causes of
secondary hypertension include renal artery stenosis, renal parenchymal disease, primary hyperaldosteronism,
pheochromocytoma, Cushing’s disease, hyperparathyroidism, aortic coarctation, and sleep apnea.
39. Hypertensive crises have historically been classified as hypertensive emergency or hypertensive urgency, although
the latter term is potentially misleading. When evaluating patients with severe elevations in blood pressure, the
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primary consideration in determining the need for rapid treatment is the presence of acute target-organ
dysfunction. Target organs affected predominately include those of the cardiovascular, renal, or central nervous
systems. Although severe hypertension is commonly defined as blood pressure greater than 180/120 mm Hg,
there is no absolute value of blood pressure that dictates urgent treatment. Patients with hypertensive emergency
and associated end-organ damage will benefit from aggressive reductions in blood pressure, while patients with
isolated severe hypertension may be harmed by similarly aggressive treatment measures. Clinical syndromes
associated with hypertensive emergency include hypertensive encephalopathy, intracerebral hemorrhage, unstable
angina/acute myocardial infarction, pulmonary edema, dissecting aortic aneurysm, or eclampsia. In general, the
initial goal for hypertensive emergencies will be to reduce mean arterial blood pressure by no more than 25% in
the first few hours, followed by further gradual reduction over the next 24 hours.
40. Patients over the age of 75 years have the highest incidence and complications of NSTEMI events. Despite similar
of greater benefit derived from intervention compared to younger patients, diagnosis and treatment is often
delayed as a result of atypical ACS symptoms, comorbidities, and concern for periprocedural complications.
41. Cardiac risk indices for perioperative risk stratification have been used in clinical practice for more than 30 years.
These indices do not inform clinicians on how to modify perioperative care specifically, but they do provide a
baseline assessment of risk and the value of different intervention strategies. The revised cardiac risk index was
developed by studying more than 5000 patients and identifying the following six risk factors: high-risk surgery,
ischemic heart disease, history of congestive heart failure, history of cerebrovascular disease, preoperative
treatment with insulin, and preoperative serum creatinine greater than 2 mg/dL.
42. Common causes of depressed left ventricular systolic dysfunction and cardiomyopathy include coronary artery
disease, hypertension, valvular heart disease, and alcohol abuse. Other causes include cocaine abuse, collagen
vascular disease, viral infection, myocarditis, peripartum cardiomyopathy, human immunodeficiency virus/acquired
immunodeficiency disease (HIV/AIDS), tachycardia-induced, hypothyroidism, anthracycline toxicity, and Chagas’
disease.
43. The classic signs and symptoms of patients with heart failure are dyspnea on exertion (DOE), orthopnea,
paroxysmal nocturnal dyspnea (PND), and lower extremity edema.
44. The most common cause of sudden cardiac death in young athletes is hypertrophic cardiomyopathy, followed by
anomalous origin of a coronary artery. Other causes of sudden cardiac death in younger persons in general
include long-QT syndrome, Brugada syndrome, CPVT, and arrhythmogenic right ventricular dysplasia/
cardiomyopathy (ARVD/C), as well as pulmonary embolism.
45. Side effects due to amiodarone treatment are common and include organ toxicity to the lung, thyroid, and liver.
Amiodarone can also cause or exacerbate sinus bradycardia. It also can cause bluish discoloration of the skin,
photosensitivity, tremor, peripheral neuropathy, ocular deposits, and optic neuropathy. Monitoring of patients while
on amiodarone varies by clinician but includes periodic laboratory testing for liver and thyroid dysfunction as well
as chest radiography and pulmonary function testing.
46. Patients with depressed ejection fractions (,40%) should be treated with agents that block the rennin-
angiotensin-aldosterone system such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor
blockers (ARBs), the combination agent sacubitril (a neprilysin inhibitor)/valsartan, and aldosterone receptor
blockers in order to improve symptoms, decrease hospitalizations, and decrease mortality. Sacubitral/valsartan is
considered preferable for long-term therapy to ACE inhibitors and ARBs. The beta-blockers metoprolol succinate,
carvedilol, and bisoprolol have been shown to decrease mortality in appropriately selected patients and are also
considered first-line agents. These agents should be initiated in euvolemic patients on stable background heart
failure therapy. Hydralazine and isosorbide dinitrate are used in patients who are unable to tolerate ACE inhibitors,
ARBs, or ARNIs because of renal failure, angioedema, or as a consideration for add-on therapy. Hydralazine and
isosorbide dinitrate should be considered in addition to an ACE inhibitor, ARB, or ARNI in Black Americans in
particular because it appears to have an added mortality benefit and can be considered as an add-on therapy in
others if the patient’s blood pressure allows.
47. Biventricular pacing (BiV) or cardiac resynchronization therapy (CRT) should be considered for patients in sinus
rhythm with NYHA class II-IV symptoms, left ventricular ejection fraction (LVEF) less than 35%, and QRS greater
than 150 milliseconds.
48. High-risk features in patients hospitalized with acute decompensated heart failure (ADHF) include low systolic
blood pressure, elevated blood urea nitrogen (BUN), hyponatremia, history of prior heart failure hospitalization,
elevated brain natriuretic peptide (BNP), and elevated troponin I or T.
49. Implantable cardioverter defibrillators (ICDs) should be considered for primary prevention of sudden cardiac death
in patients whose left ventricular ejection fractions remains less than 30% to 35% despite optimal medical
therapy or revascularization and who have good-quality life expectancy of at least 1 year.
50. Anticoagulation treatment duration for pulmonary embolism (PE) depends greatly on whether the PE was provoked
(by a clear transient risk factor that has now resolved) versus unprovoked (without a clear cause). Provoked PEs
with transient risk factors are typically treated for 3 months but can be extended up to 6 or 12 months. Patients
may qualify for indefinite therapy in the event of an unprovoked PE or the presence of ongoing risk factors such
as an active malignancy, immobility, or an inherited prothrombotic condition. These decisions must always take
into account a patient’s estimated risk of bleeding, recurrence, comorbidities, and patient preferences (e.g., fall
risk, occupation, and life expectancy).
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51. The three primary factors that promote venous thrombosis (known together as Virchow’s triad) are (1) venous
blood stasis, (2) injury to the intimal layer of the venous vasculature, and (3) abnormalities in coagulation or
fibrinolysis.
52. Transthoracic echo (TTE) has a sensitivity of 60% to 75% in the detection of native valve endocarditis. In cases
where the suspicion of endocarditis is higher, a negative TTE should be followed by a transesophageal echo (TEE),
which has a sensitivity of 88% to 100% and a specificity of 91% to 100% for native valves.
53. Normal cardiac signs and symptoms of pregnancy include hyperventilation (as a result of increased minute
ventilation), peripheral edema (from volume retention and vena caval compression by the gravid uterus),
dizziness/lightheadedness (from reduced SVR and vena caval compression), and palpitations (normal HR increases
by 10–15 beats/min). Pathologic cardiac signs and symptoms of pregnancy include the following: anasarca or
generalized edema and paroxysmal nocturnal dyspnea, which are not components of normal pregnancy and
warrant workup syncope (possibly due to pulmonary embolism, tachy/bradyarrhythmias, pulmonary hypertension,
or obstructive valvular pathology), chest pain (possibly due to aortic dissection, pulmonary embolism, angina, or
myocardial infarction), and hemoptysis (possibly due to occult mitral stenosis)
54. The main echocardiographic criteria for severe mitral stenosis are mitral valve area less than 1.5 cm2, diastolic
pressure half-time of 150 milliseconds or greater, and pulmonary artery (PA) systolic pressure greater than 50 mm
Hg. These usually occur in the setting of a mean transvalvular gradient greater than 5 to 10 mm Hg,
55. The symptoms associated with obstructive sleep apnea (OSA) include snoring, excessive daytime sleepiness, and
sudden arousals with chocking/gasping, and are important clues to suspect the diagnosis. Ventricular pauses,
second-degree atrioventricular (AV) block, premature ventricular contractions (PVCs), and nonsustained ventricular
tachycardia occur more frequently in patients with sleep apnea. Prolonged pauses up to 15 seconds have been
reported during OSA in patients in whom electrophysiological evaluation did not reveal significant intrinsic sinus or
AV nodal disease. Cardiovascular sequelae of OSA include systemic hypertension, coronary artery disease,
congestive heart failure, and pulmonary hypertension. OSA is a frequent cause of uncontrolled hypertension.
