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CONTENTS
Contributors
Preface
Credits for Figures and Tables
SECTION 1 CARDIOVASCULAR DISEASE: PAST, PRESENT, AND FUTURE
CHAPTER 1 A History of the Cardiac Diseases, and the Development of Cardiovascular Medicine as a Specialty
Questions
Answers
CHAPTER 2 The Global Burden of Cardiovascular Diseases
Questions
Answers
CHAPTER 3 Assessing and Improving the Quality of Care in Cardiovascular Medicine
Questions
Answers
SECTION 2 FOUNDATIONS OF CARDIOVASCULAR MEDICINE
CHAPTER 4 Functional Anatomy of the Heart

Questions
Answers
CHAPTER 5 Normal Physiology of the Cardiovascular System
Questions
Answers
CHAPTER 6 Molecular and Cellular Biology of the Heart
Questions
Answers
CHAPTER 7 Biology of the Vessel Wall
Questions
Answers
CHAPTER 8 Molecular and Cellular Development of the Heart
Questions
Answers
CHAPTER 9 Genetic Basis of Cardiovascular Disease
Questions
Answers
CHAPTER 10 Stem Cells and the Cardiovascular System
Questions
Answers
SECTION 3 EVALUATION OF THE PATIENT
CHAPTER 11 The History, Physical Examination, and Cardiac Auscultation

Questions
Answers
CHAPTER 12 Surface Electrocardiography
Questions
Answers
CHAPTER 13 Electrocardiographic Exercise Testing
Questions
Answers
CHAPTER 14 Cardiac Radiography
Questions
Answers
CHAPTER 15 Echocardiography
Questions
Answers
CHAPTER 16 Magnetic Resonance Imaging of the Heart
Questions
Answers
CHAPTER 17 Computed Tomography of the Heart
Questions
Answers
CHAPTER 18 Nuclear Cardiology
Questions
Answers
CHAPTER 19 Positron Emission Tomography in Heart Disease
Questions
Answers
CHAPTER 20 Cardiac Catheterization, Cardiac Angiography, and Coronary Blood Flow and Pressure Measurements
Questions
Answers
CHAPTER 21 Coronary Intravascular Imaging
Questions
Answers
CHAPTER 22 Magnetic Resonance Imaging and Computed Tomography of the Vascular System
Questions
Answers
SECTION 4 SYSTEMIC ARTERIAL HYPERTENSION
CHAPTER 23 Epidemiology of Hypertension

Questions
Answers
CHAPTER 24 Pathophysiology of Hypertension
Questions
Answers
CHAPTER 25 Diagnosis and Treatment of Hypertension
Questions
Answers
SECTION 5 METABOLIC DISORDERS AND CARDIOVASCULAR DISEASE
CHAPTER 26 The Metabolic Syndrome

Questions
Answers
CHAPTER 27 Obesity and Cardiovascular Disease
Questions
Answers
CHAPTER 28 Diabetes and Cardiovascular Disease
Questions
Answers
CHAPTER 29 Hyperlipidemia
Questions
Answers
SECTION 6 CIGARETTE SMOKING AND CARDIOVASCULAR DISEASE
CHAPTER 30 Epidemiology of Smoking and Pathophysiology of Cardiovascular Damage

Questions
Answers
CHAPTER 31 Preventing and Mitigating Smoking-Related Heart Disease
Questions
Answers
SECTION 7 ATHEROSCLEROSIS AND CORONARY HEART DISEASE
CHAPTER 32 Atherothrombosis: Disease Burden, Activity, and Vulnerability

Questions
Answers
CHAPTER 33 Coronary Thrombosis: Local and Systemic Factors
Questions
Answers
CHAPTER 34 Coronary Blood Flow and Myocardial Ischemia
Questions
Answers
CHAPTER 35 Nonobstructive Atherosclerotic and Nonatherosclerotic Coronary Heart Disease
Questions
Answers
CHAPTER 36 Definitions of Acute Coronary Syndromes
Questions
Answers
CHAPTER 37 Pathology of Myocardial Infarction and Sudden Death
Questions
Answers
CHAPTER 38 Molecular and Cellular Mechanisms of Myocardial Ischemia/Reperfusion Injury
Questions
Answers
CHAPTER 39 Evaluation and Management of Non–ST-Segment Elevation Myocardial Infarction
Questions
Answers
CHAPTER 40 ST-Segment Elevation Myocardial Infarction
Questions
Answers
CHAPTER 41 Antiplatelet and Anticoagulant Therapy in Acute Coronary Syndromes
Questions
Answers
CHAPTER 42 Percutaneous Coronary Interventions in Acute Myocardial Infarction and Acute Coronary Syndromes
Questions
Answers
CHAPTER 43 The Evaluation and Management of Stable Ischemic Heart Disease
Questions
Answers
CHAPTER 44 Coronary Artery Bypass Grafting and Percutaneous Interventions in Stable Ischemic Heart Disease
Questions
Answers
CHAPTER 45 Rehabilitation of the Patient with Coronary Heart Disease
Questions
Answers
SECTION 8 VALVULAR HEART DISEASE
CHAPTER 46 Acute Rheumatic Fever

Questions
Answers
CHAPTER 47 Aortic Valve Disease
Questions
Answers
CHAPTER 48 Degenerative Mitral Valve Disease
Questions
Answers
CHAPTER 49 Ischemic Mitral Regurgitation
Questions
Answers
CHAPTER 50 Mitral Stenosis
Questions
Answers
CHAPTER 51 Tricuspid and Pulmonary Valve Disease
Questions
Answers
CHAPTER 52 Prosthetic Heart Valves
Questions
Answers
CHAPTER 53 Antithrombotic Therapy for Valvular Heart Disease
Questions
Answers
CHAPTER 54 Management of Mixed Valvular Heart Disease
Questions
Answers
SECTION 9 CONGENITAL HEART DISEASE
CHAPTER 55 Mendelian Basis of Congenital and Other Cardiovascular Diseases

Questions
Answers
CHAPTER 56 Congenital Heart Disease in Adolescents and Adults
Questions
Answers
SECTION 10 MYOCARDIAL, PERICARDIAL, AND ENDOCARDIAL DISEASES
CHAPTER 57 Classification of Cardiomyopathies

Questions
Answers
CHAPTER 58 Dilated Cardiomyopathy
Questions
Answers
CHAPTER 59 Hypertrophic Cardiomyopathies
Questions
Answers
CHAPTER 60 Left Ventricular Noncompaction
Questions
Answers
CHAPTER 61 Restrictive Heart Diseases
Questions
Answers
CHAPTER 62 Arrhythmogenic Cardiomyopathy
Questions
Answers
CHAPTER 63 Myocarditis
Questions
Answers
CHAPTER 64 The Athlete and the Cardiovascular System
Questions
Answers
CHAPTER 65 Cardiovascular Disease in the Elderly: Pathophysiology and Clinical Implications
Questions
Answers
CHAPTER 66 Pericardial Diseases
Questions
Answers
CHAPTER 67 Infective Endocarditis
Questions
Answers
SECTION 11 HEART FAILURE
CHAPTER 68 Pathophysiology of Heart Failure

Questions
Answers
CHAPTER 69 The Epidemiology of Heart Failure
Questions
Answers
CHAPTER 70 The Diagnosis and Management of Chronic Heart Failure
Questions
Answers
CHAPTER 71 Evaluation and Management of Acute Heart Failure
Questions
Answers
CHAPTER 72 Cardiac Transplantation
Questions
Answers
CHAPTER 73 Mechanically Assisted Circulation
Questions
Answers
SECTION 12 CARDIOPULMONARY DISEASE
CHAPTER 74 Pulmonary Hypertension

Questions
Answers
CHAPTER 75 Pulmonary Embolism
Questions
Answers
CHAPTER 76 Cor Pulmonale: The Heart in Parenchymal Lung Disease
Questions
Answers
CHAPTER 77 Sleep-Disordered Breathing and Cardiac Disease
Questions
Answers
SECTION 13 RHYTHM AND CONDUCTION DISORDERS
CHAPTER 78 Electrophysiologic Anatomy

Questions
Answers
CHAPTER 79 Mechanisms of Cardiac Arrhythmias and Conduction Disturbances
Questions
Answers
CHAPTER 80 Genetics of Channelopathies and Clinical Implications
Questions
Answers
CHAPTER 81 Approach to the Patient with Cardiac Arrhythmias
Questions
Answers
CHAPTER 82 Invasive Diagnostic Electrophysiology
Questions
Answers
CHAPTER 83 Atrial Fibrillation, Atrial Flutter, and Atrial Tachycardia
Questions
Answers
CHAPTER 84 Supraventricular Tachycardia: Atrial Tachycardia, Atrioventricular Nodal Reentry, and Wolff–Parkinson–White
Syndrome
Questions
Answers
CHAPTER 85 Ventricular Arrhythmias
Questions
Answers
CHAPTER 86 Bradyarrhythmias
Questions
Answers
CHAPTER 87 Antiarrhythmic Drugs
Questions
Answers
CHAPTER 88 Catheter-Ablative Techniques
Questions
Answers
CHAPTER 89 Pacemakers and Defibrillators
Questions
Answers
CHAPTER 90 Diagnosis and Management of Syncope
Questions
Answers
CHAPTER 91 Sudden Cardiac Death
Questions
Answers
CHAPTER 92 Cardiopulmonary and Cardiocerebral Resuscitation
Questions
Answers
SECTION 14 DISEASES OF THE GREAT VESSELS AND PERIPHERAL VESSELS
CHAPTER 93 Diseases of the Aorta

Questions
Answers
CHAPTER 94 Cerebrovascular Disease and Neurologic Manifestations of Heart Disease
Questions
Answers
CHAPTER 95 Carotid Artery Stenting
Questions
Answers
CHAPTER 96 Diagnosis and Management of Diseases of the Peripheral Arteries
Questions
Answers
CHAPTER 97 Diagnosis and Management of Diseases of the Peripheral Venous System
Questions
Answers
SECTION 15 MISCELLANEOUS CONDITIONS AND CARDIOVASCULAR DISEASE
CHAPTER 98 Perioperative Evaluation for Noncardiac Surgery

Questions
Answers
CHAPTER 99 Anesthesia and the Patient with Cardiovascular Disease
Questions
Answers
CHAPTER 100 Rheumatologic Diseases and the Cardiovascular System
Questions
Answers
CHAPTER 101 The Diagnosis and Management of Cardiovascular Disease in Patients with Cancer
Questions
Answers
CHAPTER 102 HIV/AIDS and the Cardiovascular System
Questions
Answers
CHAPTER 103 Heart Disease in Pregnancy
Questions
Answers
CHAPTER 104 Traumatic Heart Disease
Questions
Answers
CHAPTER 105 The Kidney in Heart Disease
Questions
Answers
CHAPTER 106 Exercise in Health and Cardiovascular Disease
Questions
Answers
SECTION 16 POPULATIONS AND SOCIAL DETERMINANTS OF CARDIOVASCULAR DISEASE
CHAPTER 107 Social Determinants of Cardiovascular Disease

Questions
Answers
CHAPTER 108 Women and Ischemic Heart Disease: An Evolving Saga
Questions
Answers
CHAPTER 109 Race, Ethnicity, and Cardiovascular Disease
Questions
Answers
CHAPTER 110 Environment and Heart Disease
Questions
Answers
CHAPTER 111 Behavioral Cardiology: Epidemiology, Pathophysiology, and Clinical Management
Questions
Answers
CHAPTER 112 Economics and Cost-Effectiveness in Cardiology
Questions
Answers
Index
CONTRIBUTORS
MARIA L. ALCARAZ, BA
Clinical Research Assistant
Division of Clinical Epidemiology
Department of Medicine
Jewish General Hospital
McGill University
Montreal, Quebec, Canada
EMMANUEL E. EGOM, MD, MSc, PHD

Clinician-Lead for Heart Health Clinic and Hearts in Motion Program
St Martha’s Regional Hospital
Antigonish, Nova Scotia, Canada
INNA ERMEICHOUK, MSc

McGill University
CAROLINE FRANCK, MSc

Jewish General Hospital/McGill University
SARAH B. WINDLE, MPH

Clinical Research Associate
McGill University
PREFACE
Cardiology Board Review and Self-Assessment is an all-inclusive study guide written to complement the 14th Edition of Hurst’s
The Heart. Edited by Drs. Valentin Fuster, Robert A. Harrington, Jagat Narula, and Zubin J. Eapen, the 14th Edition of Hurst’s
The Heart is an exhaustive and thorough state-of-the-art review of the entire field of cardiovascular medicine.
Cardiology Board Review contains over 1100 questions and answers presented in a multiple-choice format. Each of the 112
chapters of Hurst’s The Heart is represented in Cardiology Board Review with 10 multiple-choice questions. Detailed answers
are provided for each question including not only an explanation of why the correct answer is correct but also why incorrect
answers are incorrect. Questions and answers correspond to appropriate sections of Hurst’s The Heart and include tables,
figures, and references. The more than 1100 questions presented in Cardiology Board Review span the depth and breadth of the
fascinating field of cardiovascular medicine.
Cardiology Board Review is designed to be a study guide for individuals preparing to take the Subspecialty Examination in
Cardiovascular Disease given by the American Board of Internal Medicine. Thus, Cardiology Board Review will be of particular
interest to cardiology fellows preparing to take the board examination for the first time and for practicing cardiologists preparing
to take the board examination as part of their recertification process. Cardiology Board Review will also be of interest to medical
students, residents, fellows, practicing physicians, and other health care professionals who wish to advance their knowledge of
cardiovascular medicine.
The current generation of health care professionals increasingly obtains their knowledge from nontraditional formats. To that
end, Cardiology Board Review and Self-Assessment is available in multiple electronic formats in addition to the traditional print
format. The book will be available in print, e-book, and online on McGraw-Hill Education’s cardiology web site at
www.AccessCardiology.com.
It has been my distinct pleasure to work with four coauthors while preparing Cardiology Board Review: Drs. Jonathan
Afilalo, Jacqueline E. Joza, Ravi Karra, and Patrick R. Lawler. Each of us contributed original questions and answers
corresponding to our particular areas of expertise. We would like to thank the members of the editorial and production
departments at McGraw-Hill Education with whom we worked, including Karen Edmonson, Robert Pancotti, and Shivani
Salhotra. We would also like to acknowledge the contributions and assistance of a number of other individuals, including Maria
L. Alcaraz, Emmanuel E. Egom, Inna Ermeichouk, Caroline Franck, and Sarah B. Windle. Finally, on behalf of myself and my
coauthors, we would like to express thanks to our families and colleagues for their encouragement and forbearance during the
many months it took to prepare this study guide.
Taking care of patients with cardiovascular disease is an honor and a privilege. Many of these patients have life-threatening
conditions that require advanced knowledge and highly technical skills. It is our responsibility, as health care professionals, to
ensure that our knowledge and skills match the needs of our patients. It is our hope that you will find Cardiology Board Review
and Self-Assessment to be an essential and valuable tool in your study of the ever expanding and always fascinating field of
cardiovascular medicine.
Mark J. Eisenberg, MD, MPH
CREDITS FOR FIGURES AND TABLES
The following figures and tables have been used with permission from this McGraw-Hill Education publication:
Fuster V, Harrington RA, Narula J, Eapen ZJ, eds. Hurst’s The Heart. 14th ed. New York: McGraw-Hill Education; 2017:
Chapter 9: Figure 9-1.

