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CARDIOLOGY SECRETS
To Lydia, who inspires me to try to be a better husband, friend, and person.
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
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CONTRIBUTORS
Suhny Abbara, MD
Chief, Cardiothoracic Imaging Department of Radiology Professor, Department of Radiology UT Southwestern Medical Center Dallas, Texas, USA
Richa Agarwal, MD
Associate Professor of Medicine Division of Cardiology
Duke University School of Medicine Durham, North Carolina, USA
Ali M. Agha, MD
Department of Cardiology
Baylor College of Medicine Houston, Texas, USA
David Aguilar, MD, MSc Professor of Medicine Division of Cardiovascular Medicine University of Kentucky College of Medicine Lexington, Kentucky, USA
Rami Akhrass, MD
Regional Director
Department of Thoracic and Cardiovascular Surgery Cleveland Clinic Cleveland, Ohio, USA
Mahmoud Al Rifai, MD, MPH Cardiology Fellow Department of Medicine-Cardiology
Baylor College of Medicine Houston, Texas, USA
Eric Awtry, MD
Associate Professor of Medicine Section of Cardiology
Boston University School of Medicine; Associate Chief for Clinical Affairs Section of Cardiology Boston Medical Center Boston, Massachusetts, USA
Faisal G. Bakaeen, MD Professor
Department of Thoracic and Cardiovascular Surgery Cleveland Clinic Cleveland, Ohio, USA
Gary J. Balady, MD
Director, Non Invasive Cardiovascular Laboratories
Section of Cardiology
Boston Medical Center Professor of Medicine
Boston University School of Medicine Boston, Massachusetts, USA
Neal Barshes, MD, MPH
Associate Professor of Surgery
Michael E. DeBakey Department of Surgery
Baylor College of Medicine Houston, Texas, USA
Luc M. Beauchesne, MD, FRCPC, FACC Cardiologist, Adult Congenital Heart Disease Program University of Ottawa Heart Institute Ottawa, Ontario, Canada
Jeffrey S. Berman, MD Cardiology Fellow
Department of Medicine, Division of Cardiology
Baylor College of Medicine Houston, Texas, USA
Sheilah Bernard, MD Associate Professor of Medicine
Section of Cardiology, Department of Medicine Boston Medical Center Boston, Massachusetts, USA
Gilad Birnbaum, MD Department of Medicine
Section of Cardiology
Baylor College of Medicine Houston, Texas, USA
Yochai Birnbaum, MD Professor Department of Medicine
Section of Cardiology
Baylor College of Medicine Houston, Texas, USA
Fernando Boccalandro, MD, FACC, FSCAI Pro-Care/Odessa Heart Institute Director, Cardiovascular Laboratory Medical Center Hospital Department of Cardiology
Associated Clinical Professor Texas Tech University Health Science Center Department of Internal Medicine Odessa, Texas
Michael Boone, DO
Resident, Department of Family Medicine Waco Family Health Center Waco, Texas, USA
Stephen Boone, MD, FACEP
Assistant Professor
Department of Emergency Medicine
Assistant Professor
Department of Internal Medicine
Baylor College of Medicine Houston, Texas, USA
Sanket Borgaonkar, MD
Chief Fellow, PGY-VII Department of Cardiology
Baylor College of Medicine Houston, Texas, USA
Biykem Bozkurt
Professor
Mary and Gordon Cain Chair and Professor of Medicine
Director, Winters Center for Heart Failure Research at Baylor College of Medicine Medical Care Line Executive DeBakey VA Medical Center Houston, Texas, USA
Arzu Canan, MD
Assistant Professor Department of Radiology, Cardiothoracic Imaging UT Southwestern Medical Center Dallas, Texas, USA
Kelly N. Casteel, MD
Assistant Professor Department of Benign Hematology MD Anderson Cancer Center Houston, Texas, USA
Tiffany Chen, MD
Assistant Professor of Clinical Medicine Division of Cardiovascular Medicine Hospital of the University of Pennsylvania Philadelphia, Pennsylvania, USA
Leslie T. Cooper Jr., MD
Elizabeth C. Lane, Ph.D. and M. Nadine Zimmerman, Ph.D. Professor of Internal Medicine Chair, Cardiovascular Department Jacksonville, Florida, USA