Continuous positive airway pressure (CPAP) significantly decreases systolic and diastolic BP, more notably in those
with resistant hypertension.
56. Women comprise approximately 40% of all acute coronary syndrome presentations. Women present with coronary
artery disease up to 10 years later than men. Although the prevalence of coronary disease increases with age,
prevalence is also on the rise in younger women. Women derive the same treatment benefit from beta-blockers,
statins, and antiplatelet therapy, although they are underprescribed acute care therapies, as are treatments for
secondary prevention compared to men. Women have a higher rate of death within 1 year of first myocardial
infarction (MI) and higher rate of recurrent MI within 5 years of first MI than men.
57. Hypertrophic cardiomyopathy (HCM) is a primary cardiac disorder characterized by myocardial hypertrophy and a
nondilated left ventricle (LV) in the absence of both an accountable increase in cardiac afterload (i.e., aortic
stenosis or systemic hypertension) and an underlying systemic or metabolic disease. The hypertrophy is caused
by a pathogenic variant of cardiac sarcomere proteins. Historically, and due to the fact that two basic phenotypes
(i.e., with and without obstruction to outflow, discussed later) exist within the HCM spectrum, there has been
known a confusing array of names, such as idiopathic hypertrophic subaortic stenosis (IHSS), or muscular
subaortic stenosis. Currently, hypertrophic cardiomyopathy is the preferred term.
58. In patients with pericardial effusions, echocardiography findings that indicate elevated intrapericardial pressure
and tamponade physiology include diastolic indentation or collapse of the right ventricle (RV), compression of the
right atrium (RA) for more than one-third of the cardiac cycle, lack of inferior vena cava (IVC) collapsibility with
deep inspiration, 25% or more variation in mitral or aortic Doppler flows, and 50% or greater variation of tricuspid
or pulmonic valves flows with inspiration.
59. The causes of pulseless electrical activity (PEA) can be broken down to the Hs and Ts of PEA, which are
hypovolemia, hypoxemia, hydrogen ion (acidosis), hyperkalemia/hypokalemia, hypoglycemia, hypothermia, toxins,
tamponade (cardiac), tension pneumothorax, thrombosis (coronary and pulmonary), and trauma.
60. A hypercoagulable state should be suspected in patients with idiopathic thrombosis at any age, family history of
venous thromboembolism, thrombosis at unusual sites (such as cerebral, hepatic, mesenteric, renal, or portal
veins), recurrent unprovoked/unexplained thromboses, recurrent unexplained fetal loss, warfarin-induced skin
necrosis, purpura fulminans, or recurrent superficial thrombophlebitis
61. The most common cause of culture-negative endocarditis is prior use of antibiotics. Other causes include fastidious
organisms (HACEK group, Legionella, Chlamydia, Brucella, certain fungal infections) and noninfectious causes.
62. The common inherited hypercoagulable states are factor V Leiden and prothrombin G20210A, which are due to
mutations in the genes for factor V and prothrombin. Factor V Leiden is a point mutation in factor V that renders
factor V resistant to breakdown by activated protein C (R506Q), and prothrombin G20210A is a mutation in the
noncoding region of the prothrombin gene that results in increased protein synthesis (prothrombin levels of
110%–120%). Less common inherited hypercoagulable states are due to deficiencies of the natural anticoagulant
proteins antithrombin, protein C, and protein S. Mutations in the folate-metabolizing enzyme methylene
tetrahydrofolate reductase (MTHFR) leading to elevated blood homocysteine levels are sometimes mistakenly
designated an inherited hypercoagulable state. Hemodynamically significant atrial septal defects (ASDs) have a
shunt ratio greater than 1.5 are usually 10 mm or larger in diameter and are usually associated with right
ventricular enlargement.
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63. Important causes of ventricular tachyarrhythmias include coronary artery disease, depressed LVEF, hypertrophic
cardiomyopathy, prolonged QT interval, Brugada syndrome, ARVD/C, and idiopathic VT.
64. Findings suggestive of a hemodynamically significant coarctation include small diameter (,10 mm or ,50% of
reference normal descending aorta at the diaphragm), presence of collateral blood vessels, and a gradient across
the coarctation of more than 20 to 30 mm Hg.
65. The CHA2DS2-VASc score is now used to assess the risk of stroke in patients with atrial fibrillation, replacing the
CHADS2 score. Factors used to sum the score include CHF, hypertension, diabetes, CVA/TIA, vascular disease,
female gender, and older age. Guidelines recommend a DOAC (in DOAC-eligible patients) over warfarin for atrial
fibrillation in men with a CHA2DS2-VASc risk score of 2 or more and in women with a CHA2DS2-VASc risk score
of 3 or more, except in patients with atrial fibrillation and either moderate or severe mitral stenosis or a
mechanical heart valve where warfarin is recommended regardless of CHA2DS2-VASc risk score. In men with a
CHA2DS2-VASc risk score of 1 or women with a CHA2DS2-VASc risk score of 2, anticoagulation may be
considered.
66. In general, there is no clear role for medical therapy in patients with severe (stage C or D) primary mitral
regurgitation. Surgical or transcatheter intervention (e.g., MitraClip) should be considered even before the onset of
symptoms. Secondary MR is commonly associated with LV dysfunction and systolic heart failure. As such,
optimization of guideline-directed medical therapy for heart failure is indicated. Improving LV function and
ventricular remodeling can reduce the severity of secondary mitral regurgitation. In patients who have persistent
symptoms and significant secondary mitral regurgitation despite optimal medical therapy for heart failure
(including cardiac resynchronization therapy when appropriate), surgical or percutaneous intervention could be
considered.
67. Pericardial effusions occur in up to 21% of patients with cancer. Malignancies commonly associated with
pericardial effusions include lung cancer, leukemia, lymphoma, and breast cancer. Unfortunately, overall 1-year
survival for patients with malignant cells in the pericardial fluid is only 12%
68. Active cardiac conditions for which the patient should undergo evaluation and treatment before noncardiac
surgery include unstable or severe angina, recent MI, decompensated heart failure, high-grade AV block,
symptomatic ventricular arrhythmias, symptomatic bradycardia, severe aortic stenosis, and severe mitral stenosis.
69. Transcatheter aortic valve replacement (TAVR), alternately known as transcatheter aortic valve implantation (TAVI),
is a procedure in which a diseased aortic valve is replaced via an endovascular or transapical approach, using an
expandable valve delivered with a catheter. The decision on surgical aortic valve replacement (SAVR) versus TAVR
should be based upon an individual risk-benefit analysis, performed for each patient by the Heart Valve Team.
TAVR can be considered now in patients at high, intermediate, and low surgical risk. TAVR is contraindicated for
patients with a life expectancy of less than 1 year based on noncardiac factors (e.g., metastatic malignancies), in
order to strike an appropriate balance between the risks and benefits of the procedure.
70. Myocarditis is an inflammatory disease of the myocardium that can occur as a result of exposure to a discrete
external trigger, antigens such as viruses, bacteria, parasites, toxins, or drugs, or as a result of an internal trigger,
including autoimmune activation against self-antigens. The cardiac manifestations include acute heart failure,
arrhythmias, atrioventricular block, sudden death, and chronic dilated cardiomyopathy Myocarditis causes 9% to
16% of cases of unexplained nonischemic dilated cardiomyopathy (DCM).
71. The SGLT2 class of medications, initially intended to be used for management of diabetic patients, have been shown in
patients with HFrEF to have significant benefit for heart failure–related hospitalization and death irrespective of the
presence of type-2 diabetes.