Chapter 11: Figures 11-1, 11-2, and 11-3.Chapter 14: Figures 14-1, 14-2, 14-3, and 14-4.
Chapter 15: Figures 15-1, 15-2, 15-3, 15-4, 15-5, 15-6, 15-7, and 15-8.
Chapter 16: Figures 16-1, 16-2, 16-3, 16-4, and 16-5.
Chapter 17: Figures 17-1, 17-2, 17-3, 17-4, and 17-5.
Chapter 18: Figures 18-1 and 18-2.
Chapter 19: Figures 19-1, 19-2, 19-3, and 19-4.
Chapter 39: Figure 39-1 and Tables 39-1 and 39-2.
Chapter 40: Table 40-1.
Chapter 66: Tables 66-1 and 66-2.
Chapter 76: Tables 76-1 and 76-2.
Data from Fuster V, Alexander RW, O’Rourke RA, et al. Hurst’s The Heart. 11th ed. New York: McGraw-Hill; 2004:

SECTION 1
Cardiovascular Disease: Past, Present, and Future

CHAPTER 1
A History of the Cardiac Diseases, and the Development of
Cardiovascular Medicine as a Specialty
Mark J. Eisenberg
QUESTIONS
DIRECTIONS: Choose the one best response to each question.
1-1. All of the following were experimental questions asked by William Harvey except:
A. What is the relationship of the motion of the auricle to the ventricle?
B. Do the arteries distend because of the propulsive force of the heart?
C. What purpose is served by the orientation of the cardiac and venous valves?
D. How much blood is present, and how long does its passage take?
E. All were questions asked by William Harvey
1-2. What were the primary component(s) of the clinical examination until the 17th century?
A. Palpating the pulse
B. Palpating the pulse and inspecting the urine
C. Palpating the pulse and percussion
D. Palpating the pulse and auscultation
E. Palpating the pulse, percussion, and auscultation
1-3. Which physician received the Nobel Prize for his work in electrophysiology?
A. Albert von Kölliker
B. Heinrich Müller
C. Augustus Waller
D. Willem Einthoven
E. Thomas Lewis
1-4. Who performed the first cardiac catheterization in a human?

A. Werner Forssmann
B. Claude Bernard
C. Dickinson Richards
D. Etienne Jules Marey
E. André Cournand
1-5. From which Latin word is the term angina appropriated?

A. Pain
B. Stress
C. Strangulation
D. Anxiety
E. Discomfort
1-6. Before the defibrillator and coronary care units, the in-hospital mortality associated with acute myocardial infarction was
approximately:
A. 10%
B. 15%
C. 20%
D. 30%
E. 40%
1-7. Who first described audible heart murmurs?

A. James Hope
B. John Mayow
C. William Cowper
D. René Laennec
E. Raymond Vieussens
1-8. Which procedure pioneered by Helen Taussig and Alfred Blalock was a pivotal breakthrough in thinking about congenital
heart abnormalities?
A. Balloon atrial septostomy
B. Subclavian-pulmonary artery shunt
C. Closure of atrial septal defect
D. Closure of ventricular septal defect
E. Stenting of patent ductus arteriosus
1-9. Who invented the first device for measuring blood pressure?
A. Etienne Jules Marey
B. Jean Poiseuille
C. Scipione Riva-Rocci
D. Karl von Vierordt
E. Carl Ludwig
1-10. Which of the following statements about hypertension is false?

A. In 1913, Janeway showed that patients, once diagnosed with hypertensive heart disease and symptoms, lived an average
of 4 to 5 years
B. Until the latter half of the 20th century, the asymptomatic state of most patients with hypertension and a prevalent view
that lowering the blood pressure would be deleterious to the kidney and brain lulled most physicians into accepting the
condition as being normally associated with aging
C. Effective oral treatment was available before President Franklin Roosevelt’s death in 1945 from severe hypertension
D. In the 1970s, reports from the Framingham Heart Study showed hypertension to be a major contributing cause to stroke,
heart attack, and heart and kidney failure
E. Richard Bright’s 1836 discovery of the relationship of cardiac hypertrophy and dropsy to shrunken kidneys introduced the
kidneys as a cause of heart failure long before hypertension was known
ANSWERS
1-1. The answer is E. (Hurst’s the Heart, 14th Edition, Chap. 1) Starting in 1603, Harvey dissected the anatomy and observed
the motion of the cardiac chambers and the flow of blood in more than 80 species of animals. His experimental questions
“to seek unbiased truth” can be summarized in the following questions: What is the relationship of the motion of the
auricle to the ventricle? Which is the systolic and which is the diastolic motion of the heart? Do the arteries distend
because of the propulsive force of the heart? What purpose is served by the orientation of the cardiac and venous valves?
How does blood travel from the right ventricle to the left side of the heart? Which direction does the blood flow in the
veins and the arteries? How much blood is present, and how long does its passage take? After many experiments and
without knowledge of the capillary circulation of the lungs, which was not known until 1661, Harvey stated, “It must of
necessity be concluded that the blood is driven into a round by a circular motion and that it moves perpetually; and hence
does arise the action or function of the heart, which by pulsation it performs.” This was published in 1628 as Exercitatio
Anatomica de Motu Cordis et Sanguinis in Animalibus.1 This revolutionary concept eventually became accepted in
Harvey’s lifetime and remains the foundation of our understanding of the purpose of the heart.
1-2. The answer is B. (Hurst’s the Heart, 14th Edition, Chap. 1) Until the 17th century, the clinical examination consisted of
palpating the pulse and inspecting the urine to reveal disease and predict prognosis. Percussion was first suggested in
1761 by Leopold Auenbrugger, a Viennese physician, who published a book proposing “percussion of the human thorax,
whereby, according to the character of the particular sounds thence elicited, an opinion is formed of the internal state of
that cavity.”2 It was reintroduced by Jean-Nicolas Corvisart in early 19th-century France and became an essential addition
to the chest examination until it was mostly supplanted by the chest x-ray. While auscultation of the chest was first
practiced by Hippocrates (460-370 BC), who applied his ear directly to the chest, it was not until the mid-19th century that
the stethoscope (first invented by René Laennec in Paris in 1816) moved auscultation to the forefront of the clinical
examination.3,4
1-3. The answer is D. (Hurst’s the Heart, 14th Edition, Chap. 1) In 1856, von Kölliker and Müller demonstrated that the heart
also produced electricity. Augustus Waller, with a capillary electrometer device (1887), detected cardiac electricity from
the limbs, a crude recording that he called an “electrogram.” Willem Einthoven, a physiologist in Utrecht, devised a more
sensitive string galvanometer (1902), for which he received the Nobel Prize, and the modern electrocardiogram was born.
Initially weighing 600 lb and requiring five people to operate, the three-lead electrocardiograph would eventually become
portable, 12 leads, routine, and capable of providing both static and continuous recordings of cardiac rhythm.5 With the
electrocardiogram, the activation and sequence of stimulation of the human heart could now be measured, and the
anatomic basis for the conduction system confirmed. Thomas Lewis in London was the first to realize its great potential,
beginning in 1909, and his books on disorders of the heartbeat became essential for aspiring electrocardiographers.2,6
1-4. The answer is A. (Hurst’s the Heart, 14th Edition, Chap. 1) Claude Bernard in 1844 was the first to insert a catheter into
the hearts of animals to measure temperature and pressure.2 In the early 1860s, Auguste Chauveau, a veterinary
physiologist, and Etienne Jules Marey, inventor of the sphygmograph, collaborated to develop a system of devices called
sounds, forerunners of the modern cardiac catheter, which they used to catheterize the right heart and left ventricle of the
horse.7 Cardiac catheterization in humans was thought an inconceivable risk until Werner Forssmann, a 29-year-old
surgical resident in Germany, performed a self-catheterization in 1929.8,9 Interested in discovering a method of injecting
adrenaline to treat cardiac arrest, Forssmann passed a ureteral catheter into his antecubital vein and confirmed its right
atrial position using x-ray. The next year he tried to image his heart using an iodide injection. However, he was
reprimanded by superiors and did not experiment further. Catheterization began in earnest in the early 1940s in New York
and London. André Cournand and Dickinson Richards at Bellevue, interested in respiratory physiology, developed and
demonstrated the safety of complete right heart catheterization, for which they shared the Nobel Prize with Forssmann in
1956.7,10
1-5. The answer is C. (Hurst’s the Heart, 14th Edition, Chap. 1) On July 21, 1768, William Heberden presented “Some
Account of a Disorder of the Breast” to the Royal College of Physicians, London: “But there is a disorder of the breast
marked with strong and peculiar symptoms, considerable for the kind of danger belonging to it, and not extremely rare.
The seat of it, and sense of strangling and anxiety with which it is attended, may make it not improperly be called angina
pectoris.”2,11 Heberden appropriated the term angina from the Latin word for strangling. His classic account marks the
beginning of our appreciation of coronary artery disease and myocardial ischemia. Edward Jenner and Caleb Parry were
the first to suspect a coronary etiology, which Parry published in 1799. Allan Burns, in Scotland, likened the pain of
angina pectoris to the discomfort brought about by walking with a tight ligature placed on a limb (1809), a prescient
concept that remains relevant today.
1-6. The answer is D. (Hurst’s the Heart, 14th Edition, Chap. 1) Before the defibrillator and coronary care units, the in-
hospital mortality associated with acute myocardial infarction was approximately 30%. With the development of the
defibrillator by William Kouwenhoven, Claude Beck and Paul Zoll were able to prove that rescue of cardiac arrest victims
was possible. Beck’s concept that “the heart is too good to die” instilled optimism into the care of coronary patients and
aggressiveness into their providers. Myocardial infarction was no longer a disease to be watched but rather one that might
benefit from aggressive therapeutic interventions. Zoll reported closed chest defibrillation in 1956 and cardioversion of
ventricular tachycardia in 1960. The monitoring of patients in close proximity to skilled nursing personnel who could
perform cardiopulmonary resuscitation was a logical next step suggested by Desmond Julian in 1961.
1-7. The answer is D. (Hurst’s the Heart, 14th Edition, Chap. 1) Valvular pathology was described in the 17th and 18th
centuries; however, Laennec was the first to describe audible heart murmurs, calling them “blowing, sawing, filing, and
rasping.”3 Originally, he attributed the noises to actual valvular disease, but he later decided that they were caused by
spasm or contraction of a cardiac chamber. James Hope in England was the first to classify valvular murmurs in A
Treatise on the Diseases of the Heart and Great Vessels (1832).12 He interpreted physical findings in early physiologic
terms and provided detailed pathologic correlations.13 Constriction of the mitral valve was recorded by John Mayow
(1668) and Raymond Vieussens (1715); the latter also recognized that this condition could cause pulmonary congestion.14
The presystolic murmur of mitral stenosis was described by Bertin (1824), timed as both early diastolic and presystolic by
Williams (1835), and placed on firmer grounds by Fauvel (1843) and Gairdner (1861). Aortic stenosis was first described
pathologically by Rivière (1663), and Laennec pointed out that the aortic valve was subject to ossification (1819).15
Corvisart showed an astute grasp of the natural history of aortic stenosis (1809). Early descriptions of aortic regurgitation
were by William Cowper (1706) and Raymond Vieussens (1715),16 whereas Giovanni Morgagni recognized the
hemodynamic consequences of aortic regurgitation (1761). In 1832, Corrigan provided his classic description of the
arterial pulse and murmur of aortic regurgitation. Flint added that the presystolic murmur was sometimes heard with
severe aortic regurgitation (1862).4
1-8. The answer is B. (Hurst’s the Heart, 14th Edition, Chap. 1) The pivotal breakthrough in thinking about congenital
abnormalities came from Helen Taussig and Alfred Blalock at Johns Hopkins Hospital with their “blue baby operation.”
Taussig had observed that patients with cyanotic heart disease worsened when their ductus arteriosus closed. She
suggested creating an artificial ductus to improve oxygenation.17 Blalock, assisted by Vivian Thomas, successfully
created a shunt from the subclavian to the pulmonary artery in November 1944. This innovative operation, in which a blue
baby was dramatically changed to a pink one—the Blalock-Taussig shunt—was highly publicized, and other operations
soon followed. These include closure of atrial septal defects (1950s), closure of ventricular septal defects (1954), and
tetralogy of Fallot repair (1954). In 1966, Rashkind introduced the balloon septostomy, a novel catheter therapeutic
technique that bought time for severely cyanotic infants with transposition of the great arteries.7 In the 1980s, catheters
were adapted to dilate stenotic aortic and pulmonic valves as well as aortic coarctation. Today, transcatheter closure of
patent ductus arteriosus (1971), atrial septal defects (1976), and ventricular septal defects (1987) has become routine.
Indomethacin therapy to enable closure of a patent ductus in the premature infant (1976) and prostaglandin infusion to
maintain ductal patency (1981) profoundly changed the medical management of fragile newborns. Stents now help keep
the ductus open as well as alleviate right ventricular obstruction in tetralogy of Fallot.
1-9. The answer is B. (Hurst’s the Heart, 14th Edition, Chap. 1) Stephen Hales, an English country parson, reported in his
Statical Essays (1733) that the arterial blood pressure of the cannulated artery of a recumbent horse rose more than eight
feet above the heart—the first true measurement of arterial pressure and the beginning of sphygmometry.2,18,19 His
pioneering efforts stood alone until 1828 when Jean Poiseuille introduced a mercury manometer device to measure blood
pressure.20,21 Over the next 60 years, various sphygmomanometric methods were developed—notably by Ludwig (1847),
Vierordt (1855), and Marey (1863)—to refine the measurement of the arterial pressure. An inflatable arm cuff coupled to
the sphygmograph, a device small enough to allow measurement outside the laboratory, was invented by Riva-Rocci
(1896), who also noted the “white-coat effect” on blood pressure.22 Nicolai Korotkoff, a Russian military surgeon, first
auscultated brachial arterial sounds (1905), a discovery that marked the advent of modern blood pressure recording. This
auscultatory approach eventually ensured its widespread use by the 1920s. In 1939, blood pressure recordings were
standardized by committees of the American Heart Association (AHA) and the Cardiac Society of Great Britain and
Ireland.
1-10. The answer is C. (Hurst’s the Heart, 14th Edition, Chap. 1) President Franklin Roosevelt’s death in 1945 from severe
hypertension and stroke called international attention to the consequences of hypertension and its inadequate treatment—
he had been managed with diet, digitalis, and phenobarbital. Effective oral treatment became possible in 1949, first with
reserpine and then with hydrochlorothiazide.23 Lumbar sympathectomy and adrenalectomy (1925), the last resort, was
abandoned. Subsequently, β-adrenergic blockers, calcium channel blockers, ACE inhibitors, angiotensin receptor blocking
agents, and direct renin inhibitors have brought antihypertensive relief to many. Severe salt restriction, as practiced earlier
with the Kempner rice diet, has taken a lesser role, whereas the Dietary Approaches to Stop Hypertension (DASH) diet,
exercise, and alcohol restriction are encouraged. Since 1973, recommendations published by the Joint National Committee
(JNC) on Detection, Evaluation, and Treatment of High Blood Pressure have been very helpful.
References
1. Harvey W. Anatomical Studies on the Motion of the Heart and Blood. Leake CD, trans. Springfield, IL: Charles C Thomas;
1970.
2. Acierno LJ. The History of Cardiology. London, UK: Parthenon; 1994.
3. Duffin JM. The cardiology of RTH Laënnec. Med Hist. 1989;33:42-71.
4. Hanna IR, Silverman ME. A history of cardiac auscultation and some of its contributors. Am J Cardiol. 2002;90:259-267.
5. Burch GE, DePasquale NP. A History of Electrocardiography. Chicago, IL: Year Book; 1964.
6. Fleming P. A Short History of Cardiology. Amsterdam, Netherlands: Rodopi; 1997.
7. Bing RJ. Cardiology: The Evolution of the Science and the Art. Basel, Switzerland: Harwood; 1992.
8. Forssmann-Falck R. Werner Forssmann: a pioneer of cardiology. Am J Cardiol. 1997;79: 651-660.
9. Mueller RL, Sanborn TA. The history of interventional cardiology: cardiac catheterization, angioplasty, and related
interventions. Am Heart J. 1995;129:146-172.
10. Fishman AP, Dickinson WR. Circulation of the Blood: Men and Ideas. Bethesda, MD: American Physiological Society;
1982.
11. Leibowitz JO. The History of Coronary Heart Disease. Berkeley, CA: University of California Press; 1970.
12. Flaxman N. The hope of cardiology: James Hope (1801–1841). Bull Hist Med. 1938;6:1-21.
13. Vander Veer JB. Mitral insufficiency: historical and clinical aspects. Am J Cardiol. 1958;2:5-10.
14. Rolleston H. The history of mitral stenosis. Br Heart J. 1941;3:1-12.
15. Vaslef SN, Roberts WC. Early descriptions of aortic valve stenosis. Am Heart J. 1993;125:1465-1474.
16. Vaslef SN, Roberts WC. Early descriptions of aortic regurgitation. Am Heart J. 1993;125:1475-1483.
17. Engle MA. Growth and development of state of the art care for people with congenital heart disease. J Am Coll Cardiol.
1989;13:1453-1457.
18. Willius FA, Dry TJ. A History of the Heart and the Circulation. Philadelphia, PA: Saunders; 1948.
19. Naqvi NH, Blaufox MD. Blood Pressure Measurement: An Illustrated History. New York, NY: Parthenon; 1998.
20. Dustan HP. History of clinical hypertension: from 1827 to 1970. In: Oparil S, Weber MA, eds. Hypertension: A Companion
to Brenner and Rector’s The Kidney. Philadelphia, PA: Saunders; 2000:1-4.
21. Ruskin A. Classics in Arterial Hypertension. Springfield, IL: Charles C Thomas; 1956.
22. Posten–Vinay N. A Century of Arterial Hypertension: 1896-1996. Chichester, UK: Wiley; 1996.
23. Piepho RW, Beal J. An overview of antihypertensive therapy in the 20th century. J Clin Pharmacol. 2000;40:967-977.
CHAPTER 2
The Global Burden of Cardiovascular Diseases
Mark J. Eisenberg
QUESTIONS
2-1. How many deaths worldwide are caused each year by cardiovascular disease (CVD)?
A. 10 million
B. 15 million
C. 17 million
D. 20 million
E. 23 million
2-2. Which of the following statements about global cardiovascular disease (CVD) is false?
A. There has been a steady decrease in the age-specific death rate for CVD in both sexes over the past 20 years
B. Women represent 50% of CVD deaths worldwide
C. The total number of deaths from CVD increased more than 40% between 1990 and 2013
D. Increases in gross domestic product are well correlated with reductions in cardiovascular disease mortality
E. A continued increase in the number of CVD deaths is expected as a result of demographic changes worldwide
2-3. What proportion of ischemic heart disease (IHD) patients from low-income world regions are taking none of the standard
secondary prevention medications?
A. 20%
B. 30%
C. 40%
D. 60%
E. 80%
2-4. Which noncommunicable disease (NCD) is the second most common cause of all disability globally?
A. Stroke
B. Ischemic heart disease
C. Chronic obstructive pulmonary disease
D. Lower back and neck pain
E. Depression
2-5. Which of the following cardiovascular diseases are more commonly diagnosed in men than in women worldwide?
A. Abdominal aortic aneurysm
B. Peripheral arterial disease
C. Atrial fibrillation
D. Both A and B
E. Both A and C
2-6. What is the most common complication of infective endocarditis?