Edmond M. Cronin, MB BCh BAO Associate Professor Department of Medicine Temple University Philadelphia, Pennsylvania, USA
George D. Dangas, MD, Professor of Medicine and Surgery Director, Cardiovascular Innovation Mount Sinai Hospital Icahn School of Medicine at Mount Sinai New York, USA
Amish S. Dave, MD, PhD, FACC
Assistant Professor of Medicine Department of Cardiology Houston Methodist Hospital Houston, Texas, USA
Ali E. Denktas, MD Professor of Medicine Department of Cardiology Baylor College of Medicine Houston, Texas, USA
Kim A. Eagle, MD
Albion Walter Hewlett Professor of Internal Medicine
Department of Internal Medicine University of Michigan Ann Arbor, Michigan, USA
Lothar Faber, MD, FESC, FACC
Professor Home Office
Schuerhornweg 36 Bielefeld, Germany
Savitri Fedson, MA, MD
Professor
Center for Medical Ethics and Health Policy
Baylor College of Medicine; Professor
Department of Medicine
Michael E. DeBakey VA Medical Center Houston, Texas, USA
Matthew J. Feinstein, MD, MSc
Assistant Professor of Medicine Division of Cardiology, Department of Medicine Northwestern University Feinberg School of Medicine Chicago, Illinois, USA
G. Michael Felker, MD, MHS Professor of Medicine Division of Cardiology
Duke University School of Medicine Durham, North Carolina, USA
James J. Fenton, MD
Clinical Associate Professor Pulmonary Medicine
National Jewish Health Denver, Colorado, USA
Michael E. Field, MD Professor of Medicine Department of Medicine
Medical University of South Carolina Charleston, South Carolina, USA
Scott D. Flamm, MD, MBA Professor of Radiology Department of Radiology Cleveland Clinic Cleveland, Ohio, USA
Lee A. Fleisher, MD Professor
Department of Anesthesiology and Critical Care Perelman School of Medicine at the University of Pennsylvania Philadelphia, Pennsylvania, USA
Laura Flink
The permanente medical group California, USA
Marat Fudim, MD
Assistant Professor of Medicine Division of Cardiology
Duke University School of Medicine Durham, North Carolina, USA
Sanjay Ganapathi, MD, DM Professor Department of Cardiology
Sree Chitra Tirunal Institute for Medical Sciences and Technology Trivandrum, India
Kathryn A. Gayle, MD Fellow
Department of Cardiovascular Medicine
Vanderbilt University Medical Center Nashville, Tennessee, USA
Marie Gerhard-Herman, MD
Associate Professor Department of Medicine
Mass General Brigham Boston, Massachusetts, USA
Casey Graziani, MD Fellow
Departments of Pulmonary and Critical Care Medicine
Baylor College of Medicine Houston, Texas, USA
Cindy Grines, MD Chief Scientific Officer
Cardiovascular Institute Northside Hospital Atlanta, Georgia, USA
Aakriti Gupta, MD Cardiologist
Department of Cardiology
Columbia University Irving Medical Center New York, New York, USA
Gabriel B. Habib Sr., MD, FACC, FCCP, FAHA Professor of Medicine Department of Medicine
Baylor College of Medicine Houston, Texas, USA
Ihab Hamzeh, MD
Associate Professor of Medicine Department of Medicine
Baylor College of Medicine Houston, Texas, USA
Sivadasanpillai Harikrishnan, MD, DM, DNB Professor
Department of Cardiology
Sree Chitra Tirunal Institute for Medical Sciences and Technology Trivandrum, India
Gustavo A. Heresi, MD, MS
Director, Pulmonary Vascular and CTEPH Program
Department of Pulmonary and Critical Care Medicine Cleveland Clinic Cleveland, Ohio, USA
Tomoya T. Hinohara, MD
Fellow, Department of Cardiology
Houston Methodist Hospital Houston, Texas, USA
Brian D. Hoit, MD
Professor of Medicine and Physiology and Biophysics
Department of Medicine
Case Western Reserve University; Director of Echocardiography
University Hospitals Cleveland Medical Center Cleveland, Ohio, USA
Geoffrey D. Huntley, MD
Fellow
Department of Cardiovascular Medicine
Mayo Clinic Rochester, Minnesota, USA