72. Important complications in heart transplant recipients include infection, rejection, vasculopathy (diffuse coronary
artery narrowing), arrhythmias, hypertension, renal impairment, malignancy (especially skin cancer and
lymphoproliferative disorders), and osteoporosis (caused by steroid use).
73. The classic symptoms of aortic stenosis are angina, syncope, and those of heart failure (dyspnea, orthopnea,
paroxysmal nocturnal dyspnea, edema, etc.). Once any of these symptoms occur, the average survival without
surgical intervention is 5, 3, or 2 years, respectively.
74. Class I indications for aortic valve replacement (AVR) include (1) development of symptoms in patients with severe
aortic stenosis; (2) a left ventricular ejection fraction of less than 50% in the setting of severe aortic stenosis; and
(3) the presence of severe aortic stenosis in patients undergoing coronary artery bypass grafting, other heart valve
surgery, or thoracic aortic surgery.
75. The major risk factors for venous thromboembolism (VTE) include previous thromboembolism, immobility, cancer,
and other causes of hypercoagulable state (protein C or S deficiency, factor V Leiden, antithrombin deficiency),
advanced age, major surgery, trauma, and acute medical illness.
76. The antiphospholipid syndrome is the most important cause of acquired hypercoagulability. It develops de novo or
secondary to lymphoproliferative or rheumatologic conditions. Other acquired hypercoagulable states are heparin-
induced thrombocytopenia, myeloproliferative neoplasms (MPNs), paroxysmal nocturnal hemoglobinuria (PNH),
and cancer. The prevalence of cancer-associated VTE varies with the type of malignancy and its treatment. It is
associated with an average relative risk of a first VTE of approximately 6, with an absolute 6-month incidence of
recurrence—on anticoagulation—of at least 10%
77. The Wells’ score in cases of suspected pulmonary embolism includes deep vein thrombosis (DVT) symptoms and
signs (3 points); pulmonary embolism (PE) as likely as or more likely than alternative diagnosis (3 points); heart
 TOP 100 SECRETS xxiii

rate greater than 100 beats/min (1.5 point); immobilization or surgery in previous 4 weeks (1.5 point); previous
DVT or PE (1.5 point); hemoptysis (1.0 point); and cancer (1 point).
78. Cardiogenic shock is a state of end-organ hypoperfusion due to cardiac failure and the inability of the
cardiovascular system to provide adequate blood flow to the extremities and vital organs. In general, patients with
cardiogenic shock manifest persistent hypotension (systolic blood pressure ,80–90 mm Hg or a mean arterial
pressure 30 mm Hg below baseline) with severe reduction in cardiac index (,1.8 L/min/m2) in the presence
of adequate or elevated filling pressure (left ventricular end-diastolic pressure .18 mm Hg or right ventricular
end-diastolic pressure .10–15 mm Hg).
79. Acute aortic regurgitation may result from either abnormalities of the valve cusps or aortic root. Abnormalities
of the valve cusps that may lead to acute aortic regurgitation include infective endocarditis and iatrogenic
causes, such as balloon dilation of the aortic valve. The most common causes of acute aortic regurgitation
related to the aortic root include aortic dissection and chest trauma. The physical findings of aortic
regurgitation (AR) include widened pulse pressure, a palpable dynamic left ventricular apical beat that is
displaced downward and to the left, a diastolic blowing murmur heard best along the left sternal border with
the patient sitting upward and leaning forward, and a low-pitched diastolic rumble heard to the left ventricular
(LV) apex (Austin Flint murmur).
80. The rate of ischemic stroke in patients with nonvalvular atrial fibrillation (AF) is about 2 to 7 times that of persons
without AF, and the risk increases dramatically as patients age. Both paroxysmal and chronic AF carry the same
risk of thromboembolism.
81. Class I recommended criteria for CRT include the presence of sinus rhythm, class II, III, or ambulatory class IV symptoms
despite good medical therapy, LVEF less than or equal to 35%, and QRS more than 150 milliseconds (especially if left
bundle branch block morphology is present). CRT may also be considered in those with less prolonged QRS duration
(120–150 milliseconds), although benefit is generally not as great and/or not as well established.
82. Between 40% and 70% of cardiac transplant recipients experience rejection within the first year posttransplant.
Most episodes occur in the first 6 months, with a decrease in frequency after 12 months. Acute allograft rejection
is the leading cause of death in the first year after transplant; this emphasizes the importance of early diagnosis
and treatment. Most patients are asymptomatic early in the course of rejection; therefore, routine biopsies are
necessary to assist in the diagnosis of rejection.
83. The target international normalized ratio (INR) for warfarin therapy in most cases of cardiovascular disease is 2.5,
with a range of 2.0 to 3.0. In certain patients with mechanical heart valves (e.g., older valves, mitral position), the
target is 3.0 with a range of 2.5 to 3.5.
84. The major complications of percutaneous coronary intervention (PCI) include periprocedural MI, acute stent
thrombosis, coronary artery perforation, contrast nephropathy, access site complications (e.g., retroperitoneal
bleed, pseudoaneurysm, arteriovenous fistula), stroke, and a very rare need for emergency CABG.
85. Chronic aortic regurgitation may result from abnormalities of the aortic valve cusps or aortic root. In the United
States, the two most common abnormalities of valve cusps leading to chronic aortic regurgitation are calcific
aortic valve disease and congenitally bicuspid aortic valve. Other abnormalities of valve cusps that may lead to
chronic aortic regurgitation include infective endocarditis, inflammatory diseases (including lupus, rheumatoid
arthritis, ankylosing spondylitis, Takayasu arteritis, and Crohn’s disease), myxomatous degeneration
of the aortic valve, and prosthetic aortic valve dysfunction. Abnormalities of the aortic root that may lead to
chronic aortic regurgitation include Marfan’s syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta,
annuloaortic ectasia, ascending aortic dissection, aortic aneurysm, and aortic degeneration resulting from
hypertension and age-related aortic dilation.
86. Anticoagulation improves survival in patients with acute symptomatic pulmonary embolism (PE). In patients with
acute PE, a therapeutic level of anticoagulation should ideally be achieved within 24 hours because this reduces
the risk of recurrence. The three different types of “acute aortic syndromes” are aortic dissection, intramural
hematoma, and penetrating atherosclerotic ulcer.
87. The new definition of pulmonary hypertension is a mean pulmonary arterial pressure (mPAP) greater than
20 mm Hg as measured during invasive hemodynamic testing. The change in mPAP criteria (from previous
threshold of 25 mm Hg) reflected research in normal subjects suggesting mPAP of 20 mm Hg as the likely
upper limit of normal.
88. The most important risk factors for ischemic stroke are a prior stroke and age. The most important modifiable risk
factor for stroke is hypertension. Other risk factors for ischemic stroke include diabetes, smoking, carotid stenosis,
and a lipid profile with low HDL, high triglycerides, and high LDL. Cardiac diseases such as atrial fibrillation and
valvular disease are ischemic stroke risk factors. The most significant risk factor for the commonest type of
hemorrhagic stroke is chronic hypertension.
89. Indications for surgery in cases of endocarditis include acute aortic insufficiency or mitral regurgitation leading to
congestive heart failure, cardiac abscess formation/perivalvular extension, persistence of infection despite
adequate antibiotic treatment, recurrent peripheral emboli, cerebral emboli, infection caused by microorganisms
with a poor response to antibiotic treatment (e.g., fungi), prosthetic valve endocarditis (particularly if hemodynamic
compromise exists), “mitral kissing infection”, and large (.10 mm) mobile vegetations.
90. Complications of aortic dissection include cardiac tamponade, aortic insufficiency, myocardial infarction, proximal
or distal malperfusion syndromes, and aortic rupture.
 xxiv TOP 100 SECRETS

91. General criteria for surgical intervention in cases of thoracic aortic aneurysm are, for the ascending thoracic
aorta, aneurysmal diameter of 5.5 cm (4.5–5.0 cm in patients with Marfan’s syndrome and 5.0–5.5 cm in
patients with bicuspid aortic valves and aortopathy), and for the descending thoracic aorta, aneurismal diameter
of 6.5 cm (6 cm in patients with Marfan’s syndrome).