A. Stroke
B. Embolization other than stroke
C. Heart failure
D. Intracardiac abscess
E. Intracardiac fistula
2-7. Which of the following statements about Chagas disease is false?
A. Chagas disease is primarily transmitted through the bites of the Triatoma infestans insect
B. No rapid diagnostic tests are available to detect the causative parasite
C. The acute phase immediately following infection is often asymptomatic, but it produces fever and malaise in up to 5% of
people
D. More than 50% of those infected will not progress to chronic Chagas disease
E. Approximately 30% of those infected will develop chronic cardiovascular Chagas disease
2-8. What percentage of patients with acute rheumatic fever will develop rheumatic heart disease (RHD)?
A. 50%
B. 60%
C. 70%
D. 80%
E. 90%
2-9. Which modifiable cardiovascular risk factor is responsible for the most morbidity and mortality worldwide?
A. Low fruit intake
B. High body mass index
C. High sodium
D. High blood pressure
E. Smoking
2-10. In 2013, the WHO and all member states (194 countries) agreed to a Global Non-Communicable Disease (NCD) Action
Plan, which aims to reduce the number of premature deaths from NCDs by 25% by 2025 through nine voluntary global
targets. Which of the following is not one of the nine voluntary targets?
A. A 20% relative reduction in daily exposure to outdoor and indoor air pollution
B. A 30% relative reduction in the prevalence of current tobacco use in persons aged 15 years and over
C. A 25% relative reduction in the prevalence of raised blood pressure or else containing the prevalence of raised blood
pressure, according to national circumstances
D. A halt in the rise of diabetes and obesity
E. At least 50% of eligible people receiving drug therapy and counseling (including glycemic control) to prevent heart
attacks and strokes
ANSWERS
2-1. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 2) In 2013, more than 17 million people died from CVDs, with
an estimated US $863 billion in direct health care costs and productivity losses worldwide.1 As a result of the large
populations in many low- and middle-income countries (LMICs), nearly 70% of CVD deaths occurred in LMICs. CVDs
account for 50% of all NCD deaths in the world each year and represent a significant threat to human welfare and
sustainable development. CVDs are the leading cause of death in every region of the world, with the exceptions of sub-
Saharan Africa—where infectious diseases are still the leading cause of death—and South Korea and Japan, where
cancers cause more deaths. The leading cause of CVD-related death was IHD, accounting for more than eight million
deaths, followed by ischemic and hemorrhagic strokes, with more than three million deaths each. Rheumatic heart
disease, although not the leading cause of death, was a significant contributor to the global burden and a leading cause of
highly preventable death, with approximately 275,000 deaths in 2013.
2-2. The answer is D. (Hurst’s The Heart, 14th Edition, Chap. 2) Despite the steady decrease in death rate for both sexes over
the past 20 years, the total number of deaths is increasing as a result of population growth and aging, which
disproportionately affects low- and middle-income countries (LMICs). Globally, the total number of CVD deaths
increased from 12.3 to 17.3 million, a 41% increase between 1990 and 2013.2 Women represent 50% of these deaths.
Although most countries have seen an increased national income per capita over this time, the decrease in the number of
CVD deaths cannot be entirely explained by economic growth. The decline in age-specific CVD mortality does not
correlate well with increases in country income, except weakly in upper-middle income countries. Therefore, it appears
unlikely that economic growth alone will improve a country’s burden of CVD. Despite an overall decrease in the global
age-specific CVD death rate, a continued increase in the number of CVD deaths is expected as a result of demographic
changes. The United Nations estimated that the global population in 2015 was 7.3 billion and will increase to a total of 8.5
billion by 2025 and 9.7 billion by 2050. When population growth slows down as a result of a reduction in fertility, the
population ages, and the proportion of older persons aged 60 or older increases over time. In 2015, about 10% of the
population was aged 60 or older, and the number of adults in this age group is projected to more than double by 2050 and
more than triple by 2100, with more than two-thirds of these older adults residing in LMICs.
2-3. The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 2) Ischemic heart disease is the leading cause of death
worldwide, encompassing myocardial infarction and all other acute coronary syndromes as well as long-term sequelae of
coronary heart disease, including angina pectoris and ischemic cardiomyopathy. Since the 1990s, the high-income
regions, specifically Australasia, Western Europe, and North America, have seen dramatic declines in the age-
standardized IHD mortality.3 However, IHD mortality has increased in other regions, including Central Asia, South Asia,
and East Asia. Although IHD burden falls largely on those aged older than 70 years in high-income regions, the age of
IHD deaths is much lower in other regions, with a mean age of onset of IHD events before age 50 years in more than 29%
of males and 24% of females in North Africa/Middle East and South Asia.3,4 As more patients with IHD survive their
initial event, the IHD death rate and case fatality will no longer be the sole public health benchmark for success; improved
symptom control and overall quality of life and access to adequate treatment will be important secondary outcomes.3 The
mainstays of treatment include standard, low-cost medications that are insufficiently used in low- and middle-income
countries (LMICs). The Prospective Urban Rural Epidemiological (PURE) study found that only 11% of patients from
high-income countries were not taking standard secondary prevention medications, whereas 80% of low-income-region
patients were taking none of the recommended medications.5,6
2-4. The answer is A. (Hurst’s The Heart, 14th Edition, Chap. 2) Stroke was the second largest contributor to disability
globally and in developing countries, whereas it was the third largest contributor to disability in developed countries (after
IHD and lower back and neck pain).7 Globally, the proportional contribution of stroke-related disability-adjusted life
years (DALYs) as a proportion of all diseases increased from 3.5% in 1990 to 4.6% in 2013. The deaths caused by stroke
also increased from 9.7% in 1990 to 11.8% in 2013. In order to reduce the rising burden of stroke worldwide, urgent
prevention and management strategies are needed. Prevention of risk factors remains key to reversing the stroke
pandemic, and universal access to organized stroke services must remain a priority, especially in LMICs.8 In 2013, the top
five noncommunicable causes of disability globally (from most to least) were: IHD, stroke, lower back and neck pain,
chronic obstructive pulmonary disorder, and depression.9
2-5. The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 2) Abdominal aortic aneurysm (AAA) and atrial fibrillation
(AF) are more commonly diagnosed in men than in women worldwide, while peripheral arterial disease (PAD) is equally
common among men and women in developed countries, and it is more often diagnosed in women than in men in
developing countries. AAA is a focal dilation of the abdominal aorta of at least 1.5 times the normal diameter or an
absolute value of 3 cm or greater. Risk factors include male sex, smoking, hypertension, atherosclerosis, and history of
AAA in a first-degree relative. In 2010, the age-specific prevalence rate per 100,000 ranged from 7.9 to 2274. Prevalence
was higher in developed versus developing nations. The age-specific annual incidence rate per 100,000 ranged between
0.83 and 164.6.10 AF and atrial flutter are irregular heart rhythms that often cause a rapid heart rate and can increase the
risk of stroke, heart failure, and other heart-related complications. In 2010, the estimated age-standardized DALYs
resulting from AF was 65 per 100,000 population in males and 46 in females, which was an increase of 18.8% and 19%
for males and females since 1990, respectively.11 Higher burden in men compared with women may reflect actual disease
rates or poorer access to medical care among women in resource-poor settings. PAD is a circulatory problem in which
narrowed arteries reduce blood flow to the limbs and cause symptoms of leg pain with walking (claudication). PAD is
defined as an ankle brachial index lower than or equal to 0.90. In developed countries, among adults aged 45–49 years,
the prevalence is similar for males and females and is around 5%. The prevalence increases to around 18% for males and
females in those aged 85 to 89 years.12 In developing countries, for the same age groups, the prevalence is around 6% for
females and 3% for males and increases to 15% in females and 14% in males.12
2-6. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 2) Infective endocarditis (IE) is an infection caused by
bacteria, or other infectious pathogens, that enter the bloodstream and cause inflammation in the heart tissues, often on a
valve. Because of the lack of direct blood supply, the heart valves are particularly susceptible to bacterial colonization and
are neither protected by the typical immune response nor easily reached by antibiotics. IE is a serious illness, with up to
22% in-hospital and 40% five-year mortality rates.13 A global collaboration was formed to assess the current
characteristics of patients with IE via a large, prospective multicenter registry, called the International Collaboration on
Endocarditis (ICE). ICE found that contemporary infective endocarditis is most often an acute disease with a high rate of
infection with Staphylococcus aureus and involving the mitral (41.1%) and aortic (37.6%) valves. Common complications
included stroke (16.9%), embolization other than stroke (22.6%), heart failure (32.3%), and intracardiac abscess (14.4%);
these often required surgical intervention (48.2%). In-hospital mortality was high (17.7%).14 Unfortunately, there were
few sites in Asia and Africa included in the registry, which limits the ability to assess geographic differences in patient
and microbiologic characteristics in these areas. IE is estimated to have resulted in 65,000 deaths and 1.9 million DALYs
in 2013. More complete knowledge and improved surveillance are needed in all world regions.15
2-7. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 2) Chagas disease is a disease of poverty and is localized to
Latin America because it is primarily transmitted through bites from the nocturnal “kissing bug,” Triatoma infestans,
which is endemic to this region. The infection can be asymptomatic, but it can eventually lead to premature morbidity and
mortality, especially in young women of childbearing age. There are rapid diagnostic tests that can detect the causative
parasite, Trypanosoma cruzi, in serum and can diagnose chronic infections. Pesticides have been developed for vector
control programs, but much is still unknown about this disease. In any case, prevention and elimination of the vector
remain the keys to Chagas control. The disease has three phases: acute, indeterminate, and chronic. The acute phase
immediately follows infection and is often asymptomatic, but it produces fever and malaise in up to 5% of people. The
indeterminate phase is asymptomatic, with more than 50% of those infected remaining in this phase for life without any
long-term sequelae. After a decade or more, approximately 30% of people will experience chronic cardiovascular Chagas
disease, with symptoms including heart failure, arrhythmias, and thromboembolism.16 Deaths are rare in the acute phase,
and most deaths attributable to Chagas disease result from downstream cardiovascular sequelae. In addition,
approximately 15%–20% of people will experience chronic gastrointestinal disease sequelae, including megaesophagus
and megacolon. Between 5 and 18 million people are currently infected, and the infection is estimated to cause more than
10,000 deaths annually.17
2-8. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 2) Rheumatic heart disease is an endemic disease that is
common in settings of poverty. It is caused by group A streptococcus infection and leads to mitral stenosis and premature
mortality, particularly in young, predominantly female, poorer individuals living in Oceania, South Asia, Central Asia,
Africa, and the Middle East. Approximately 60% of all acute rheumatic fever cases will develop RHD, based on data from
Aboriginal Australian populations, and 1.5% of patients with RHD will die each year.18 Globally in 2010, RHD affected
more than 34 million people, causing more than 345,000 deaths, almost all in LMICs.19 The disease can progress to cause
moderate to severe multivalvular disease, leading to congestive heart failure, pulmonary hypertension, or AF. RHD also
contributes (3%–7.5%) to an estimated 144,000–360,000 incident strokes each year.
2-9. The answer is D. (Hurst’s The Heart, 14th Edition, Chap. 2) Elevated blood pressure is estimated to be the single largest
contributor to the global burden of disease and global mortality. There are gaps in the awareness, treatment, and control of
hypertension globally. High blood pressure in populations appears to occur in tandem with economic development, but
notably in the highest income countries, individuals with lower socioeconomic status are the group most likely to be
untreated.20,21 In Africa, hypertension is thought to be the leading cause of heart failure, whereas at global levels,
hypertension is linked to the development of atherosclerotic vascular disease. In high-income countries, it is estimated to
be responsible for 25% of deaths from stroke, 20% of deaths from IHD, and more than 17% of all global deaths.22 The
number of people with uncontrolled hypertension was 978 million in 2008, a substantial increase from 605 million in
1980, largely because of population growth and aging.23 Other modifiable cardiovascular risk factors are: high body mass
index, low fruit intake, smoking, high sodium, and high total cholesterol.24
2-10. The answer is A. (Hurst’s The Heart, 14th Edition, Chap. 2) While a reduction in exposure to outdoor and indoor air
pollution is not one of the nine targets, such pollution ranks as the largest single environmental health risk factor, with
more than 2.9 million deaths attributed to outdoor air pollution and a similar number attributed to indoor air pollution.25
Air pollution has been shown to increase preclinical cardiovascular risk factors such as atherosclerosis, endothelial
dysfunction, and hypertension. The estimated excess risk of cardiovascular mortality rises 11% per 10 μg/m3 rise in levels
of particulate matter, with no threshold level below which long-term exposure to urban air pollution has no ill effect on
cardiovascular health.26 Answers B through E: Modeling studies have shown that significant reductions in premature
CVD are possible by 2025 if multiple risk factor targets are achieved. Globally, the risk factor change that would lead to
the largest reduction in premature mortality would be the decreased prevalence of hypertension, followed by tobacco
smoking prevalence for men and obesity for women.
References
1. Bloom DE, Cafiero E, Jané-Llopis E, et al. The global economic burden of noncommunicable diseases. Program on the
Global Demography of Aging, World Economic Forum, 2011.
2. Roth GA, Huffman MD, Moran AE, et al. Global and regional patterns in cardiovascular mortality from 1990 to 2013.
Circulation. 2015;132:1667-1678.
3. Moran AE, Forouzanfar MH, Roth GA, et al. The global burden of ischemic heart disease in 1990 and 2010: the Global
Burden of Disease 2010 study. Circulation. 2014;129:1493-1501.
4. Moran AE, Tzong KY, Forouzanfar MH, et al. Variations in ischemic heart disease burden by age, country, and income:
The Global Burden of Diseases, Injuries, and Risk Factors 2010 study. Glob Heart. 2014;9:91-99.
5. Yusuf S, Islam S, Chow CK, et al. Use of secondary prevention drugs for cardiovascular disease in the community in high-
income, middle-income, and low-income countries (the PURE Study): a prospective epidemiological survey. Lancet.
2011;378:1231-1243.
6. Khatib R, McKee M, Shannon H, et al. Availability and affordability of cardiovascular disease medicines and their effect on
use in high-income, middle-income, and low-income countries: an analysis of the PURE study data. Lancet. 2016;387:61-
69.
7. Barker-Collo S, Bennett DA, Krishnamurthi RV, et al. Sex differences in stroke incidence, prevalence, mortality and
disability-adjusted life years: results from the Global Burden of Disease study 2013. Neuroepidemiology. 2015;45:203-214.
8. Feigin VL, Krishnamurthi R, Bhattacharjee R, et al. New strategy to reduce the global burden of stroke. Stroke. 2015
Jun;46(6):1740-1747.
9. Murray CJL, Barber RM, Foreman KJ, et al. Global, regional, and national disability-adjusted life years (DALYs) for 306
diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990–2013: quantifying the epidemiological
transition. Lancet. 2015;386:2145-2191.
10. Sampson UK, Norman PE, Fowkes FG, et al. Estimation of global and regional incidence and prevalence of abdominal
aortic aneurysms 1990 to 2010. Glob Heart. 2014;9:159-170.
11. Chugh SS, Roth GA, Gillum RF, Mensah GA. Global burden of atrial fibrillation in developed and developing nations. Glob
Heart. 2014;9:113-119.
12. Fowkes FGR, Rudan D, Rudan I, et al. Comparison of global estimates of prevalence and risk factors for peripheral artery
disease in 2000 and 2010: a systematic review and analysis. Lancet. 2013;382:1329-1340.
13. Bannay A, Hoen B, Duval X, et al. The impact of valve surgery on short- and long-term mortality in left-sided infective
endocarditis: do differences in methodological approaches explain previous conflicting results? Eur Heart J. 2011;32:2003-
2015.
14. Murdoch DR. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International
Collaboration on Endocarditis–Prospective Cohort Study. Arch Intern Med. 2009;169:463.
15. Chu VH, Park LP, Athan E, et al. Association between surgical indications, operative risk, and clinical outcome in infective
endocarditis: a prospective study from the International Collaboration on Endocarditis. Circulation. 2015;131:131-140.
16. Nunes MC, Dones W, Morillo CA, Encina JJ, Ribeiro AL. Chagas disease: an overview of clinical and epidemiological
aspects. J Am Coll Cardiol. 2013;62:767-776.
17. Stanaway JD, Roth G. The burden of Chagas disease. Glob Heart. 2015;10:139-144.
18. Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal diseases. Lancet Infect Dis.
2005;5:685-694.
19. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a
systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015;385:117-171.
20. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560-2572.
21. Colhoun HM, Hemingway H, Poulter NR. Socio-economic status and blood pressure: an overview analysis. J Hum
Hypertens. 1998;12:91-110.
22. Forouzanfar MH, Alexander L, Anderson HR, et al. Global, regional, and national comparative risk assessment of 79
behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a
systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015;386:2287-2323.
23. Danaei G, Finucane MM, Lin JK, et al. National, regional, and global trends in systolic blood pressure since 1980:
Systematic analysis of health examination surveys and epidemiological studies with 786 country-years and 5·4 million
participants. Lancet. 2011;377:568-577.
24. Institute for Health Metrics and Evaluation (IHME). GBD Compare. Seattle, WA: IHME, University of Washington, 2015.
Available from http://vizhub.healthdata.org/gbd-compare (Accessed February 2, 2016).
25. GBD 2013 Risk Factors Collaborators. Global, regional and national comparative risk assessment of 79 behavioural,
environmental/occupational and metabolic risks or clusters of risks in 188 countries 1990-2013: a systematic analysis for the
GBD 2013. Lancet. 2015;5;386(10010):2287-3223.
26. Cosselman KE, Navas-Acien A, Kaufman JD. Environmental factors in cardiovascular disease. Nat Rev Cardiol.
2015;12:627-642.
CHAPTER 3
Assessing and Improving the Quality of Care in
Cardiovascular Medicine
Mark J. Eisenberg
QUESTIONS
3-1. Which of the following statements concerning health care expenditures in the United States is false?
A. Health care expenditures accounted for nearly 17.5% of the gross domestic product in 2014
B. The United States invested an estimated $3.0 trillion in health care in 2014
C. Expenditures related to cardiovascular disease were estimated to be $656 billion in 2015
D. The United States health system ranked lowest among 11 similar countries with respect to access, equity, quality,
efficiency, and healthy lives, despite spending the most on health care
E. Increasing the use of expensive medical care is associated with better quality of care and patient outcomes
3-2. Which of the following factors influences the variability and appropriateness of health care delivery?
A. Patients’ clinical status
B. Sociodemographic factors
C. Providers and facilities
D. Geographic location
E. All of the above
3-3. How many years, on average, does it take for guidelines to be incorporated into clinical practice?
A. 4 years
B. 10 years
C. 13 years
D. 17 years
E. 21 years
3-4. Which of the following is not generally considered a part of defining quality of care?
A. Cost of care
B. Evidence-based care
C. Improving outcomes
D. Patient satisfaction
E. All of the above are important for defining quality of care
3-5. Which constitute the primary domains of the Donabedian framework for quality assurance?
A. Structure, process, and outcome
B. Process, outcome, and evaluation
C. Research, guidelines, and implementation
D. Research, structure, and outcome
E. Research, outcome, and cost
3-6. Which of the following is not a principal thematic dimension in the Institute of Medicine (IOM)’s landmark report on
quality improvement initiatives, Crossing the Quality Chasm: A New Health System for the 21st Century?
A. Safety
B. Cost
C. Timeliness
D. Efficiency
E. Equity
3-7. What is the specific function of clinical data standards?