Aliza Hussain, MD
Fellow Physician
Department of Medicine, Section of Cardiology
Baylor College of Medicine Houston, Texas, USA
Scott E. Janus, MD Physician
Department of Cardiology
University Hospitals of Cleveland Cleveland, Ohio, USA
Xiaoming Jia, MD
Fellow, Department of Medicine
Baylor College of Medicine Houston, Texas, USA
Hani Jneid, MD, FACC, FAHA, FSCAI
Associate Professor of Medicine Department of Cardiology
Baylor College of Medicine Houston, Texas, USA
Jose A. Joglar, MD
Professor of Internal Medicine
Department of Internal Medicine
UT Southwestern Medical Center Dallas, Texas, USA
Thomas A. Kent, MD
Robert Welch Chair Professor Center for Genomic and Precision Medicine
Institute of Biosciences and Technology
Texas A&M Health Science Center-Houston
Adjunct Professor
Stanley H. Appel Department of Neurology
Houston Methodist Hospital Houston, Texas, USA
Umair Khalid, MD, FACC
Assistant Professor of Medicine – Cardiology
Baylor College of Medicine Houston, Texas, USA
Sarah Kohnstamm, MD
Clinical Assistant Professor Department of Cardiovascular Medicine
Michigan Medicine
Ann Arbor, Michigan, USA
Nitin Kondamudi, MD
House Staff
Division of Cardiology, Department of Internal Medicine
University of Texas Southwestern Medical Center Dallas, Texas, USA
Chayakrit Krittanawong, MD
House Staff Section of Cardiology
Baylor College of Medicine Houston, Texas, USA
Michael H. Kroll, MD
Professor
Department of Benign Hematology UT MD Anderson Cancer Center Houston, Texas, USA
Richard A. Lange, MD, MBA
President
Texas Tech University Health Sciences Center El Paso Dean, Paul L. Foster School of Medicine El Paso, Texas, USA
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
Paul Litvak, MD
Assistant Professor Department of Neurology
Baylor College of Medicine Houston, Texas, USA
Jing Liu, MD
Cardiology Fellow
Department of Internal Medicine-Cardiology
Baylor College of Medicine Houston, Texas, USA
Melissa A. Lyle, MD
Assistant Professor of Medicine
Cardiologist, Department of Cardiovascular Medicine Mayo Clinic Jacksonville, Florida, USA
Thomas Maddox, MD, MSc
Professor Division of Cardiology
Washington University School of Medicine St. Louis, Missouri, USA
Jamal H. Mahar, MD, MEd
Cardiology Fellow
Department of Cardiology
Baylor College of Medicine Houston, Texas, USA
Salvatore Mangione, MD
Associate Professor of Medicine
SKMC of Thomas Jefferson University Philadelphia, Pennsylvania, USA
Rita Marr, BS, MD
Staff Cardiologist
Department of Cardiology
Michael E. DeBakey VA Medical Center Houston, Texas, USA
Sharyl R. Martini
Medical Director
VA National Telestroke Program
Department of Veterans Affairs
Assistant Professor Department of Neurology
Baylor College of Medicine Houston, Texas, USA
Jim McCord, MD
Professor of Medicine, Wayne State Medical School
Heart and Vascular Institute
Cardiology Director Observation Unit
Henry Ford Hospital Detroit, Michigan, USA
Roxana Mehran, MD, FACC, FAHA, MSCAI
Mount Sinai Professor in Cardiovascular Clinical Research and Outcomes
Professor of Medicine (Cardiology), and Population
Health Science and Policy
Director, the Center for Interventional Cardiovascular Research and Outcomes
Icahn School of Medicine at Mount Sinai New York, New York, USA
Lisa A. Mendes, MD
Professor of Medicine
Department of Cardiovascular Medicine
Vanderbilt University Medical Center Nashville, Tennessee, USA
Geno J. Merli, MD, MACP, FHM, FSVM
Professor of Medicine and Surgery
Department of Surgery
Sydney Kimmel Medical College at Thomas Jefferson University
Co-Director
Jefferson Vascular Center
Thomas Jefferson University
Senior Vice President & Associate CMO
Thomas Jefferson University Hospital Philadelphia, Pennsylvania, USA
Hassan Mir, MD, FRCPC
Cardiologist and Clinician Investigator
Cardiology
University of Ottawa Heart Institute;