92. Pericarditis is the most common cardiac manifestation of systemic lupus erythematosus and can occur with or
without a pericardial effusion. Nonbacterial thrombotic endocarditis (NBTE) is also common, particularly in patients
with antiphospholipid antibodies. The vegetations seen in NBTE are generally small and most often affect the
mitral valve. These vegetations carry a high risk of thromboembolism, necessitating lifelong anticoagulation.
Systemic lupus erythematosus is an independent risk factor for premature coronary artery atherosclerosis,
particularly in patients with antiphospholipid antibodies, lupus nephritis, and/or severe disease activity.
93. The ankle-brachial index (ABI) is the ratio of systolic blood pressure at the level of the ankle to the systolic blood
pressure measured at the level of the brachial artery. A normal ankle-brachial index should be greater than 1.00.
Using a diagnostic threshold of 0.90 to 0.91, several studies have found the sensitivity of the ABI to be 79% to
95% and the specificity to be 96% to 100% to detect stenosis of 50% or more reduction in lumen diameter. An
ABI of 0.40 or less is associated with an increased risk of rest pain, ischemic ulceration, or gangrene. Patients
with long-standing diabetes or end-stage renal disease on dialysis and elderly patients may have
noncompressible leg arterial segments caused by medial calcification, resulting in false elevation of the ABI.
These patients are best evaluated using digital pressures and with assessment of the quality of the arterial
waveform in the PVR studies or by measuring toe-brachial index.
94. The acutely ill medical patient admitted to the hospital with congestive heart failure or severe respiratory
disease, or who is confined to bed and has one or more additional risk factors, including active cancer, previous
venous thromboembolism, sepsis, acute neurologic disease, or inflammatory bowel disease, should receive DVT
prophylaxis with either unfractionated heparin, a low molecular weight heparin, or fondaparinux.
95. The incidence of detected AAA in studies of older men, smokers, and those with family history of AAA is 5.5%.
Screening for AAA with ultrasound examination in older (.65 years) men has been shown to decrease AAA-
related mortality. In the European guidelines, screening for AAA is recommended in all men above 65 years of
age and may be considered in women above 65 years of age with history of current or past smoking. In the US
guidelines, screening is recommended in men 60 years of age or older who are either the siblings or offspring of
patients with AAA and in men age 65 to 75 who have ever smoked.
96. Temporary or permanent pacing is indicated in the setting of acute MI, with or without symptoms, for (1) complete
third-degree block or advanced second-degree block that is associated with block in the His-Purkinje system (wide
complex ventricular rhythm) and (2) transient advanced (second-degree or third-degree) AV block with a new bundle
branch block.
97. Class I indications for aortic valve replacement in patients with aortic regurgitation (AR) include (1) the presence
of symptoms in patients with severe AR, irrespective of left ventricular systolic function; (2) chronic severe AR
with left ventricular systolic dysfunction (ejection fraction 50% or less), even if asymptomatic; and (3) chronic,
severe AR in patients undergoing coronary artery bypass grafting (CABG), other heart valve surgery, or thoracic
aortic surgery.
98. Myocardial contusion is a common, reversible injury that is the consequence of a nonpenetrating trauma to the
myocardium. It is detected by elevations of specific cardiac enzymes with no evidence of coronary occlusion
and by reversible wall motion abnormalities detected by echocardiography.
99. Classical signs for cardiac tamponade include Beck’s triad of (1) hypotension caused by decreased stroke
volume, (2) jugulovenous distension caused by impaired venous return to the heart, and (3) muffled heart sounds
caused by fluid inside the pericardial sac, as well as pulsus paradoxus and general signs of shock such as
tachycardia, tachypnea, and decreasing level of consciousness.
100. Tumors metastasize to the heart by direct extension, venous extension, hematogenous spread, or lymphatic
spread. Pericardial involvement is the most common cardiac site of metastatic disease. The most common tumors
that spread to the heart are those of the lung, breast, and leukemias, due to the high prevalence of these
malignancies. Melanoma and mesothelioma have the greatest propensity to spread to the heart. Patients with
cocaine-induced chest pain should be treated with intravenous benzodiazepines, which can have beneficial
hemodynamic effects and relieve chest pain, and aspirin therapy, as well as nitrate therapy if the patient remains
hypertensive. Beta-blockers (including labetalol) should not be administered in the acute setting of cocaine-
induced chest pain.
 I
Diagnostic
Examinations
And Procedures

1
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CARDIOVASCULAR PHYSICAL

CHAPTER 1
EXAMINATION
Glenn N. Levine, Salvatore Mangione

Editor’s Note to Readers: For an excellent and more detailed discussion of the cardiovascular physical examination,
read Physical Diagnosis Secrets, 2nd edition, by Salvatore Mangione.

1. What is the meaning of a slow rate of rise of the carotid arterial pulse?
A carotid arterial pulse that is reduced (parvus) and delayed (tardus) suggests the presence of aortic valvular
stenosis. Occasionally, this also may be accompanied by a palpable thrill. If ventricular function is good, a slower
upstroke correlates with a higher transvalvular gradient. In left ventricular failure, however, parvus and tardus may
occur even with mild aortic stenosis (AS).
2. What is the significance of a brisk carotid arterial upstroke?
It depends on whether it is associated with normal or widened pulse pressure. If associated with the normal pulse
pressure, a brisk carotid upstroke usually indicates two conditions:
• Simultaneous emptying of the left ventricle into a high-pressure bed (the aorta) and a lower pressure bed: The
latter can be the right ventricle (in patients with ventricular septal defect [VSD]) or the left atrium (in patients
with mitral regurgitation [MR]). Both will allow a rapid left ventricular emptying, which in turn generates a brisk
arterial upstroke. The pulse pressure, however, remains normal.
• Hypertrophic cardiomyopathy (HCM): Despite its association with left ventricular obstruction, this disease is
characterized by a brisk and bifid pulse, due to the hypertrophic ventricle and its delayed obstruction. An
example of the carotid pulsation in HCM and other conditions is given in Fig. 1.1.
If associated with the widened pulse pressure, a brisk upstroke usually indicates aortic regurgitation (AR).
In contrast to MR, VSD, or HCM, the AR pulse has rapid upstroke and collapse.
3. In addition to aortic regurgitation, which other processes cause rapid upstroke and widened
pulse pressure?
The most common are the hyperkinetic heart syndromes (high-output states). These include anemia, fever, exercise,
thyrotoxicosis, pregnancy, cirrhosis, beriberi, Paget disease, arteriovenous fistulas, patent ductus arteriosus, AR, and
anxiety—all typically associated with rapid ventricular contraction and low peripheral vascular resistance.
Examples of the carotid pulse waveform and its correlation to heart sounds are provided in Fig. 1.2.
4. What is pulsus paradoxus?
Pulsus paradoxus is an exaggerated fall in systolic blood pressure during quiet inspiration. In contrast to
evaluation of arterial contour and amplitude, it is best detected in a peripheral vessel, such as the radial
artery. Although palpable at times, optimal detection of the pulsus paradoxus typically requires a sphygmo­­
manometer. Pulsus paradoxus can occur in cardiac tamponade and other conditions.
5. What is pulsus alternans?
Pulsus alternans is the alternation of strong and weak arterial pulses despite regular rate and rhythm. First de-
scribed by Ludwig Traube in 1872, pulsus alternans is often associated with alternation of strong and feeble heart
sounds (auscultatory alternans). Both indicate severe left ventricular dysfunction (from ischemia, hypertension, or
valvular cardiomyopathy), with worse ejection fraction and higher pulmonary capillary pressure. Hence, they are
often associated with an S3 gallop. A tracing indicating pulses alternans is given in Fig. 1.3.