A. To measure and improve access to evidence-based care
B. To enable the reproducible collection of data across hospitals and settings
C. To measure physician performance
D. To measure the quality of clinical trial data
E. To enable the assessment of standards of care
3-8. The ACC/AHA guidelines indicate that percutaneous aortic balloon dilation may be considered a bridge to surgical aortic
valve replacement or transcatheter aortic valve replacement for symptomatic patients with severe aortic stenosis (Class IIb,
level C).23 A Class IIb level C recommendation could indicate that the intervention is:
A. Probably indicated, based on data from multiple randomized trials
B. Probably indicated, based on expert opinion
C. Probably indicated, based on case studies
D. Possibly indicated, based on expert opinion
E. Possibly indicated, based on a single randomized trial
3-9. Which of the following tools for improving the quality of cardiovascular care involves quantifying a range of health care
processes and outcomes, identifying multiple points in the continuum of care for which clinical inertia (the failure to
implement or titrate recommended therapies) can occur, and then selecting those with the strongest evidence and highest
correlation with clinically meaningful outcomes?
A. Clinical practice guidelines
B. Clinical data standards
C. Performance measures
D. Appropriate use criteria
E. Procedural registries
3-10. Some of the most exciting opportunities to improve care come from the combination of registries and national coalitions
to target significant gaps in care. A dramatic example of this is the Door-to-Balloon (D2B) initiative. Which of the following
was not a performance recommendation in the D2B initiative?
A. Prompt data feedback to the emergency department and cath lab staff
B. Expectations of having the cath lab team assembled within 30 minutes
C. Targeted times to first ECG acquisition for chest pain patients within 15 minutes
D. Emergency medicine physician activates cath lab
E. Single-call activation of the cath lab
ANSWERS
3-1. The answer is E. (Hurst’s the Heart, 14th Edition, Chap. 3) In the United States, health care expenditures accounted for
nearly 17.5% of the gross domestic product in 2014 (an estimated $3 trillion) and are expected to reach 19.6% by 2024.1
Cardiovascular disease (CVD) remains the leading cause of death and disability,2 with an estimated annual total cost of
$656 billion in 2015.3 In a recent report, the US health system ranked lowest among 11 countries with respect to access,
equity, quality, efficiency, and healthy lives,4 despite spending the most on health care.5 It is often thought that high-
quality health care is dependent on the continued discovery and delivery of novel diagnostic and therapeutic interventions.
However, studies suggest that greater use of expensive medical care is actually associated with lower quality and worse
outcomes.6,7 Woolf and Johnson8 have extended this concept to mathematically quantify the trade-off between the
development of new interventions and the more consistent delivery of known therapies. They argue that despite
tremendous scientific and technologic advancements, the failure to consistently deliver proven therapies dilutes and
reduces the overall quality of a health care system. Thus, money spent on improving this actual delivery of care may be
equally or even more critical than money spent on improving technology to result in improved quality of both routine and
specialized health care.
3-2. The answer is E. (Hurst’s the Heart, 14th Edition, Chap. 3) A critical goal of efforts to disseminate high-quality care is
to ensure rational and efficient use of effective treatment to those who derive the most benefit.9 Yet surveys evaluating
processes of care have shown that, on an average, only one in two US adults receives recommended care when receiving
health care services.10 Several studies have suggested that there are marked variations in the use of evidence-based
treatments of cardiovascular disease (CVD) based on gender, age, race, education, income, and insurance status.10,11,12,13
A study examining differences in the treatment of myocardial infarction showed that although blacks lived closer than
whites to hospitals with revascularization capability that were considered high-quality, they were less likely than whites to
be admitted to revascularization-capable and high-quality hospitals.14 Further emphasizing the need to monitor the quality
of care has been the observation of marked variations in the processes of care by geographic region. Pioneering work from
the Dartmouth Atlas series, a comprehensive evaluation of health care services provided to Medicare beneficiaries, has
documented broad variation in the use of both diagnostic and treatment modalities in CVD as a function of the site of
care.15 Beyond concerns about overall disparities in care, there is emerging evidence that among the patients eligible for
treatments, those with the least potential to benefit are preferentially treated, whereas those with the most to gain are
systematically undertreated. This finding is referred to as the risk-treatment paradox. Many investigators have shown that
high-risk patients—who would be expected to benefit more than lower-risk patients—are treated less aggressively,
whereas lower-risk patients are treated more aggressively.16,17
3-3. The answer is D. (Hurst’s the Heart, 14th Edition, Chap. 3) It is estimated that, on average, it takes about 17 years for
guidelines to be incorporated into clinical practice,9 even with an intervention as simple as aspirin use at the time of
myocardial infarction (> 20 years for full adoption). There can be several levels of barriers to the effective implementation
of clinical evidence and guidelines in routine practice. These exist at policy, societal, system/organizational, provider, and
patient levels. These can be addressed through the use of frameworks for quality metrics and tools to improve quality of
care in cardiovascular disease.
3-4. The answer is E. (Hurst’s the Heart, 14th Edition, Chap. 3) Lohr and Schroeder broadly define quality of care as “the
degree to which health services for individuals and populations increase the likelihood of desired health outcomes and are
consistent with current professional knowledge.”18 The US Agency for Healthcare Research and Quality has proposed a
similar definition: “Quality healthcare means doing the right thing at the right time in the right way for the right person
and having the best results possible.”19 The Institute for Healthcare Improvement recommends that to improve the United
States’ health care system requires simultaneous pursuit of three aims, called the “Triple Aim”—improving the patient
experience of care (including satisfaction), improving outcomes (of individuals and populations), and reducing the per
capita cost of health care.20 Achieving the best quality of care as marked by highest quality patient outcome and
experience with the lowest possible cost is what a health care system usually strives to achieve. Although the concept of
quality health care is intuitive and relatively easy to understand, to actually measure, monitor, and improve quality
requires the use of a clear conceptual framework that encompasses important, relevant aspects of health care.
3-5. The answer is A. (Hurst’s the Heart, 14th Edition, Chap. 3) One of the earliest approaches to conceptualizing the
components of quality assurance was proposed by Donabedian.21 This framework considers quality to comprise three
main domains: structure, process, and outcome. Structure refers to the attributes of settings where care is delivered and
includes aspects that exist independently of the patient. Examples of structural attributes include provider training and
experience, the availability of specialized treatments, nurse-to-patient ratios, and treatment and discharge plans. Process
refers to whether or not good medical practices are followed, and it incorporates concepts such as the medications given
and the timing of their administration, the use of diagnostic and therapeutic procedures, and patient counseling. Outcome
refers to tangible measures that capture the consequences of care and range from manifestations of disease progression
(eg, mortality and hospitalizations) to patient-centered outcomes of health status and treatment satisfaction. As noted by
Donabedian, these three components of quality are interdependent and are built on a framework that focuses mainly on
linking the delivery of care to outcomes.
3-6. The answer is B. (Hurst’s the Heart, 14th Edition, Chap. 3) The current driving force and roadmap for quality
improvement initiatives in American health care is the Institute of Medicine (IOM)’s landmark report, Crossing the
Quality Chasm: A New Health System for the 21st Century.9 The IOM recognized the following principal thematic
dimensions needed to guide QI in health care:
• Safety—avoiding injuries to patients from the care that is intended to help them
• Effectiveness—providing services based on scientific knowledge to those who could benefit while refraining from
providing services to those not likely to benefit
• Patient-centeredness—providing care that is respectful of and responsive to individual patient preferences, needs, and
values, and ensuring that patient values guide all clinical decisions
• Timeliness—reducing waits and sometimes harmful delays in care
• Efficiency—avoiding waste, including waste of equipment, supplies, ideas, and energy
• Equity—providing care that does not vary in quality because of personal characteristics such as sex, ethnicity,
geographic location, and socioeconomic status
Cost is not one of the principal themes of the IOM report, but it is considered among the outcomes in the Donabedian
framework for quality assurance.
3-7. The answer is B. (Hurst’s the Heart, 14th Edition, Chap. 3) To measure and improve care, one first needs to know both
how and what to measure. It is critical to have standardized data definitions that enable the reproducible collection of data
across different hospitals and settings. To create the foundation for clear, explicit data capture, the ACC/AHA Clinical
Data Standards were developed to serve as a foundation for implementing and evaluating the other ACC/AHA quality
tools.22 These data standards are a set of standardized definitions of particular conditions and treatments that can and
should be applied in both QA/QI activities and, importantly, clinical trials. Inclusion in clinical trials is especially
important to support both comparability across studies and their incorporation into guidelines, performance measures, and
clinical care. In particular, standardized definitions support the consistent definition of symptoms, comorbidities, and
outcomes in many areas of CVD (eg, acute coronary syndromes, congestive heart failure, PCI).22 The more these data
standards are used in clinical trials, observational registries, and QA/QI efforts, the greater the ability will be to translate
the emerging knowledge from clinical research to clinical care.
3-8. The answer is D. (Hurst’s the Heart, 14th Edition, Chap. 3) To distill the rapidly expanding body of cardiovascular
literature, professional agencies, such as the AHA and ACC, have commissioned expert committees to synthesize the
available evidence into clinical practice guidelines.24-25 The creation of guidelines requires writing committees to
systematically review the medical literature and to assess the strength of evidence for particular treatment strategies. This
necessitates ranking the types of research from which knowledge is generated. Randomized controlled trials are given the
highest weight. When these are not available, other study designs, including preintervention and postintervention studies,
observational registries, and clinical experience are used. To transparently communicate the strength of a recommendation
and the evidence on which it is generated, a class recommendation (Class I = strongly indicated, Class IIa = probably
indicated, Class IIb = possibly indicated, or Class III = not indicated) and strength of the evidence (level A evidence [data
derived from multiple randomized trials] through level C [data derived from expert opinion, case studies, or standard of
care]) are provided.25 An intervention that is probably indicated, based on data from multiple randomized trials (option A)
is a Class IIa level A recommendation. An intervention that is probably indicated, based on expert opinion (option B) or
probably indicated, based on case studies (option C) are both Class IIa level C recommendations. An intervention that is
possibly indicated, based on a single randomized trial (option E), is a Class IIb level B recommendation.
3-9. The answer is C. (Hurst’s the Heart, 14th Edition, Chap. 3) At times, the evidence supporting (or for avoiding) a
particular diagnostic or therapeutic action is so strong that failure to perform such actions jeopardizes patients’ outcomes.
Performance measures represent that subset of the clinical practice guidelines (option A) for which the strongest evidence
exists and for which their routine use (or avoidance) is felt to be an important advance to elevating quality.26,27,28
Performance measures are often constructed as a set of measures that quantify a range of health care processes and
outcomes; they are designed to identify multiple points in the continuum of care for which clinical inertia—the failure to
implement or titrate recommended therapies—can occur.28,29 Once the relevant domains are identified, then those
guideline recommendations with the strongest evidence and highest correlation with clinically meaningful outcomes are
selected for performance measure creation. Clinical data standards (option B) are a set of standardized definitions of
particular conditions and treatments that can be applied in both quality assurance/improvement activities and clinical
trials. Appropriate use criteria (option D) help identify what specific tests and procedures to perform and when and how
often, based on estimates of the relative benefits and harms of a procedure or a test for a specific indication. Procedural
registries (option E) support the prospective collection of data for assessing performance and guideline compliance within
hospitals.
3-10. The answer is C. (Hurst’s the Heart, 14th Edition, Chap. 3) First ECG acquisition for chest pain patients was
recommended within 10 minutes. Launched in 2006, the Door-to-Balloon (D2B) initiative sought to increase the
proportion of ST-segment elevation myocardial infarction patients receiving primary PCI within 90 minutes of hospital
presentation from approximately 50% to more than 75%.30 This program supplemented data collected through the NCDR
CathPCI registry with explicit recommendations about how to improve performance,31 including (1) activation of the
catheterization laboratory (cath lab) by emergency department physicians, (2) single-call activation of the cath lab, (3)
expectations of having the cath lab team assembled within 30 minutes, (4) prompt data feedback to the emergency
department and cath lab staff, and (5) activation of the cath lab based on prehospital ECGs and targeted times to first ECG
acquisition for chest pain patients within 10 minutes. Between January 2005 and September 2010, this effort led to a
decline in median D2B time, from 96 minutes in December 2005 to 64 minutes in September 2010.32 There were
corresponding increases in the proportion of patients undergoing primary PCI within 90 minutes (from 44.2% to 91.4%),
and within 75 minutes (from 27.3% to 70.4%). The declines in median times were greatest among groups that had the
highest median times during the first period.32
References
1. Centers for Medicare & Medicaid Services. National health expenditure data. https://www.cms.gov/Research-Statistics-
Data-and-Systems/Statistics-Trends-and-Reports/NationalHealthExpendData/NationalHealthAccountsProjected.html.
Accessed December 8, 2015.
2. NHLBI Morbidity and Mortality Chart Book: National Heart, Lung, and Blood Institute.
https://www.nhlbi.nih.gov/research/reports/2012-mortality-chart-book. Accessed December 9, 2015.
3. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2015 update: a report from the American
Heart Association. Circulation. 2015;131(4): e29-322.
4. Davis K, Stremikis K, Suires D, Schoen C. Mirror, mirror on the wall, 2014 update: how the U.S. health care system
compares internationally. The Commonwealth Fund. June 2014; http://www.commonwealthfund.org/publications/fund-
reports/2014/jun/mirror-mirror. Accessed December 8, 2015.
5. Squires D, Anderson C. Health care from a global perspective: spending, use of services, prices, and health in 13 countries.
The Commonwealth Fund. October 2015; http://www.commonwealthfund.org/publications/issue-briefs/2015/oct/us-health-
care-from-a-global-perspective.
6. Skinner JS, Staiger DO, Fisher ES. Is technological change in medicine always worth it? The case of acute myocardial
infarction. Health Affairs (Project Hope). 2006;25(2): w34-47.
7. Fisher ES, Bynum JP, Skinner JS. Slowing the growth of health care costs—lessons from regional variation. N Engl J Med.
2009;360(9):849-852.
8. Woolf SH, Johnson RE. The break-even point: when medical advances are less important than improving the fidelity with
which they are delivered. Ann Family Med. 2005;3(6):545-552.
9. Committee on Quality of Health Care in America; Institute of Medicine. Crossing the Quality Chasm: A New Health System
for the 21st Century. Washington, DC: National Academy Press; 2001.
10. Asch SM, Kerr EA, Keesey J, et al. Who is at greatest risk for receiving poor-quality health care? N Engl J Med.
2006;354(11):1147-1156.
11. Mody P, Gupta A, Bikdeli B, Lampropulos JF, Dharmarajan K. Most important articles on cardiovascular disease among
racial and ethnic minorities. Circ Cardiovasc Qual Outcomes. 2012;5(4):e33-41.
12. Daly C, Clemens F, Lopez Sendon JL, et al. Gender differences in the management and clinical outcome of stable angina.
Circulation. 2006;113(4):490-498.
13. Blomkalns AL, Chen AY, Hochman JS, et al. Gender disparities in the diagnosis and treatment of non-ST-segment elevation
acute coronary syndromes: large-scale observations from the CRUSADE (Can Rapid Risk Stratification of Unstable Angina
Patients Suppress Adverse Outcomes With Early Implementation of the American College of Cardiology/American Heart
Association Guidelines) National Quality Improvement Initiative. J Am Coll Cardiol. 2005;45(6):832-837.
14. Popescu I, Cram P, Vaughan-Sarrazin MS. Differences in admitting hospital characteristics for black and white Medicare
beneficiaries with acute myocardial infarction. Circulation. 2011;123(23):2710-2716.
15. The Center for the Evaluative Clinical Sciences, Dartmouth Medical School; The Center for the Evaluative Clinical
Sciences, Maine Medical Center. The Dartmouth Atlas of Cardiovascular Health Care. Chicago, IL: AHA Press; 1999.
16. Spertus JA, Decker C, Gialde E, et al. Precision medicine to improve use of bleeding avoidance strategies and reduce
bleeding in patients undergoing percutaneous coronary intervention: prospective cohort study before and after
implementation of personalized bleeding risks. BMJ. 2015;350:h1302
17. Marso SP, Amin AP, House JA, et al. Association between use of bleeding avoidance strategies and risk of periprocedural
bleeding among patients undergoing percutaneous coronary intervention. JAMA. 2010;303(21):2156-2164.
18. Lohr KH. Medicare: A Strategy for Quality Assurance, Volume I. Washington: National Academy of Sciences; 1990.
19. US Department of Health & Human Services, The US Agency for Healthcare Research and Quality Archive. A Quick Look
at Quality. Available at: http://archive.ahrq.gov/consumer/qnt/qntqlook.htm. Accessed December 11, 2015.
20. Institute for Healthcare Improvement: The IHI Triple Aim.
http://www.ihi.org/engage/initiatives/tripleaim/Pages/default.aspx. Accessed December 11, 2015.
21. Donabedian A. The quality of care. How can it be assessed? JAMA. 1988;260(12): 1743-1748.
22. Hendel RC, Bozkurt B, Fonarow GC, et al. ACC/AHA 2013 methodology for developing clinical data standards: a report of
the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards. J Am Coll
Cardiol. 2014;63(21): 2323-2334.
23. Nishimura, et al. (2017). 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients
with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on
Clinical Practice Guidelines. http://circ.ahajournals.org/content/early/2017/03/14/CIR.0000000000000503. Accessed April
7, 2017.
24. Gibbons RJ, Smith S, Antman E. American College of Cardiology/American Heart Association clinical practice guidelines:
Part I: where do they come from? Circulation. 2003;107(23):2979-2986.
25. Halperin JL, Levine GN, Al-Khatib SM, et al. Further evolution of the ACC/AHA clinical practice guideline
recommendation classification system: a report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2016;67(13):1572-1574.
26. Bonow RO, Masoudi FA, Rumsfeld JS, et al. ACC/AHA classification of care metrics: performance measures and quality
metrics: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures.
Circulation. 2008;118(24):2662-2666.
27. Spertus JA, Eagle KA, Krumholz HM, Mitchell KR, Normand SL. American College of Cardiology and American Heart
Association methodology for the selection and creation of performance measures for quantifying the quality of
cardiovascular care. J Am Coll Cardiol. 2005;45(7):1147-1156.
28. Turner BJ, Hollenbeak CS, Weiner M, Ten Have T, Tang SS. Effect of unrelated comorbid conditions on hypertension
management. Ann Intern Med. 2008;148(8):578-586.
29. Phillips LS, Twombly JG. It’s time to overcome clinical inertia. Ann Intern Med. 2008;148(10):783-785.
30. Krumholz HM, Bradley EH, Nallamothu BK, et al. A campaign to improve the timeliness of primary percutaneous coronary
intervention: Door-to-Balloon: an alliance for quality. JACC Cardiovasc Interv. 2008;1(1):97-104.
31. Bradley EH, Nallamothu BK, Herrin J, et al. National efforts to improve door-to-balloon time results from the Door-to-
Balloon Alliance. J Am Coll Cardiol. 2009;54(25):2423-2429.
32. Krumholz HM, Herrin J, Miller LE, et al. Improvements in Door-to-Balloon Time in the United States: 2005-2010.
Circulation. 2011;124(9):1038-1045.
SECTION 2
Foundations of Cardiovascular Medicine