Assistant Professor Department of Medicine
University of Ottawa Ottawa, Ontario, Canada
Arunima Misra, MD
Associate Professor Department of Internal Medicine
Baylor College of Medicine
Houston, Texas, USA
Ajith Nair, MD
Assistant Professor of Medicine Department of Medicine
Baylor College of Medicine Houston, Texas, USA
Vijay Nambi, MD, PhD
Staff Cardiologist Department of Medicine
Michael E DeBakey Veterans Affairs Hospital; Associate Professor
Division of Atherosclerosis and Vascular Medicine, Section of Cardiovascular Research Department of Medicine
Baylor College of Medicine Houston, Texas, USA
G. Titus Ngeno, MBCHB, MSc Assistant Professor Department of Medicine Duke University Durham, North Carolina, USA
Vuyisile T. Nkomo, MD, MPH Professor of Medicine Director, Valvular Heart Disease Clinic Department of Cardiovascular Medicine
Mayo Clinic Rochester, Minnesota, USA
E. Magnus Ohman, MD, FRCPI, FESC, FACC Professor Department of Medicine
Duke University School of Medicine Durham, North Carolina, USA
Nicolas L. Palaskas, MD Assistant Professor Department of Cardiology UT MD Anderson Cancer Center Houston, Texas, USA
Ambarish Pandey, MD, MSCS
Assistant Professor Division of Cardiology, Department of Medicine University of Texas Southwestern Medical Center Dallas, Texas, USA
Shivda Pandey, MBBS
Assistant Professor of Medicine Section of Cardiology
Boston University School of Medicine Boston, Massachusetts, USA
Lavannya M. Pandit, MD, MS Associate Professor of Medicine Department of Pulmonary, Critical Care, and Sleep Medicine
Baylor College of Medicine/Michael E. DeBakey VA Medical Center Houston, Texas, USA
Maria A. Parekh, MD Chief Resident Department of Neurology
Baylor College of Medicine Houston, Texas, USA
W. Frank Peacock, MD, FACEP, FACC Vice Chair for Research Department of Emergency Medicine
Baylor College of Medicine Houston, Texas, USA
Lawrence Phillips, MD Director, Nuclear Cardiology Division of Cardiology, Department of Medicine
NYU Langone Health
New York, New York, USA
June K. Pickett, MD Fellow
Department of Cardiology/Internal Medicine
Baylor College of Medicine Houston, Texas, USA
Andrew Pipe, BA, MD, LLD(Hon), DSc(Hon), FRCPSC(Hon) Professor
Faculty of Medicine, University of Ottawa; Division of Cardiac Prevention and Rehabilitation University of Ottawa Heart Institute Ottawa, Ontario, Canada
Stuart B. Prenner, MD
Assistant Professor of Clinical Medicine
Section of Advanced Heart Failure and Cardiac Transplant University of Pennsylvania Philadelphia, Pennsylvania, USA
Prabhakar Rajiah, MBBS, MD,FRCR Professor of Radiology Department of Radiology, Mayo Clinic Rochester, Minnesota, USA
Pattara Rattanawong, MD Fellow in Cardiovascular Medicine
Assistant Professor of Medicine Department of Cardiovascular Diseases Mayo Clinic Phoenix, Arizona, USA
Heidi Reich, MD
Cardiothoracic Surgeon Department of Surgery
Central California Heart and Lung Surgery Fresno, California, USA
Eric E. Roselli, MD, FACS Chief, Adult Cardiac Surgery
Surgical Director, Aorta Center Department of Thoracic and Cardiovascular Surgery Heart Vascular and Thoracic Institute, Cleveland Clinic Cleveland, Ohio, USA
Smita Scholtz Clinic for General and Interventional Cardiology/Angiology Herz- und Diabeteszentrum NRW, Ruhr University Bochum Bad Oeynhausen, Germany
Associate Professor of Cardiology & Senior Consultant Interventional Cardiologist
Sri Ramachandra Institute of Higher Education and Research
Adjunct Faculty, Indian Institute of Technology-Madras Chennai, Tamil Nadu, India
Hirak Shah, MD
Department of Cardiology
Duke University Durham, North Carolina, USA
Nishant R. Shah, MD, MPH
Assistant Professor
Department of Medicine, Division of Cardiology
Alpert Medical School of Brown University Providence, Rhode Island, USA
Sanjiv J. Shah, MD