6. What is the Duroziez double murmur?
The Duroziez murmur is a to-and-fro double murmur over a large central artery—usually the femoral but also the
brachial. It is elicited by applying gradual but firm compression with the stethoscope’s diaphragm. This produces
not only a systolic murmur (which is normal) but also a diastolic one (which is pathologic and typical of AR). The
Duroziez murmur has 58% to 100% sensitivity and specificity for AR.
7. What is the carotid shudder?
Carotid shudder is a palpable thrill felt at the peak of the carotid pulse in patients with AS, AR, or both. It repre-
sents the transmission of the murmur to the artery and is a relatively specific but rather an insensitive sign of
aortic valvular disease.

3
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reach Greybridge, and, on arriving there, found the dog-cart in
waiting.
The driver this time was not his old friend Dawson, but a much
less communicative person, whose observations were confined to
“Gently then, old lady,” and “Wo-ho now.” He was evidently not
accustomed to driving the “quality,” and his whole attention was
given to his steed; so they drove on for a mile or two in silence.
Suddenly a turn in the road made visible a little group of figures in
front; they were those of a man and a woman and a horse, walking
slowly along side by side. Mr. Guildford observed them with a sort of
half idle curiosity, but before the dog-cart was near enough for him to
distinguish the features of the man and the girl, they separated, the
girl entering a road to the right, the man mounting his horse and
riding on quickly; but, before separating, they had stood still for a
moment, evidently saying “Good-bye,” thus giving the carriage time
to approach them more nearly. Suddenly Mr. Guildford was surprised
by a remark from his companion.
“She’s a nice little mare, sir, isn’t she—her as the young squire’s
on?”
He pointed with his whip to the gentleman in front, now fast
leaving them far behind.
“The young squire?” repeated Mr. Guildford.
“Yes, sir, young Mr. Fawcett.”
“Oh! I did not recognize him,” said Mr. Guildford; “that was Mr.
Fawcett in front of us then leading his horse?”
“Yes, sir, him as were walking with the young lady—
Maddymuzelle.”
Then he relapsed into silence again.
When they came to where the Abbey road branched off, the figure
of Geneviève walking quickly in front was again distinctly visible; but
before they overtook her, Mr. Guildford had made a little change in
his plans.
 “Is there not a short cut to Dr. Farmer’s house somewhere about
here?” he inquired of the groom, and finding that it was so, and that
ten minutes’ quick walking across the fields would save a long round
by road, he left the dog-cart, sending by the servant a message to
Colonel Methvyn explaining the delay in his appearance.
Half an hour later Mr. Guildford entered the Abbey grounds,
having executed the little commission entrusted to him by Dr.
Farmer. He walked slowly up the drive, enjoying the sight of the
pleasant, quaint old garden, which as yet he had hardly seen by
daylight in its summer dress; it was a garden such as there are few
of nowadays,—the paths edged with box, whole beds of lavender
and sweet William, sweet peas and clove-pinks, marigold, and snap-
dragon; for on this side of the house the good taste of its owners
allowed of no “new-fangled” gardening; all—from the moss-grown
sun-dial on the lawn, to the curiously cut yew-trees guarding the
entrance to the bowling green,—remained as it might have been in
many a long, long ago summer, when the ever-young flower faces
smiled to old-world Cicelys in hoop and farthingale, just as they did
now to the fair-haired girl who came swiftly across the smooth short
grass to meet the stranger, the mellow light of the afternoon sun
falling full upon her.
The young man started when he first caught sight of her, yet at
that very instant she had been in his thoughts.
“I am so very glad you have come today,” she said, as she drew
near; “my mother and I have just come back from Haverstock,—and
oh! by the bye, I must apologise for that stupid old Hodge having
been sent to meet you at Greybridge; he can’t drive a bit, but the
coachman was away, and Dawson out with us, when your telegram
came,—and we have found my father in a perfect fever of eagerness
to go out a little. He has not been out since the day before you were
here last, it has been so much colder, you know; do you think he
may come out this?”
“I don’t see any reason against it,” said Mr. Guildford; “the air is
fresh, but perfectly mild. Shall I go and talk about it to Colonel
Methvyn before it gets later?”
 “Yes,” said Cicely, “I think he is anxious to see you.”
She turned and walked back again with him across the lawn in the
direction of the house.
“I should have been here earlier,” said Mr. Guildford, “but I came
round by Dr. Farmer’s; he wrote to ask me to look out some books
and papers that he wants forwarded, and that his servants could not
have found.”
“Did he say how he was?” asked Cicely.
“Yes, he says he is better,” replied Mr. Guildford; “but I thought the
tone of his letter seemed dull, and he says he finds it rather lonely
work travelling about all by himself.”
“Yes, poor old man,” said Miss Methvyn thoughtfully; “I think it is
very sad to see any one grow old with no one belonging to them. Dr.
Farmer has nobody at all.”
“Was he never married?” asked Mr. Guildford.
“No,” said Cicely, “but he was going to be married once. There
was some story about it, my father knows it I think—Dr. Farmer
belongs to this neighbourhood—the girl died I believe. Fancy! it must
be nearly fifty years ago, and I speak of her as a girl; but she will
always have seemed a girl to him.”
“Yes,” replied the young man, “to him she will always have been
sweet-and-twenty. And if she had lived to be Mrs. Farmer, she would
probably have grown stout and buxom, and not impossibly the cares
of life would have developed a temper.”
Miss Methvyn glanced at her companion with some curiosity.
Then she said quietly, “You are not really the least cynical, Mr.
Guildford, why do you talk as if you were?”
He smiled, “Do you dislike it?”
“I think I do,” she said. “Don’t think me rude for saying that that
tone of talk is so commonplace nowadays, that—”
She stopped short. He smiled again, but with a slight change of
expression, “You mean that the affectation of it is commonplace, I
think,” he said. “It is very easily affected, but I was in earnest. I think
it is well to look on both sides of a possible picture, and a
disappointed bachelor should surely be allowed the consolation of
thinking that, after all, the fairest flowers do fade, or at least lose their
beauty.”
“But youth and beauty are not everything,” remonstrated Cicely
with a very unusual colour in her cheeks.
“They are a good deal,” said Mr. Guildford drily.
A slight look of disappointment over-clouded the girl’s fair face,
but she said nothing. A curious feeling came over her that the man
beside her was not expressing his true sentiments, and this instinct
made her averse to say more. But Mr. Guildford understood her
better than she thought.
“You are disgusted with me, Miss Methvyn,” he said. “You think I
am worse than commonplace, that I don’t believe in there being
women whose grandeur and real beauty have little to say to ‘the
beauty that must die.’ But you are mistaken.”
Cicely’s face cleared; but she still looked puzzled.
“Then I must confess I don’t understand you,” she said.
“You can’t reconcile my having a high ideal of woman, with my
talking in a commonplace matter-of-fact way of marriage? But do not
facts strengthen my position? Don’t think I mean to compare myself
with such people; but isn’t it true that the giants among men have not
looked for, or wished for anything out of the way in their wives? And
when a man is by no means a giant, but still feels he has it in him to
do something, surely his best strength lies in keeping his powers
concentrated, in deprecating any overwhelming outside influence?”
He spoke almost as if he were trying to argue his theory out to
himself, to prove its soundness for his own satisfaction rather than
for that of his hearer. And his hearer was not to be so readily
convinced.
“But, appealing to facts, as you say,” she objected, “you cannot
maintain that women’s influence has not in innumerable instances,
been an elevating and ennobling one, as well as a softening and
purifying one? Of course whatever softens and purifies ennobles, in
a sense, but I mean ennobling in the sense of strengthening and
widening.”
“Women’s influence has certainly done all you say,” he replied;
“but it has seldom been the influence of wives. The grandest women
make splendid friends; but I still appeal to past experience to support
the side of my position which I see you dislike.”