CHAPTER 4
Functional Anatomy of the Heart
Jacqueline Joza
QUESTIONS
4-1. Which of the following statements is false?

A. The main pulmonary artery, portions of both venae cavae, distal pulmonary veins, and nearly the entire ascending aorta
are intrapericardial
B. The right and left pulmonary arteries are extrapericardial structures
C. The transverse sinus forms a tunnel-like passageway that separates the great arteries anteriorly from the great veins
posteriorly
D. The oblique sinus lies posterior to the right atrium
E. The serous pericardium forms the inner lining of the fibrous pericardium; over the heart, it is referred to as the epicardium
4-2. A 35-year-old woman presents to your clinic for evaluation of a murmur. She describes intermittent regular palpitations
that have been associated with lightheadedness. Auscultation reveals a midsystolic click and a crescendo systolic murmur. The
S1-click distance increases with squatting and decreases with standing. Regarding this valve or valve defect, which statement
is true?
A. The valve leaflets are characteristically thin
B. Annular dilatation is not typically present
C. Prolapse of the anterior leaflet occurs more frequently
D. The anterolateral papillary muscle is commonly single and usually has a dual blood supply from the left coronary
circulation
E. The posteromedial papillary muscle usually has a single head and is most commonly supplied by the left anterior
descending artery
4-3. Regarding Figure 4-1, select the statement that is false:
FIGURE 4-1 Superior view of the heart. (Reproduced with permission from McAlpine W. Heart and Coronary Arteries: An
Anatomic Atlas for Radiologic Diagnosis and Surgical Treatment. New York: Spring-Verlag; 1975.)
A. The central structures labelled L, P, and R are supplied by the conus artery
B. The * depicts the right atrial appendage
C. The arrowhead points to a circumflex marginal branch
D. An ablation catheter positioned at P will reveal atrial electrogram signals
E. The oblique sinus is not visualized in this figure
4-4. All of the following are used to differentiate the right ventricle from the left ventricle except:
A. The presence of a moderator band
B. Free wall typically < 0.4 mm thick
C. A prominent arch-shaped muscular ridge known as the crista supraventricularis separates the tricuspid and pulmonary
valves
D. The apex is thin and lacks trabeculation
E. The tricuspid valve always follows the morphological right ventricle
4-5. Which of the following statements regarding structures within the right atrium is false?
A. The cavotricuspid isthmus is targeted during typical right atrial flutter ablation
B. The cavotricuspid isthmus is a well-defined region of atrial tissue that is bordered by the eustachian ridge and valve
posteriorly, and the tricuspid valve annulus anteriorly
C. The right atrial free wall is a very thin structure between pectinate muscles and can perforate during catheter positioning
D. Inferior vena caval blood flow is directed by the eustachian valve toward the foramen ovale, and superior vena caval
blood is directed toward the tricuspid valve
E. The right atrial appendage abuts the left aortic sinus of Valsalva
4-6. A patient undergoes a transesophageal echocardiography (TEE) as workup for possible left atrial appendage (LAA) closure.
Regarding the LAA, which of the following statements is false?
A. There is no known relationship between stroke and LAA morphology
B. There are four basic morphologic patterns to the LAA: windsock, cactus, cauliflower, and chicken wing
C. Age is not a determinant for the dimensions of an LAA
D. All lobes of the LAA should be visualized during TEE to rule out a thrombus
E. Both the right and the left atrial appendages are located close to the right ventricular outflow tract
4-7. All of the following are true statements except:

A. The left anterior descending artery courses within the epicardial fat of the anterior interventricular groove
B. The first septal perforating branch of the left anterior descending artery supplies the AV (His) bundle and proximal left
bundle branch
C. Dominance is left in 70% of human hearts, right in 10%, and shared in 20%
D. A patient who presents acutely with an anterior ST elevation myocardial infarction secondary to a left anterior descending
artery occlusion is at risk for a mechanical complication
E. The right coronary artery typically arises nearly perpendicularly from the aorta
4-8. In a typical right-dominant system, which of the following left ventricular segments would most likely not be affected in a
patient with left anterior descending artery occlusion?
A. Mid anterior wall
B. Mid inferolateral wall
C. Basal anterior septum
D. Basal anterior wall
E. Mid anterolateral wall
4-9. Regarding the great vessels, which of the following statements is true?
A. Most coarctations occur just proximal to the left subclavian artery
B. When the eustachian or the adjacent thebesian valve of the coronary sinus is large and fenestrated, it is referred to as the
ligamentum arteriosum
C. The ligamentum arteriosum represents the vestigial remnant of the fetal ductal artery, which, when patent, connects the
proximal right pulmonary artery to the undersurface of the aortic arch
D. The ostium of the superior vena cava (SVC) is guarded by a crescent-shaped, often fenestrated flap of tissue called the
eustachian valve
E. The ligament of Marshall is the vestigial remnant of the vein of Marshall, which forms the terminal connection between a
persistent left SVC and the coronary sinus
4-10. Which of the following statements is false concerning the triangle of Koch?
A. It is bordered by the coronary sinus ostium, the septal tricuspid annulus, and the tendon of Todaro
B. The AV node is a subendocardial structure that is located within the upper portion of the triangle of Koch
C. The His bundle is located within the triangle of Koch. The apex of the triangle corresponds to the central fibrous body of
the heart where the His bundle penetrates
D. The atrial end of the fast pathway in AV nodal reentrant tachycardia inserts near the ostium of the coronary sinus, while
the slow pathway lies closer to the apex of the triangle near the AV node
E. AV node displacement occurs in Ebstein malformation and persistent left SVC
ANSWERS
4-1. The answer is D. (Hurst’s The Heart, 14th Edition, Chap. 4) The reflections along the pulmonary veins and venae cavae
are continuous and form a posterior midline cul-de-sac known as the oblique sinus. The oblique sinus lies immediately
posterior to the left atrium, not the right atrium (option D). The main pulmonary artery, portions of both venae cavae,
distal pulmonary veins, and nearly the entire ascending aorta are intrapericardial (option A). The right and left pulmonary
arteries are extrapericardial structures (option B). The transverse sinus forms a tunnel-like passageway that separates the
great arteries anteriorly from the great veins posteriorly (option C). The serous pericardium forms the delicate inner lining
of the fibrous pericardium and continues onto the surface of the heart and great vessels at the pericardial reflection.1 Over
the heart, it is referred to as the epicardium, and it contains the epicardial coronary arteries and veins, autonomic nerves,
lymphatics, and a variable amount of adipose tissue (option E).
4-2. The answer is D. (Hurst’s The Heart, 14th Edition, Chap. 4) The anterolateral papillary muscle is single and usually has
a dual blood supply from the left coronary circulation (option D).2 Mitral valve prolapse is characterized by thickened and
redundant leaflets (option A), annular dilatation (with or without calcium) and thickened and elongated chordae tendineae
(with or without rupture) (option B). Prolapse of the posterior leaflet occurs more often than that of the anterior leaflet
(option C). The posteromedial papillary muscle usually has multiple heads and is most commonly supplied only by the
dominant coronary artery (option E).2 Small left atrial branches supply the most basal aspects of the mitral leaflets.3
4-3. The answer is A. (Hurst’s The Heart, 14th Edition, Chap. 4) The figure shows a superior view of the heart, including the
aortic and pulmonic valves, the origins of the left and right coronary arteries, the superior aspect of the left atrium, the
SVC, and the right upper pulmonary vein. The aortic cusps (labeled L for left aortic cusp; P for posterior aortic cusp; and
R for right aortic cusp) form pocketlike tissue flaps that are avascular (option A). The conus artery is the first branch of
the right coronary artery in 50%–60% of persons; it supplies the right ventricular outflow tract and forms an important
collateral anastomosis (circle of Vieussens) just below the pulmonary valve with an analogous branch from the left
anterior descending coronary artery.1-3 The * symbol (option B) represents the right atrial appendage, which is retracted
by the rod to disclose the sinus node artery (SNA). The arrowhead (option C) is pointing to a marginal branch of the left
circumflex artery. An ablation catheter positioned at the posterior (or noncoronary) cusp (option D) will reveal atrial
electrogram signals due to its close proximity to the interatrial septum. The oblique sinus (option E) is not seen in this
figure. It is formed from the reflections along the pulmonary veins and venae cavae that form a posterior midline cul-de-
sac that lies posterior to the left atrium.
4-4. The answer is D. (Hurst’s The Heart, 14th Edition, Chap. 4) The right ventricular apex is heavily trabeculated.1,3 This
apical trabecular zone extends inferiorly beyond the attachments of the papillary muscles toward the ventricular apex and
about halfway along the anterior wall. This muscular meshwork is the usual site of insertion of transvenous ventricular
pacemaker electrodes, and it is the preferred site for positioning the tip of an implantable cardioverter defibrillator lead.
The moderator band (option A) forms an intracavitary muscle that connects the septal band with the anterior tricuspid
papillary muscle. The right ventricular wall is thin in normal adults, usually less than 0.4 cm (regional variation between
0.2 and 0.7 cm) (option B). A prominent arch-shaped muscular ridge known as the crista supraventricularis separates the
tricuspid and pulmonary valves. It is made up of three components (parietal band, infundibular septum, and septal band)
that can appear as distinct structures or can merge together (option C).1,3 The tricuspid valve always follows the
morphological right ventricle, which is an important consideration when evaluating patients with congenital heart disease
(option E).
4-5. The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 4) The right atrial appendage abuts the right aortic sinus of
Valsalva and overlies the proximal right coronary artery (option E). The cavotricuspid isthmus, a frequent target of atrial
flutter ablation, is a well-defined region of atrial tissue that is bordered by (1) the eustachian ridge and valve posteriorly
and (2) the tricuspid valve annulus anteriorly (options A, B). The right atrial free wall is paper-thin between pectinate
muscles and therefore can be perforated easily by stiff catheters (option C).1-3 The atrial lead of a dual-chamber
pacemaker is normally positioned within the trabeculations of the right atrial appendage. Inferior vena caval blood flow is
directed by the eustachian valve toward the foramen ovale, and superior vena caval blood is directed toward the tricuspid
valve (option D).4
4-6. The answer is A. (Hurst’s The Heart, 14th Edition, Chap. 4) The left atrial appendage is usually multilobed and narrower
than its right atrial counterpart, and it exhibits more variability in shape.1-3,5 The chicken wing variety of LAA
morphology has the least likelihood for embolic events (option A).6 There are four basic morphologic patterns: windsock,
cactus, cauliflower, and chicken wing (option B).6 Age and sex are both determinants for LAA dimension (option C).4
There may be multiple lobes in the LAA; all lobes must be visualized in order to rule out thrombus prior to planned
cardioversion, electrophysiology or structural procedure, or percutaneous balloon valvuloplasty procedures (option D).
Either atrial appendage may serve as a vantage point from which to access and ablate arrhythmias in the adjacent segment
of the right ventricular outflow tract (option E).7
4-7. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 4) Dominance is right in 70% of human hearts, left in 10%,
and shared in 20%.1-3 In patients with a congenitally bicuspid aortic valve, the incidence of left coronary dominance is
25% to 30%.3 The left anterior descending artery (LAD) courses within the epicardial fat of the anterior interventricular
groove (option A). The first septal perforating branch supplies the AV (His) bundle and the proximal left bundle branch
(option B).3 In patients with symptomatic hypertrophic obstructive cardiomyopathy, nonsurgical septal reduction by
percutaneous transluminal occlusion of septal branches of the LAD is a therapeutic approach aimed at reducing the
outflow gradient.8 Anterior infarcts have been shown to be independent predictors of ventricular septal defects post
myocardial infarction (option D). Whereas the right coronary artery arises almost perpendicularly from the aorta, the left
arises at an acute angle (option E).4
4-8. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 4). The midventricular inferolateral wall is typically supplied
by the circumflex artery, not the left anterior descending artery (LAD). In a typical right-dominant system, the LAD
supplies the midventricular and basal segments of the anterior (options A and D), anterolateral walls (option E) and
anterior septum (option C) and all apical segments. The left circumflex artery supplies the midventricular and basal
inferolateral segments, and the right coronary artery supplies the midventricular and basal inferior wall and inferior
septum. In the setting of a large obtuse marginal branch of the circumflex artery, the anterolateral or inferior wall may not
be supplied by the LAD. However, because the patterns of coronary distribution are so highly variable, these correlations
between coronary blood flow and regional anatomy are not precise. For example, a hyperdominant right coronary artery
can supply the apex, and a large, obtuse marginal branch of the circumflex artery can supply the anterolateral or inferior
wall.1-3 Ventricular septal defects are more common in the setting of a wrap-around LAD.
4-9. The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 4) The vein of Marshall forms the terminal connection between
a persistent left SVC and the coronary sinus. Its vestigial remnant in normal adults is the ligament of Marshall; it is a
potential source of arrhythmias and a common site for recurrences after pulmonary vein isolation (option E). Most
coarctations occur just distal to the left subclavian artery (option A). The ostium of the inferior vena cava is guarded by a
crescent-shaped, often fenestrated flap of tissue, the eustachian valve,1-3 which is readily seen by echocardiography.
Although generally small, the eustachian valve can become so large that it can produce a double-chambered right atrium.2
Also, when either the eustachian or the adjacent thebesian valve of the coronary sinus is large and fenestrated, it is
referred to as a Chiari network (option B).1-3 The ligamentum arteriosum represents the vestigial remnant of the fetal
ductal artery, which, when patent, connects the proximal left pulmonary artery to the undersurface of the aortic arch
(option C). The ostium of the inferior vena cava (not the SVC) is guarded by the eustachian valve. It is an important
structure during cavotricuspid isthmus ablation (option D).
4-10. The answer is D. (Hurst’s The Heart, 14th Edition, Chap. 4) The atrial end of the fast pathway in AV nodal reentrant
tachycardia inserts closer to the AV node at the apex of the triangle, whereas the slow pathway (target for radiofrequency
ablation) inserts near the ostium of the coronary sinus (option D). The triangle of Koch is bordered by the coronary sinus
ostium posteroinferiorly, the septal tricuspid annulus anteriorly, and the tendon of Todaro posteriorly (option A). The
tendon of Todaro is a fibrous extension of the Eustachian valve (option B). The body of the AV node is found near the
apex of the triangle. The His bundle, also located in the triangle of Koch, penetrates through the central fibrous body
separating the atria and ventricles (option C). The bundle of His then bifurcates into right and left main bundle branches,
which branch further to become Purkinje fibers that spread conduction to the ventricles. Differences in the conduction
system primarily reside in the arrangement of the transitional and compact components of the AV node and in the length
and route of the His bundle. In both Ebstein’s anomaly and persistent left SVC syndrome with a grossly enlarged CS
ostium, the size of the triangle of Koch is reduced, resulting in a shorter distance between the compact AV node and the
CS ostium (option E).
References
1. Edwards WD. Anatomy of the Cardiovascular System: Clinical Medicine. Vol 6. Philadelphia, PA: Harper & Row; 1984:1-
24.
2. Edwards WD. Cardiac anatomy and examination of cardiac specimens. In: Emmanouilides G, Reimenschneider T, Allen H,
Gutgesell H, eds. Moss & Adams’ Heart Disease in Infants, Children, and Adolescents. 5th ed. Baltimore, MD: Williams &
Wilkins; 1995:70-105.
3. Edwards WD. Applied anatomy of the heart. In: Giuliani ER, Fuster V, Gersh BJ, et al, eds. Cardiology Fundamentals and
Practice. Vol 1. 2nd ed. St Louis, MO: Mosby-Year Book; 1991:47-112.
4. Kitzman D, Edwards WD. Minireview: age-related changes in the anatomy of the normal human heart. J Gerontol Med Sci.
1990;45:M33-M39.
5. Veinot JP, Harrity PJ, Gentile F, et al. Anatomy of the normal left atrial appendage: a quantitative study of age-related
changes in 500 autopsy hearts: implications for echocardiographic examination. Circulation. 1997;96:3112-3115.
6. Di Biase L, Santangeli P, Anselmino M, et al. Does the left atrial appendage morphology correlate with the risk of stroke in
patients with atrial fibrillation? Results from a multicenter study. J Am Coll Cardiol. 2012;60(6):531-538.
7. Tabatabaei N, Asirvatham SJ. Supravalvular arrhythmia identifying and ablating the substrate. Circ Arrhythm
Electrophysiol. 2009;2:316-326.
8. Naqueh SF, Lakkis NM, He ZX, et al. Role of myocardial contrast echocardiography during nonsurgical septal reduction
therapy for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 1998;32:225-229.
CHAPTER 5
Normal Physiology of the Cardiovascular System
Ravi Karra
QUESTIONS
5-1. Which of the following is true about Figure 5-1?
FIGURE 5-1 Phases of the action potential and major associated currents in ventricular myocytes.
A. Sodium influx during phase 1 depolarization is decreased by membrane depolarization

B. Sodium influx is limited after phase 1 by the closure of inactivation gates
C. The phase 2 plateau of the action potential is the result of a decrease in intracellular calcium through the L-type calcium
channel
D. Phase 3 repolarization is the result of potassium influx into the cell through the funny channel (IF)
E. Maintenance of the membrane potential during diastole is an energy-independent process
5-2. Please select the true statement about Figure 5-2.

A. Calcium-induced calcium release occurs by calcium influx through ion channel B with release of calcium from the
sarcoplasmic reticulum via ion channel C
B. The magnitude of the calcium transient is, in part, determined by calcium influx into the cell via channels B and D
C. The decline in the calcium transient occurs via channel C and is energy-independent
D. Increased cytoplasmic calcium results in contraction, in part, by the binding of calcium to TnI
E. None of the above
FIGURE 5-2 Major components of excitation–contraction coupling in cardiomyocytes. (Adapted with permission from Scoote
M, Poole-Wilson PA, Williams AJ, et al. The therapeutic potential of new insights into myocardial excitation-contraction
coupling. Heart. 2003 Apr;89(4):371-376.)
5-3. A 54-year-old woman was recently started on furosemide for pedal edema related to prolonged standing. Shortly after
starting furosemide, she feels fatigued and confirms dizziness with standing. Her past medical history is notable for
hypertension that had not been treated. Her blood pressure is 158/82 sitting and her heart rate is 85. Her physical exam is
notable for flat neck veins, a nondisplaced apical impulse, and a soft S4. Which of the following is not true for this patient?
A. Discontinuation of her diuretic and increased fluid intake would increase the peak tension in her cardiac muscle fibers
following muscle contraction
B. Increasing preload through hydration would increase cardiac output, in part by the increased sensitivity to calcium by
myofilaments at longer sarcomere lengths
C. Increased heart rate would result in faster cardiac relaxation
D. Increasing afterload would increase myofilament shortening velocity
E. A cup of coffee could increase contractility
5-4. Which of the following is true regarding the cardiac cycle?

A. The c wave occurs during isovolumic contraction
B. The v wave occurs just after the QRS complex on the ECG, but before the T wave
C. The change in ventricular pressure during ventricular filling is a property of ventricular stiffness
D. Ventricular stiffness is constant during contraction and relaxation
E. The area enclosed within the pressure–volume loop (PVA) is proportional to myocardial oxygen consumption
Questions 5-5 through 5-7 relate to the following vignette.
A 54-year-old woman is brought to the catheterization laboratory to assess her hemodynamics for shortness of breath. A
precatheterization echocardiogram revealed normal ventricular function. Moreover, her filling pressures are normal.
5-5. Which of the following is not true regarding ventricular function?

A. A modest volume challenge would be expected to increase stroke volume
B. Left ventricular (LV) compliance is determined entirely by the intrinsic elastic properties of the left ventricle
C. A bolus of norepinephrine would be expected to decrease the velocity of LV shortening
D. The rate of LV pressure development (dP/dt) is dependent on preload but relatively independent of afterload
E. Increasing the heart rate from 80 to 95 is unlikely to increase cardiac output
5-6. Which of the following is true regarding her diastolic function?