Stone Professor of Medicine Department of Medicine/Cardiology Northwestern University Chicago, Illinois, USA
Tina Shah, MD
Staff Cardiologist
Kaiser Permanente Seattle, Washington, USA
Fidaa Shaib, MD
Associate Professor
Departments of Pulmonary, Critical Care, and Sleep Medicine
Baylor College of Medicine Houston, Texas, USA
Win K. Shen, MD
Professor and Consultant Department of Cardiovascular Diseases
Mayo Clinic Arizona Phoenix, Arizona, USA
Katherine Shreyder, MD, PhD
Cardiology Fellow
Department of Cardiovascular Medicine
Lahey Hospital and Medical Center
Tufts University School of Medicine Burlington, Massachusetts, USA
Mohita Singh, MD
Cardiology Fellow
Department of Internal Medicine UT Southwestern Dallas, Texas, USA
Gulmohar Singh-Kucukarslan, MD, MS
Department of Internal Medicine
Henry Ford Hospital Detroit, Michigan, USA
Audrey E. Spelde, MD
Clinical Instructor
Department of Anesthesiology and Critical Care
The University of Pennsylvania Philadelphia, Pennsylvania, USA
Sarah A. Spinler, BS Pharm, PharmD
Professor and Chair
Department of Pharmacy Practice
Binghamton University School of Pharmacy and Pharmaceutical Sciences Johnson City, New York, USA
Deepthi Sudhakar, MD, MS Fellow Department of Cardiology
Baylor College of Medicine
Houston, Texas, USA
John M. Suffredini, DO
Cardiology Fellow
Section of Cardiology
Baylor College of Medicine
Houston, Texas, USA
Luis A. Tamara, MD
Chief of Nuclear Medicine/PET-CT Department of Nuclear Medicine
MEDVAMC
Houston, Texas, USA
Jeremy J. Thaden, MD
Assistant Professor Department of Cardiovascular Medicine
Mayo Clinic
Rochester, Minnesota, USA
Paaladinesh Thavendiranathan, MD, MSc
Cardiologist, Associate Professor of Medicine
Division of Cardiology and Joint Division of Medical Imaging
Peter Munk Cardiac Center, TGH, UHN, University of Toronto Toronto, Ontario, Canada
Kara A. Thompson, MD, FACC
Associate Professor, Department of Cardiology
MD Anderson Houston, Texas, USA
Miguel Valderrábano, MD
Lois and Carl Davis Centennial Chair, Methodist DeBakey Heart and Vascular Center
Associate Professor of Medicine, Weill College of Medicine, Cornell University
Director, Division of Cardiac Electrophysiology
Department of Cardiology
Houston Methodist Hospital
Patrick R. Vargo, MD
Associate Staff
Department of Thoracic and Cardiovascular Surgery
Cleveland Clinic Cleveland, Ohio, USA
Mahesh K. Vidula, MD
Fellow in Cardiovascular Medicine
Department of Medicine, Division of Cardiovascular Medicine
University of Pennsylvania
Philadelphia, Pennsylvania, USA
Shilpa Vijayakumar, MD
Cardiology Fellow
Department of Medicine, Division of Cardiology
Alpert Medical School of Brown University
Providence, Rhode Island, USA
Salim S. Virani, MD, PhD
Professor
Sections of Cardiovascular Research, Department of Medicine
Baylor College of Medicine
Houston, Texas, USA
Birgit Vogel, MD
Cardiovascular Imaging Fellow
Mount Sinai Morningside Hospital
Icahn School of Medicine at Mount Sinai New York, New York, 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 cardiovascular 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.
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
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.
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.
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
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 renninangiotensin-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).
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.
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 heparininduced 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
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.
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 AAArelated 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 cocaineinduced chest pain.