“Do I dislike it?” said Cicely. “I don’t know. Is it true, I wonder? I
am not clever enough to prove that it is not; but still a strong instinct
tells me it should not be true.”
An earnest questioning stole into her blue eyes, and, as she
spoke she looked up into her companion’s face without a shadow of
embarrassment. They had reached the front of the house by now,
and were standing just within the old grey porch. The dark leaves of
the thick-growing ivy creeping round its entrance seemed to make a
frame for the girl’s fair quiet face, and to throw out in relief the
delicate features and pure complexion. For a moment Mr. Guildford
forgot, in looking at her, what they had been talking about. But
recovering his wits he repeated quietly, “I am afraid it is true.
Sometimes I have wished it were not, but then again I see that it is
better as it is. But I am sorry to destroy your faith in beautiful
impossibilities.”
She turned upon him with a merry laugh.
“Don’t distress yourself about that,” she exclaimed. “I am much
more obstinate than you think. I am by no means an optimist in the
sense of not thinking that what is might not be made a good deal
better. And even your giants may have been short-sighted, and one-
sided in some directions, may they not? Are you shocked at my
irreverence? As for disliking your theory, I am by no means sure that
I do dislike it. If I were an ideal woman—that sounds silly, but you
know what I mean—hif I were worthy of such a thing, I mean, I
should feel infinitely more honoured by being the chosen friend of a
clever man than of being—” she stopped abruptly and blushed a
little. Then seemingly ashamed of her confusion, she went on
bravely, “than by his just falling in love with me,” she added, with a
slight tinge of contempt in her tone.
“Then you do agree with me,” said Mr. Guildford triumphantly.
And judging it wise to retire while master of the field, he went into
the house and ran upstairs to Colonel Methvyn’s room.
Cicely stood in the porch, thinking. Then she went away to see if
the cushions of her father’s Bath chair were properly aired, and was
standing ready beside it at the door when the invalid was brought
down for his little airing.
Poor Colonel Methvyn enjoyed the sun shine and the flowers and
the soft fresh air very much. His expressions of pleasure and
Cicely’s satisfaction in his enjoyment touched Mr. Guildford infinitely
more than the weary complaints, but too often well founded, which
so many of his Sothernbay patients seemed to think necessary to
enlist his sympathy.
“It is a nice old place of its kind; is it not, Guildford?” said Cicely’s
father, when the chair was brought to anchor in a sheltered corner,
whence the principal beauties of the garden—the rose fence
enclosing “the lady’s walk,” the yew “peacocks,” the ancient sun-dial
—were all visible. “It is a home a man may be forgiven for feeling
reluctant to leave, surely? It has always been my home; it would
break my heart to think of its ever going away to strangers.”
“I can understand the feeling,” said the young doctor quietly.
Thanks to Colonel Methvyn’s gentleness, his egotism did not go the
length of repelling sympathy; but yet the sympathy Mr. Guildford felt
for him was tinged with fully as much pity as respect. “It must be very
natural where one’s associations have been so concentrated. But,”
he hesitated a little, “I see no reason why it should not be your home
for many years to come.”
“You give me a chance of seeing my grand-children playing about
the old garden, do you, eh, Guildford?” asked the invalid, with an
affectation of cheerfulness which did not conceal his real anxiety.
Miss Methvyn was standing at some little distance, too far off to
overhear what was said, still Mr. Guildford lowered his voice as he
replied,
“Certainly, I do, my dear sir.”
Colonel Methvyn closed his eyes and leaned back. “I think I could
die happily if I could see it so,” he murmured. Then as if afraid of
having betrayed too much feeling, he went on speaking. “It is a
curious thing how few sons there have been in our branch of the
family. I was an only son, and so was my father; this place came to
him from his mother, and now there is only my little girl there for it to
go to.”
“But, happily, that prevents any fear of its going to strangers,” said
Mr. Guildford, more for the sake of showing interest in his
companion’s train of thought, than from any special remembrance of
his remarks.
“Of course, of course,” replied Colonel Methvyn, “of course that
could never be. It was a foolish idea that crossed my imagination. I
grow morbid, quite ridiculously morbid sometimes.”
He spoke with a nervous eagerness that made Mr. Guildford
regret the observation he had made, and he was glad that just at this
moment Cicely rejoined them.
“Here is mother coming,” she exclaimed. “Mr. Guildford, will you
help me to move papa a yard or two this way, and then she can see
him all the way from the house? You have sent Barry in? Ah, that’s
right! it is so much more comfortable without him. Mr. Guildford and I
can push you beautifully, can’t we papa?”
Her father laughed.
“Is there anything you don’t think you can do for me better than
any one else, my darling?” he said fondly, stroking the fair head, as
Cicely knelt on the grass beside him, looking up in his face with
bright tenderness in her blue eyes.
Mrs. Methvyn was not alone when she joined them. Geneviève
had seen her leave the house and ran after her, so the two came
across the lawn together.
 “I have finished my letters at last, I am glad to say,” said Cicely’s
mother, after she had shaken hands with Mr. Guildford, “so now I
have nothing to do till dinner-time, and we can all stay out till the last
moment—till Mr. Guildford orders you in, I mean, Philip. What a
delicious afternoon it is!”
“Yes, here it is perfect,” said Cicely; “the sun was just a little too
hot driving to Haverstock, though the road is pretty shady. Did you
not find it disagreeable coming from Greybridge, Mr. Guildford—that
road is so unsheltered?”
“It was rather hot, but it is not a long drive,” he replied. “You must
have found it rather a tiring walk, did you not, Miss Casalis?” he
added, thoughtlessly, turning to Geneviève.
The girl looked at him with a curious half-terrified, half-appealing
expression. Her lips parted as if she were going to speak, but before
she had time to say anything, Mrs. Methvyn and Cicely interrupted
her.
“Geneviève has not been at Greybridge, Mr. Guildford,” they
exclaimed; “you must have been mistaken.”
“I did not mean to say I saw Miss Casalis at Greybridge,” he
replied quietly. “It was on my way here I thought I saw you in the
distance,” he went on, turning to Geneviève.
“Oh! that may be,” said Mrs. Methvyn. “You did go for a little walk
you told me, I think, my dear, but of course you would not dream of
going so far as Greybridge alone—that would never do.”
“I did not see Mr. Guildford when I was out,” said Geneviève.
“Was it at the distance you thought you saw me?”
The words sounded simple in the extreme, and her tone of voice
was quiet and collected, but as the young man turned to reply, he
saw in her eyes the same expression of mute appeal. A slight chill
seemed to run through him; so young, yet so disingenuous! Yet
surely, surely, more to be pitied than blamed; and with this reflection
there set in a strong feeling of contemptuous indignation against Mr.
Fawcett, the man who could in the least take advantage of a young
girl’s ignorance and inexperience. Not that Mr. Guildford was a man
of the world in the sense of being ready to give the worst explanation
to even the faintest appearances of evil, or of crediting his fellow-
beings in advance with wrong-doing; he would not have given a
second thought to what he had seen but for Geneviève’s
unmistakable terror of its being known to her aunt. That she had
really been at Greybridge, unknown to her friends, and that this, and
not the meeting with Mr. Fawcett, was the terrible secret, naturally,
never occurred to him. Had he known it, he would have been saved
some present regret and future embarrassment. He looked at
Geneviève gravely, as he answered her question.
“Yes, Miss Casalis, when I thought I saw you it was at some
distance.”
Something in his tone inclined Cicely to start up in her cousin’s
defence—defence from what, she knew not, but she fancied there
was a coldness and constraint in his manner to Geneviève, which
annoyed her. “Poor little Geneviève is looking quite frightened
again,” she thought to herself. “Mr. Guildford may be very clever and
estimable—I have no doubt he is, but he would be much pleasanter
if he were less abrupt.”
But aloud she only said, “If it was at a distance you thought you
saw her, I dare say it was not Geneviève at all. One requires to know
a person very well indeed—their appearance, I mean—to recognise
them at a distance.”
“Perhaps so,” said Mr. Guildford.