A. Ventricular relaxation is energy-independent
B. Tau, the time constant of LV relaxation, is increased with β-adrenergic receptor stimulation
C. The end-diastolic pressure–volume relationship is influenced by changes in intrathoracic pressure, pericardial constraint,
and ventricular interaction
D. The sarcomeric protein titin does not meaningfully contribute to diastolic function
E. The PV relationship during systole reflects the lusitropic state of the heart
5-7. Right heart catheterization revealed a right atrial pressure of 5 mm Hg, a right ventricular (RV) pressure of 25/5 mm Hg, a
pulmonary artery (PA) pressure of 25/10 mm Hg, and a wedge pressure of 10 mm Hg. The aortic pressure was 120/85 mm
Hg, and heart rate was 85. The cardiac output was calculated to be 6 L/min. Which of the following is correct?
A. The mean arterial pressure (MAP) is 108 mm Hg
B. The mean PA pressure is 15 mm Hg
C. The systemic vascular resistance (SVR) is 14.5 Wood units
D. The pulmonary vascular resistance (PVR) is 2.5 Wood units
E. None of the above
5-8. Which of the following is true about the coronary circulation?

A. Collateral vessels around a coronary obstruction have myocardial blood flow during exercise similar to that of the native
coronary artery
B. To meet the increased oxygen demands during exercise, the myocardium dramatically increases its extraction of oxygen
from the blood
C. Adenosine is a major mediator of coronary autoregulation
D. Coronary vascular resistance is greater in the subendocardial coronary circulation than in the subepicardial coronary
circulation
E. The principal endothelial derived relaxing factor is adenosine
5-9. Which of the following is true about control of the circulation?

A. Arterial pressure regulation is controlled primarily by the parasympathetic nervous system
B. One result of carotid baroreflex resetting is increased receptor firing for a given mean arterial blood pressure
C. The Bezold–Jarisch reflex occurs with a decrease in ventricular distension and results in bradycardia and hypotension
D. Endothelins constrict arterioles and decrease preload
E. Endocannabinoids increase contractility
5-10. With reference to the venous return curves in Figure 5-3, which of the following is incorrect?
FIGURE 5-3 Venous pressure–cardiac output return curve.
A. Line A is the effect of volume loading or increasing venous pressure

B. Line B is the effect of arteriolar vasodilation
C. The flat portion of the curve in C represents the maximal cardiac output as venous return is reduced
D. The shift in the Frank–Starling curve to curve D is the effect of increased sympathetic tone
E. Point E is the equilibrium point where the ability of the venous system to provide enough return at a given pressure is
matched by the ventricle’s ability to pump that return when distended to that pressure
ANSWERS
5-1. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 5). Cardiomyocytes are specialized cells that couple membrane
depolarization with cellular contraction. Phase 1 depolarization is the result of sodium influx through Na+ channels.
Sodium influx is regenerative, in that increasing membrane depolarization opens more Na+ channels (option A). Rapid
depolarization is limited by K+ efflux but also by the closure of inactivation gates on Na+ channels that prevent reopening
of individual channels only after the membrane has been fully repolarized (option B). The phase 2 plateau is the result of
balanced K+ efflux and Ca2+ influx through L-type Ca2+ channels (option C). Phase 3 repolarization is the result of K+
efflux primarily through the delayed outward K current (IK). The funny current (IF) is a specialized channel found in
pacemaker cells that results in spontaneous depolarization of the cell during phase 4 and in automaticity (option D). Phase
4 occurs during diastole and requires the Na+/K+ ATPase to restore and maintain low intracellular Na+ and high
intracellular K+ concentrations (option E).
5-2. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 5). In Figure 5-2, channel A is the ryanodine receptor on the
sarcoplasmic reticulum (SR). Channel B is the L-type Ca2+ channel on the sarcolemma. Channel C is the SERCA pump
on the sarcoplasmic reticulum, and channel D is the Na+/Ca+ exchanged (NCX) on the sarcolemma. Calcium-uptake
calcium release is the result of calcium release from the SR through the ryanodine receptor (A) after calcium influx into
the cell through the L-type Ca2+ channel (B) (option A). The calcium transient is a result of (1) Ca2+ influx through the L-
type Ca2+ channel and the reverse mode NCX; (2) the amount of calcium in the SR; (3) the amount of calcium released by
the SR for a given calcium current; and (4) intracellular Ca2+ buffers. NCX can operate in the reverse mode during
cellular depolarization, when the intracellular Na+ content is high. The net effect is Na+ extrusion and Ca2+ uptake. This is
a minor contribution to the calcium transient (option B). The calcium transient declines largely because the SERCA
ATPase sequesters calcium into the SR. This requires ATP and is energy-dependent (option C). Calcium concentrations
are coupled to contraction. Calcium bound TnC essentially pulls TnI off actin. Thus, TnI can no longer inhibit the
formation of myosin-actin crossbridges (option D).
5-3. The answer is D. (Hurst’s The Heart, 14th Edition, Chap. 5) Options A and B reflect the Frank–Starling mechanism. A
key property of healthy cardiac muscle is faster relaxation times with increasing heart rates (option C). This occurs by
increased SERCA activity as a result of phospholamban phosphorylation. By the force–velocity relationship, the initial
velocity of shortening is inversely related to afterload (option D). Caffeine is a calcium sensitizer and can result in an
increased force of contraction (option E).
5-4. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 5) The c wave is the result of increased atrial pressure as the
mitral valve bulges into the atrium during isovolumic contraction (option A). The v wave occurs as the atrium fills during
ventricular systole and atrial pressure falls with mitral valve opening. The v wave occurs after the T wave (option B).
During ventricular filling, change in ventricular pressure is a function of ventricular compliance (option C). Isolated,
perfused hearts have been instrumental in the development of our understanding of ventricular mechanics. These models
have allowed for the determination that ventricular elastance increases during ventricular contraction and decreases with
ventricular relaxation (option D). The PVA is proportional to the myocardial oxygen consumption but includes the area
within the PV loop as well as the area between the end-systolic pressure relation and the end-diastolic P–V relation
(option E).
5-5. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 5) The woman in the vignette has a normal right heart
catheterization and likely is short of breath for noncardiac reasons. Increasing preload is expected to increase stroke
volume (option A). LV compliance in vivo is determined by pericardial pressure, right ventricular pressure and volume,
coronary artery perfusion, and the intrinsic elastic properties of the LV (option B). An increase in afterload, such as with a
bolus of norepinephrine, is expected to decrease stroke volume and the velocity of LV shortening (option C). Changes in
heart rate from 60 to 160 beats per minute are unlikely to increase cardiac output because the small increase in
contractility is offset by the decrease in diastolic filling time and the resulting preload (option E).
5-6. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 5) Ventricular relaxation is an energy-dependent process
requiring ATP for SERCA sequestration of calcium into the sarcoplasmic reticulum, among other processes (option A). β-
adrenergic stimulation leads to the activation of PKA and the phosphorylation of phospholamban, resulting in increased
SERCA activity. Increased SERCA activity results in faster relaxation, and a decrease of Tau (option B). Chamber
stiffness is affected by intrinsic LV factors and extrinsic factors such as pericardial constraint, atrial contraction,
intrathoracic pressures, and ventricular interaction (option C). In addition to active relaxation, diastolic function is also
related to the viscoelastic properties of the LV. LV recoil is affected by titin and the extracellular matrix (option D). The
P–V relationship during diastole reflects the lusitropic state of the heart (option E).
5-7. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 5) The MAP is (120 + 2 * 85)/3 = 97 (option A). The PA
pressure is (25 + 2 * 10)/3 = 15 (option B). SVR is (97 − 5)/6 = 15.33 Wood units (option C). The PVR is (15 − 10)/6 =
0.83 Wood units (option D).
5-8. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 5) Collateral vessels that become prominent with obstructive
coronary disease cannot augment coronary flow similar to that of the native artery with stress or exercise (option A).
Unlike skeletal muscle, the myocardium operates at nearly peak oxygen extraction at rest. Increased oxygen needs are met
by increases in blood flow through the coronary circulation (option B). Adenosine levels increase with the breakdown of
ATP, and adenosine is a potent coronary vasodilator. If coronary blood flow decreases, local adenosine levels increase,
making adenosine an integral component of coronary autoregulation (option C). To maintain equal coronary flow
throughout the myocardium, the subendocardial vessels have less resistance than the subepicardial vessels. This is
important because subendocardial vessels have a limited ability to further vasodilate in time of stress, and subendocardial
zones are more prone to ischemia (option D). The principal endothelial derived relaxing factor is nitric oxide (NO) (option
E).
5-9. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 5). Parasympathetic nerves supply only a small portion of the
resistance in vessels; the sympathetic nervous system is the primary regulator of vascular resistance (option A). Carotid
baroreflex resetting results in decreased receptor firing for a given mean arterial blood pressure (option B). The Bezold–
Jarisch reflex is mediated by ventricular C fibers, which are activated by hypovolemia. The net result is a paradoxical
bradycardia and hypotension (option C). Endothelin constricts arterioles and venules. The effect on venules serves to
increase preload (option D). Endocannabinoids decrease contractility (option E).
5-10. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 5). The venous return curve describes the relationship of
cardiac output and venous pressure. Volume loading or venoconstriction shifts the curve up and to the right (option A). By
contrast, arteriolar vasoconstriction shifts the curve down and to the left (option B). The flat portion of the curve in C
represents the maximal cardiac output as venous return is reduced (option C). The Frank–Starling curve describes the
effect of ventricular loading with cardiac output and moves up and to the left at higher levels of contractility (option D).
The intersection of the Frank–Starling curve and the venous return curve represents the equilibrium point of venous return
and ventricular performance (option E).
CHAPTER 6
Molecular and Cellular Biology of the Heart
Ravi Karra
QUESTIONS
6-1. A 55-year-old man presents with exertional dyspnea and a 10 lb weight gain. His physical exam is notable for an elevated
jugular venous pressure, a soft apical holosystolic murmur, and an S3 gallop. Echocardiography reveals a dilated left ventricle
with an ejection fraction of 35%. Which of the following is most likely true regarding β-adrenergic signaling in this patient?
A. β2-adrenergic receptors (β2-AR) are the dominant type of β-adrenergic receptor in the heart
B. An increase in GRK2 activity contributes to β-adrenergic receptor desensitization
C. β1-AR density is increased in this patient’s myocytes
D. This patient’s heart is more sensitive to β-agonists now than before developing decompensated heart failure
E. β1-AR signaling is likely to protect against apoptosis in his cardiomyocytes
6-2. Which of the following is incorrect regarding excitation–contraction coupling?

A. Depolarization of the cardiomyocyte membrane results in the opening of L-type calcium channels
B. The SERCA ATPase functions to sequester calcium in the sarcoplasmic reticulum during relaxation
C. In a healthy heart, tachycardia results in decreased calcium in the cytoplasm of the cardiomyocyte and increased
contractile force
D. PKA and CaMKII maintain SERCA activity by phosphorylating and inactivating phospholamban
E. The efficiency of the ryanodine receptor response to cytoplasmic calcium is dependent on the ryanodine receptor’s
proximity to the L-type calcium channel
6-3. A 54-year-old patient with a history of heart failure with reduced ejection fraction is admitted following 3 shocks from his
internal cardiac defibrillator. Which of the following could contribute to a proarrhythmic state in this patient?
A. Hyperphosphorylation of the ryanodine receptor contributes to a calcium leak from the sarcoplasmic reticulum
B. Increased systolic calcium concentrations in myocytes
C. An increased force-frequency relationship
D. A shortened relaxation phase
E. Increased SERCA expression and activity
6-4. Which of the following is not true regarding signaling pathways in heart failure?
A. An increased intracellular concentration of calcium leads to increased activity of calcineurin in failing myocytes
B. CaMKII contributes to hypertrophy by phosphorylating transcription factors such as MEF2 and class II histone
deacetylases
C. Prohypertrophic growth factors tend to work through heterotrimeric proteins of the Gq family
D. Mechanical stretch alone can induce many hypertrophic signaling pathways
E. Hallmarks of a fetal-gene expression program during hypertrophy include the expression of BNP, ANF, and α-MHC
Questions 6-5 through 6-7 refer to the following vignette.
A 52-year-old man presents to your office for a follow-up appointment. He has a long-standing history of hypertension. His
ECG is suggestive of left ventricular hypertrophy, and his echocardiogram shows a left ventricular wall thickness of 1.4 cm.
6-5. Which of the following is not true regarding signaling pathways in this patient?
A. Protein synthesis is dramatically upregulated through the PI3K and mTOR pathways
B. Extracellular signal-related kinases (ERKs) are activated
C. GSK-3β activity is reduced in cardiomyocytes undergoing hypertrophic growth
D. Hypertrophic signaling has a strong overlap with factors known to broadly regulate organ size
E. mTORC1 has an important role in pathologic, but not physiologic hypertrophy
6-6. Which of the following is not true regarding microRNA signaling in this patient?
A. The miR212/132 family of microRNAs promotes hypertrophy by the inhibition of the antihypertrophic transcription
factor FoxO3
B. MiR-133 levels are increased and promote hypertrophy and fibrosis
C. Anti-miRs are an approach to pharmacologically modulate microRNA signaling
D. MiRs that promote myocardial glucose utilization are investigational approaches to prevent the progression to heart
failure
E. Exosomes secreted from the heart allow for the systemic circulation of miRNAs to other organ beds
6-7. Which of the following is true regarding lncRNAs in this patient?

A. The lncRNA CHAST is likely to be upregulated
B. LncRNAs, by definition, are not translated into protein products
C. LncRNAs exert their effects solely through the inhibition of complementary transcripts
D. LncRNAs are found only in intergenic regions
E. LncRNAs are highly conserved across phyla
6-8. Which of the following is not true regarding cell death in the development of heart failure?
A. Cytochrome C release marks cells about to undergo necrotic cell death in the failing heart
B. Prolonged ER stress can trigger cell death pathways
C. Apoptotic cell death is programmed cell death that does not typically result in an inflammatory response
D. Necrotic cell death is marked by a loss of membrane integrity, extrusion of intracellular contents, and inflammation
E. Apoptotic cell death is energy dependent, but necrotic cell death is energy independent
6-9. Which of the following is not true regarding cardiac fibroblasts?

A. Cardiac fibrosis is the result of collagen production in excess of collagen degradation
B. Cardiac fibroblasts differentiate into myofibroblasts that express contractile proteins
C. The main components of cardiac extracellular matrix are proteoglycans and elastin
D. Pathologic cardiac fibrosis is proarrhythmogenic, in part, because of electrical isolation of regions of the myocardium
E. Cardiac fibroblasts in the adult heart are primarily derived from resident fibroblasts
6-10. Which of the following is true regarding cardiac microRNAs?