Then he turned to Colonel Methvyn, and began talking of some
different subject, but somehow the brightness and harmony of the
pleasant afternoon seemed to have fled.
But Cicely had no idea of allowing such desirable guests to take
their departure without making an effort to detain them.
“Papa,” she said, suddenly, “do you know what this day week will
be?”.
“This day week, my dear?” repeated her father, “this day week?—
no, I don’t remember. Oh! yes, to be sure, it will be—”
 “My birthday,” she interrupted. “What shall we do to celebrate it?
Geneviève, help us to an idea.”
“Let us have a picnic,” exclaimed Geneviève, clapping her hands,
her eyes dancing with excitement and glee in a manner that
altogether nonplussed Mr. Guildford’s new opinion of her. He looked
at her in amazement.
“How can she be so childishly light hearted, and yet so deceitful?”
he thought.
Then he wondered if this could be “acting,” but a glance at her
pretty flushed face, at her dark eyes raised to Cicely’s in sweet
eagerness as they discussed the possibilities of the scheme,
altogether put to flight so terrible a suspicion, and the young man
was fain to take refuge in the old commonplace axiom of the
incomprehensible nature of even the most apparently transparent of
women. But, once or twice in the course of the afternoon, a certain
something in Geneviève’s manner to him touched his gentler
feelings; she seemed to be tacitly appealing to his forbearance and
pity. “Don’t judge me till I can explain it all,” she seemed to say, and
though he made no effort to reassure her, he grew unconsciously
softened by her trust in him. She certainly succeeded in making him
think a good deal more about her than would have been the case but
for the confidence thus forced upon him, and which he was the last
man in the world to welcome.
They all went on talking over Geneviève’s suggestion, but Mr.
Guildford hardly noticed what they were saying till he found himself
suddenly appealed to.
“Yes, the Lingthurst Copse would be the nicest after all,” Cicely
was saying. “If we could get you to the Witch’s Ladder, papa,
wouldn’t it be delightful? Think how many times we have had
birthday treats there when Amy and Trevor and I were children!
Would you not like to see the copse again dreadfully, papa?”
Colonel Methvyn laughed, half sadly. “You want to coax me into
fancying myself well again, Cicely,” he said. “But you forget, dear, it
is four years since I have been outside the gates except for those
weary journeys to town. No, you must go without me.”
“But we won’t; if you can’t come we shall give it up,” persisted
Cicely. Then she turned to Mr. Guildford, and unfolded her scheme in
full to him. Her father was to be driven in her low pony-carriage to
the Copse Farm, and there to be met by Barry and the Bath chair. “It
can be sent in a cart to the farm the day before,” she said, “and
Barry can go in it if it’s too far to walk, lazy creature that he is! And
the paths through the copse are quite wide enough for the chair. It is
so pretty there, Geneviève,” she exclaimed to her cousin, “prettier
even than in the woods we go to church by. And don’t you think it
would do my father good, Mr. Guildford? It is only a three miles’
drive.”
Mr. Guildford was able honestly to agree with her, for he had seen
enough of Colonel Methvyn to judge more favourably of his case
than at first sight, and to be of opinion that his general health would
be improved by less vigorous adherence to invalid rules. So it was
settled that Geneviève’s idea should be actually carried out, and that
Mr. Guildford’s next visit should be timed so that he should make one
of the party.
“Is it not inconvenient for you to promise to come on any particular
day?” said Cicely, as she was bidding him good-bye, after her father
had been wheeled back to the house again.
“Not now,” he said, “I have not much to do except what I give
myself; and before another busy season comes round, I shall
probably have left Sothernbay, so I don’t care much about extending
my acquaintance—my “business”—there,” he said lightly.
“Are you going to leave Sothernbay? Oh! I am so sorry,”
exclaimed Cicely in sudden alarm, “my father will miss you so!”
“I am not thinking of leaving at present,” he replied quickly. “I
should certainly not leave till I have done what I undertook to do; that
is to say, till I can resign my charge of Colonel Methvyn to Dr. Farmer
again.”
 “Oh! thank you. I am so glad to be assured of it,” said Cicely
gently, but in a tone of great relief.
“Eventually,” continued Mr. Guildford, “I have quite made up my
mind that it will be best to leave. I think I see my way to doing more
good elsewhere and in a different way.”
But though Miss Methvyn listened courteously she made no reply
which could have led him to say more.
“She thinks of me only as her father’s doctor,” reflected Mr.
Guildford with a little bitterness when he had said good-bye and was
on his way home. It was disappointing. He had rather looked forward
to telling her of his change of plan, of his rapidly maturing belief that
by increased study and research, he might fit himself for a position
which he had long aspired to, and had considerable chance of
attaining—a position which would put him in the way of fulfilling his
darling ambition, that of doing something worth the doing for the
science of medicine. He had fancied she was the sort of woman to
have entered into his hopes and sympathised with his aspirations—
he had, in his own mind, begun to think of her, young as she was, as
belonging to the rare class of women of whom a man might make
friends. He had all but said so to her this very afternoon, and she
had then seemed thoroughly to enter into his feelings and opinions.
But this evening he felt unreasonably chilled and disappointed.
“After all,” he reflected, “I suspect it is safest to restrict one’s
relations with women in every direction. There are plenty of good
staunch men in the world to make friends of, fortunately—and a
gentle, clinging creature like poor little Geneviève even, would be
more satisfactory in the end. What can that fellow Fawcett be
thinking of to involve her in any underhand flirtation—I can’t make it
out.”
His brow darkened as he meditated upon what he had seen. He
determined to watch for an opportunity of giving Geneviève a word of
advice.
END OF VOL. I.
VOLUME II.
CHAPTER I.
 WORK AND PLAY.

“If all the world and love were young

And truth in every shepherd’s tongue”
The Nymph’s Reply.

EARLY summer was the time of all others for seeing Lingthurst Copse
to advantage, for the soil thereabouts was dry and gravelly, and a
few weeks of hot weather destroyed the freshness of the tints and
made all the vegetation look thirsty. It was only a copse, and the
trees which composed it were somewhat stunted and meagre, but
still it was a very pretty spot in itself, and worth driving more than
three miles to, for the sake of the loveliness of the view from the top
of the rugged old rock, one side of which was skirted by the
miniature forest. The latter part of the ascent of this rock was very
steep—in places almost perpendicular, but a series of rough steps
greatly facilitated matters in the hardest parts of the climb—these
were the steps known as the Witch’s Ladder. Who the witch was and
from what uncanny motive she had devoted herself to thus amiably
preparing the way for those who were to come after her, had been
matter for much grave speculation, but had never been satisfactorily
explained, and remained a pleasantly tantalising mystery to the
visitors of her ancient haunts. That there had never been a witch at
all, and that the steps were but natural irregularities on the rock’s
surface, worn, in the lapse of time, to more definite shape by the feet
of many climbers, was a theory which had suggested itself to some
few irreverent minds. But, as a rule, these scoffers had the grace to
keep their scepticism to themselves, and the witch, young or old, fair
or hideous, was allowed to retain undisputed possession of
Lingthurst Copse and Rock.
Cicely’s—or rather Geneviève’s picnic—had assumed unexpected
dimensions. Sir Thomas and Lady Frederica had been invited to join
the expedition and had asked leave to bring with them two young
ladies, no longer in the very first blush of youth, the daughters of the
Haverstock rector, whom Lady Frederica had invited to spend a
week with her, from a vague notion that “it would be nice for them to
meet Mr. Hayle, poor girls!”—a young and unmarried clergyman
being an unprecedented novelty in the neighbourhood. But though
the “poor girls” were very ready to come, Lady Frederica found the
entertaining of them by no means so easy a matter as she had
anticipated. She asked Mr. Hayle to dinner every other day at least,
and in her innocent way prepared him to be captivated by one, if not
by both, of the Misses Kettering by telling him beforehand what dear
good girls they were, how indefatigable in the manufacture of
ecclesiastical cushions and altar cloths, how unfailing in their
attendance at the daily service instituted since the opening of the
new Haverstock church. And Mr. Hayle listened gravely, expressed
his satisfaction at finding that the neighbourhood contained such
right thinking young women, came to dinner when he was asked,
disgusted the elder Miss Kettering the very first evening by
remarking that he wondered she had never thought of joining a
sisterhood if the secular tone of her home life was not to her mind,
and still more desperately offended the younger and better-looking
sister by not admiring her rendering of Liszt’s ‘Ave Maria,’ got up by
her with considerable labour for the occasion. So Lady Frederica’s
benevolent intentions were defeated, and her guests lay heavy on
her mind, and the news of the Methvyns’ picnic was welcome
indeed, not only to the young ladies themselves but to all their
entertainers, including Miss Winter and Mr. Fawcett who were
growing very tired indeed of the labours Lady Frederica’s good
nature had imposed upon them.
Mr. Hayle, in happy unconsciousness of the offence he had given,
accompanied the Lingthurst party to the rendezvous at the Copse
Farm, and almost reinstated himself in Miss Kettering senior’s favour
by calmly declining to agree with her, when she gushingly demanded
of him if he did not think that lovely Miss Casalis the most exquisitely
beautiful girl he had ever seen.”
“I don’t care about that sort of beauty,” said Mr. Hayle, and then
he walked away to where Cicely and Mr. Guildford were improvising
a comfortable couch for Colonel Methvyn with the cushions of the
carriages, as the invalid declared himself able to join the lowly
luncheon party instead of remaining in the solitary state of his Bath
chair.
He really looked and felt better than he had done for years, and
Mr. Guildford was not a little elated at the success of his new mode
of treatment. Long, long afterwards Cicely looked back with pleasure
on that bright morning in the copse, and felt warm gratitude to the
man whose care and kindness had enabled her suffering father to
enjoy again a breath of the out-door life he had loved so well. And to-
day the sight of the invalid’s pleasure seemed to cheer every one
else. To all outward appearance they were a very happy little party.
Geneviève’s clear soft laugh rang as merrily as if its owner had
never known a care or perplexity, and the tender brightness of
Cicely’s face was sunshine in itself. Mr. Hayle looked at her and
wondered. Edmond Guildford forgot all his cynical theories in the
unconscious happiness of the present, forgot even to marvel at his
own inconsistency—only Trevor looked moody and dissatisfied,
unlike his usual equable contented self.
There were more reasons than one for his gloom. Good-natured
and kindly as he was, Cicely’s extreme devotion to her parents and
home interests at times tried his patience, and suggested unpleasing
comparisons. And a long conversation he had had the night before
with his father was also on his mind. Nor was the day to close
without yet further annoyance falling to his share.
Mr. Guildford had not forgotten his intention of coming to some
sort of understanding with the little lady whose eyes had so
successfully appealed to his forbearance. After luncheon the able-
bodied members of the party felt themselves in duty bound to scale
the Witch’s Ladder; in the ascent they naturally fell apart into little
groups of twos and threes, and Mr. Guildford found himself alone
with Miss Casalis. He had not sought the opportunity, and she had
not evaded it, but now that it occurred, both were plainly conscious
that the sooner what had to be said could be got over, the more
comfortable they would feel. Somewhat to Mr. Guildford’s surprise,
Geneviève herself hastened to break the ice.
“I fear much you thought me very strange the last day you came
to Greystone,” she began, with some timidity, but on the whole less
trepidation than he had expected. “I know well you did see me on the
road, and it grieved me—indeed it grieved me to seem deceitful. But
I was so frightened, oh! oh! so frightened, that my aunt would be
very angry. And I would not for all the world make her angry. She is
so very good for me. And I thank you so much that you did not insist
that it was me that you had seen.”
Mr. Guildford was rather taken aback by the calmness of this
confession—the girl did not seem by any means ashamed of herself,
even though tacitly owning that her conduct deserved her aunt’s
serious displeasure—he walked on (they were just now on a
comparatively speaking level piece of ground, a sort of landing
between the flights of stairs), for a few moments in silence; then he
said abruptly,
“Why do you do what would make Mrs. Methvyn angry, if you
dread her anger so much?”.
“I could not help it—indeed I could not,” said Geneviève
penitently, without appearing in the least to resent his tone. “I was
obliged to go to Greybridge, and at the first I did not think how it
might displease my aunt.”
 Mr. Guildford grew still more puzzled.
“I didn’t know you had been at Greybridge,” he said. “It was not
there I saw you—indeed it was not very far from home. It wasn’t on
account of—of the distance from home I thought Mrs. Methvyn would
be displeased.”
“How then?” exclaimed Geneviève, looking up at him in perplexity.
“What else for could I have feared? I went but to Greybridge to the
post-office—” and in a few words she explained to him the reason of
her secret expedition—the same reason that she had given to Mr.
Fawcett, the wish to post unobserved the letter she feared she might
be “thought silly” for having written. It sounded sincere enough,
indeed; so far as her explanation went, it actually was so, but still Mr.
Guildford felt puzzled. Was she telling him all? Had there been no
second motive for her walk? Hitherto Mr. Fawcett had not been
named, and it had actually not occurred to Geneviève that he was in
any way connected with Mr. Guildford’s disapproval of her behaviour.
So she looked up with some anxiety, but without embarrassment, to
read in her companion’s grave face the effect of her explanation.
And something in her expression made him ashamed of his
suspicions, though it was not without an effort that he made up his
mind to discard them.
“I have done you injustice, Miss Casalis,” he said at last, and I
beg your pardon. Don’t you see that if I had had any idea that the
mere fact of your being out on the road would have displeased your
aunt, I would not have mentioned it so carelessly and casually as I
did?”
“Yes,” said Geneviève, after a little cogitation; “I see, but I
understand not. You saw nothing wrong, yet you spoke as if you
thought I had done wrong. What then was there?”
“There was nothing,” replied the young man, half annoyed, half
inclined to laugh. “I should have thought nothing of seeing you
walking along the road, had you not immediately shown me you
were afraid of its being known, Then, of course, I began to wonder
why, and pitched upon the most natural explanation. Now I know
why you were afraid, so there is nothing more for me to say except
to repeat that I am sorry for having misunderstood you.”
But Geneviève was not satisfied. Light was beginning to dawn
upon her. She stood still, her hands clasped together, the colour
coming and going in her face.
“What then was it you thought I feared?” she exclaimed
vehemently. “I must know. Mr. Guildford, you shall then tell. You are
not kind.”
She seemed on the point of tears, and Mr. Guildford was not fond
of tears. Still he was sorry for her, and provoked with himself.
“I wish you would believe me, Miss Casalis,” he said earnestly,
“that I saw nothing in your conduct that I even fancied unbecoming—
nothing that I would have given a second thought to.”
“But what thought you then when you saw that I feared?” she
persisted, beginning to lose command both of her temper and her
English. “Was it that you have seen me walk with Mr. Fawcett? I
thought not that one was so little amiable, so little kind in England!
What then was there of wrong in what I have done? I meet the
nephew of my aunt, he speaks to me, I answer him—voilà tout!
Would you that I should run away—would you—?”
But by this time the tears have come in earnest—the rest of the
sentence is lost in sobs.
“My dear Miss Casalis,” exclaimed Mr. Guildford in desperation, “I
really entreat you to be reasonable. Have I not told you half-a-dozen
times that your behaviour so far as I know was irreproachable? Nor,
whatever I had thought of it, would I have presumed to express an
opinion but for this unfortunate misunderstanding, brought about—
you must do me the justice to allow—by yourself. You appealed to
me, silently it is true, but still you did appeal to me, to refrain from
drawing attention to what I had seen, and to-day you honoured me
with an explanation of the whole. I understand it all now, and for the
third time I beg your pardon.”
“Then you do not think I—I was to blame for—for speaking to Mr.
Fawcett?” said Geneviève, calming down, but still sobbing.