A. The majority of transcripts in the genome encode proteins
B. MicroRNAs, PIWI-interacting RNAs, and endogenous short interfering RNAs are types of long ncRNAs
C. MiRNAs regulate gene expression by binding to mRNAs, resulting in degradation
D. The number of ncRNAs decreases with increasing complexity of the species
E. Long ncRNAs are more than 2000 base pairs long
ANSWERS
6-1. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 6) This patient presents with classic findings of heart failure
with reduced ejection fraction. In the normal heart, 60% to 80% of β-adrenergic receptors are of the β1 subtype.1 With
heart failure, β1-AR is downregulated, and the β1-AR/β2-AR ratio nearly normalizes (options A and C).2 A molecular
hallmark of heart failure is the desensitization of the β-adrenergic signaling axis. A failing heart is less sensitive to
exogenous β-AR ligands than is a normal heart (option D). At the molecular level, this occurs by a decreased density of
β1-AR in cardiomyocytes and increased levels of GRK2. GRK2 phosphorylates β-ARs and reduces their sensitivity
(option B).3 Chronic β-AR signaling through the β1-AR is believed to contribute to cardiomyocyte apoptosis seen in heart
failure (option E).3
6-2. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 6) Following depolarization of the cardiomyocyte membrane,
L-type calcium channels open, and calcium influxes into the cardiomyocyte (option A).4 In response, ryanodine receptors
release calcium from the sarcoplasmic reticulum. The net result is an increase in cytoplasmic calcium that leads to
increased myofilament contractility. Activation of ryanodine receptors is more efficient when they are in close proximity
to the calcium influx through L-type calcium channels (option E).5 An increase in force with increasing heart rate is due
to increased cytoplasmic calcium and is known as the force-frequency relationship (option C). The force-frequency
relationship is an important feature of the healthy heart. During relaxation, cytoplasmic calcium is sequestered in the
sarcoplasmic reticulum by the SERCA ATPase (option B). SERCA activity is negatively regulated by phospholamban.6,7
PKA and CaMKII can phosphorylate and inactivate phospholamban, thus maintaining SERCA activity (option D).
6-3. The answer is A. (Hurst’s The Heart, 14th Edition, Chap. 6) Intracellular calcium homeostasis is altered in the failing
cardiomyocyte. Hallmarks of the failing cardiomyocyte include (1) decreased systolic calcium, (2) increased diastolic
calcium, and (3) a prolonged relaxation phase (options B and D).4 Additionally, the force-frequency relationship is altered
such that contractile force decreases with increasing heart rate (option D). Biochemically, the L-type calcium channel
does not activate the ryanodine receptor as efficiently, and hyperphosphorylation leads to an increased sensitivity of the
ryanodine receptor.8 Calcium leak from the ryanodine receptor can result in delayed afterdepolarizations, an important
contributor to arrhythmogenesis (option A).4,9 Finally, SERCA expression has been demonstrated to be reduced in animal
and human models of heart failure, and the restoration of normal SERCA levels has been a focus of gene therapy efforts
for patients with heart failure (option E).7,8
6-4. The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 6) Hypertrophic signaling results from complex inputs at the
membrane and within the cell. Mechanical stretch alone can activate many of the signaling pathways involved in
hypertrophy through surface-bound integrins and mechanically activated ion channels (option D).10 Additionally,
prohypertrophic growth factors such as angiotensin II work through heterotrimeric G-proteins (option C). The Gq family
is particularly important because overexpression of Gq is sufficient to cause hypertrophy.11 A key feature of hypertrophic
signaling is an increase in intracellular calcium that binds to calmodulin, resulting in the activation of calcineurin and
CaMKII (option A). Both calcineurin and CaMKII lead to the activation of transcription factors that promote hypertophic
gene expression programs. CaMKII activates the transcription factors MEF2 and HDAC2 by phosphorylation (option
B).12 One result of hypertrophic signaling is re-expression of factors from cardiac development, such as BNP, ANF, and
β-MHC (option E).13
6-5. The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 6) Hypertrophic cardiomyocytes have dramatic upregulation of
protein synthesis via the PI3K and mTORC pathways (option A). Many stimuli that result in cardiac hypertrophy also
activate PI3K signaling. mTORC1 signaling is one example of several growth pathways that are activated with cardiac
hypertrophy. mTORC1 appears to be broadly related to cardiac growth as inhibition compromises both physiologic and
pathologic hypertrophy (options D and E).14 Additionally, MAPK activity is thought to be increased and GSK-3β activity
reduced during hypertrophy (option C).15
6-6. The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 6) The importance of microRNA signaling to the pathologic
hypertrophy and the progression of heart failure is being increasingly recognized. MicroRNAs regulate multiple
processes, such as hypertrophic signaling pathways, tissue fibrosis, vascular density, and cardiac metabolism (option D).16
MiR-133 is downregulated with cardiac stress and has protective effects against hypertrophy and tissue fibrosis (option
B).17 By contrast, miR212/132 are increased with cardiac stress and promote hypertrophic signaling by repressing the
antihypertrophic transcription factor FoxO3 (option A).18-20 MicroRNAs are promising therapeutic targets and can be
specifically targeted by modified nucleic acids that function as anti-miRs (option C). Finally, the systemic roles of cardiac
microRNAs are being increasingly understood because cardiac microRNAs can be found in the circulation within small
vesicles called exosomes (option E).21
6-7. The answer is A. (Hurst’s The Heart, 14th Edition, Chap. 6) LncRNAs were originally defined as noncoding RNAs
greater than 200 base pairs in length.22 LncRNAs can be found within coding genes and intergenic regions (option D).
LncRNAs have emerged as complex molecules with a diverse set of regulatory functions.23 They can repress transcription
by binding transcripts, and they directly interact with proteins to regulate their function (option C). More recently, some
lncRNAs have been identified that encode small proteins, such as the protein DWORF that activates the SERCA pump
(option B).24 LncRNAs tend to be poorly conserved across phyla (option E). The lncRNA CHAST is an exception, and
elevations have been identified in murine models of pressure overload and in hypertrophied human heart tissue (option
A).25
6-8. The answer is A. (Hurst’s The Heart, 14th Edition, Chap. 6) Cardiomyocyte cell death is an important contributor to the
progression to heart failure. Cell death can occur via necrotic cell death following injuries to the heart or programmed
apoptotic cell death. Necrotic cell death is an energy independent process that is marked by a loss of membrane integrity,
resulting in extrusion of intracellular contents and inflammation (option D).26 Apoptotic cell death, by contrast, is
programmed and triggered by both intracellular and extracellular stimuli (options C and E). For example, prolonged ER
stress can lead to the triggering of death pathways (option B). In failing hearts, some myocytes exhibit features of
apoptotic cell death, such as mitochondrial cytochrome C release, but they can survive and maintain intact nuclei (option
A).27 These cells are thought to undergo reversible damage.
6-9. The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 6) In response to stress, the heart undergoes pathologic
remodeling, with proliferation of resident fibroblasts to make more fibroblasts (option E).28 These fibroblasts tip the
balance of extracellular matrix turnover toward excess production compared to degradation (option A).28,29 Extracellular
matrix is a complex network of collagens, elastin, glycoproteins, and proteoglycans. However, type I collagen is the main
component (option C).30 Cardiac fibrosis stiffens the heart and can be proarrhythmic by electrically isolating parts of the
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While still hurrying forward, his excited ear detected a faint gobble in
the woods, as if a lost turkey were calling its companions; and
proceeding stealthily onward, he suddenly came upon a gobbler, that
was wandering about disconsolately, as if indeed lost. Before it could
get out of his reach, Hezekiah discharged his piece, but only
wounded it.
It started off on a rapid run, and, fearful that it would escape him if he
paused to load his rifle, he dashed after it at the top of his speed,
and now commenced a most interesting race.
All things considered, perhaps, in the condition of the gobbler,
Hezekiah could outrun it, that is, where both were given the same
chance; but the bird had a way of slipping through the undergrowth,
jumping under the bushes, and trotting over fallen trees, as though
they were not there, that gave him an immense advantage over his
pursuer.
The latter tore headlong through the bushes, sometimes a rod or two
in the rear, sometimes almost upon it, his hope constantly kept up to
a most exciting point, by the hairbreadth escapes it made from him.
More than once, he made a frenzied leap forward, and, as he fell on
his face, caught perhaps the tail feather of the bird, while the bird
itself glided through his grasp, leaving a most vivid impression of its
tapering form upon his hands, which had slipped over it so neatly.
Then, again, he would strike at it with his rifle, and perhaps pin
another feather to the ground.
"Drat it," exclaimed Hezekiah, after one of those fruitless attempts.
"It's enough to make me swear. I'll chase him as long as I can stand,
but what I shall get him."
It is a fact, to which all hunters will testify, that, in the exciting pursuit
of their game, they can travel mile after mile, with hardly any
sensible fatigue. It is not until they come to retrace their steps, that
they realize how great a distance they have passed over. The
attendant, perhaps, whose mind does not participate in the same
excitement, is exhausted even in following the hunter.
Thus it happened that Hezekiah Smith, who would not have believed
he had gone more than half a mile, chased the gobbler for fully ten
times that distance, at the end of which it did not seem fatigued in
the least, the wild turkey, as our readers are aware, being a noted
runner. With no thought of giving it up, Hezekiah still pursued it at the
top of his speed, occasionally making a leap forward at it, and the
bird as often eluding him, as cleverly as ever.
Suddenly he caught the glimmer of something through the trees, and
to his joy, saw that they were approaching the banks of a river. He
was now sure of the bird; he had fairly earned it; and his tormenting
hunger was about to be satisfied.
Gracefully, and majestically, as the bird reached the edge of the river,
it spread out its wings, and, sailing through the air, landed upon the
Ohio side, and disappeared in the woods.
"That is unpleasant. If my rifle had only been loaded, I would have
finished him."
In chasing the gobbler, with all his turnings and doublings, Hezekiah
had become "turned around," himself, so that it seemed to him the
Ohio River was running in the wrong direction, and that he was on
the other side of it. Concluding however, that such a phenomena
would be a miracle, he kept on down the river, having decided that it
would be useless to retrace his steps, in the hope of finding Waring.
He was walking slowly forward, panting and fatigued, when it struck
him that there was a peculiar smell in the air. It seemed as though
something were burning, and, knowing that he was in the midst of an
Indian country, he guarded his steps, and kept a more watchful eye
upon his surroundings.
It turned out as he had expected. He was close upon an Indian
encampment. He caught a glimpse of the gaudy, fantastic costumes
of the savages through the trees, and approaching as nigh as he
could, he concealed himself, as well as his position would admit.
It was with singular emotions, that Hezekiah recognized this party as
the identical Shawanoes who had attacked his party, and who held
Pat Mulroony and Virginia Lander as captives. The fact that they
must have been here some time, proved that they had broken their
last night's encampment at an early hour, and departed even before
he himself had awakened.
The party seemed to have lost several of their number—some four
or five—but there was no mistaking the others. Hezekiah recognized
them at once. What surprised him still more, was that none of the
captives were visible. What had become of them? Had they been
sent in advance, in chance of a smaller party? What possible cause
could the Shawanoes possess for taking such a step?
These questions ran rapidly through the mind of the New Englander,
but there was another which constantly presented itself, and that
was the one in regard to obtaining food, for satisfying his hunger,
which was constantly growing greater. There seemed but one course
left for him, and that was to take to the woods again. He was on the
point of doing so, when his heart leaped at what appeared a most
fortunate occurrence to him.
Several times he thought he had detected the smell of burning meat,
and the cause of it was now explained. Some twenty rods to the right
of the encampment of the savages, was a smaller fire, at which a
single squaw was cooking. At the moment that Hezekiah caught
sight of it, this squaw had left it, and the meat was entirely
unguarded.
The temptation was too great; Hezekiah was only sensible of his
intolerable hunger. Running back into the woods a few rods, he
came in the rear of the fire, and totally unmindful of his imminent
danger, snatched the meat, and seating himself upon the ground,
commenced devouring it like a wolf.
The first mouthful was dropped suddenly upon the lawn, being so hot
that his tongue was blistered. But he soon became used to it, and in
a few moments had swallowed the entire piece of meat, and was
wiping his fingers upon his hair.
"Just as much as I could possibly get down me," he muttered. "I
couldn't possibly swallow another mouthful, and—"
A shrill whoop suddenly broke the stillness of the woods, and turning
his alarmed gaze behind him, he saw the squaw, standing within a
dozen feet of him. She was fairly blue with fury, and was screaming
as if to split her lungs.
"Heavens!" exclaimed Hezekiah, who now saw how foolhardy he
had been, "the old woman is riled considerably, and if I ain't mistaken
them Indians are likewise."
The outcries of the infuriated squaw had attracted the instant
attention of the Shawanoes, who had caught a sight of the white
man as he was rising to his feet, and three of their fleetest runners
started in pursuit.
Hezekiah Smith's frame was gaunt and attenuated, and he was
sinewy and muscular. He was not only very fleet, but possessed
bottom, and was capable of holding his own against any one, and he
now darted into the woods at a rate that excited the admiration of his
pursuers. The three separated, so as to make sure of the fugitive,
and called all their energies into play to overtake him.
The forest for a considerable distance was open, and afforded a
good field for the runners. The distance between Hezekiah and the
Shawanoe remained about the same for five or ten minutes, when
one of the latter discharged his rifle, and the white sprang high in the
air with a loud yell.
But he hadn't been struck. It was only fright. The report of the gun
gave an impetus to his flight, and soon carried him far ahead of the
redskins. Dodging hither and thither, flitting in and out among the
trees, it was impossible for the latter to gain anything like an
accurate aim, and they did not repeat the attempt to bring him down.
All was now going well for the fugitive, and he would have escaped
had he understood the woods. But his ignorance was fatal. Directly
ahead of him was a deep gorge, or ravine, toward which the
Shawanoes had managed to turn his face without much difficulty,
and unconsciously to himself he was running directly into a trap.
It was not until he was on the very brink that Hezekiah realized his
peril. His hair fairly rose on his head, then, as he glanced about him.
To the right and left, stretched the deed yawning gorge, too broad to
be leaped over, and offering no means of access except a sheer
precipice, down which it would have been certain death for him to
have gone. Escape was cut off! There was no help for him! He was
fairly at bay!
"It's no use of talking," he exclaimed, wheeling round, and placing his
back toward the gorge. "I'm cornered this time, and there's going to
be a row!"
So saying, he clubbed his rifle, and awaited the onset of the
Shawanoes!
CHAPTER XIII.
A STRUGGLE OF LIFE AND DEATH.
The Shawanoes, as we have before stated, had separated during
the pursuit, and were now some distance apart. The center one
being directly in the rear, was the closest to the fugitive, and came
up to him considerably in advance of the others. This was fortunate,
in one sense, for Hezekiah Smith, as he then had but a single
opponent with which to contend.
The lithe, agile Indian was all eagerness to secure the white as his
captive and forgetful of the axiom, "a stag at bay is a dangerous foe,"
he halted not in the least, but came at full speed toward him. When
within a rod or so, he whirled his tomahawk in a circle over his head,
and hurled it with tremendous force full at the breast of his dauntless
adversary. The latter, from the motion of his arm, comprehended
what was coming, and dodging his head with lightning quickness, the
weapon flashed over him, and went spinning end over end down the
steep ravine.
Both of the combatants had dropped their rifles and drawn their
knives. With a demoniac yell of triumph the painted Indian leaped
high in air, and swinging his knife, sprang upon his foe. In a twinkling
both were disarmed in a singular manner.
It so happened that the two struck at each other at precisely the
same moment, the knives encountered with such force that the
Shawanoe's shot out of his hand and followed the tomahawk down
the ravine, while Hezekiah's was turned so suddenly that it fell to the
ground several yards distant. Both were now entirely unarmed, and
glaring at each other for a second, like baffled tigers, they closed in
the struggle of life and death.
In point of strength the two were very nearly equally matched. In
activity the redskin had decidedly the advantage, but the white man
being an expert wrestler, and the savage a perfect novice, the former
was in a fair way to end the contest in his own favor. The instant he
grappled with his dusky adversary, he felt that he was at his power.
By a trick, or rather art, well known to wrestlers, Hezekiah twisted the
savage off his feet, and threw him with stunning violence upon the
ground, falling heavily upon him. Allowing him to rise, he repeated
the performance several times, the redskin becoming more and
more exhausted each moment, until it was manifest to himself that
he had not the shadow of a chance in such warfare as this.
The cunning Shawanoe had noticed where the knife of his adversary
fell, and each time that he went down he managed to work himself
nearer to it. Hezekiah did not comprehend what he was at, until the
savage clutched it with the quickness of thought, and rising again to
his feet, confronted him with the weapon.
Not the least daunted, for he was now terribly excited—he closed
again with the Indian, receiving an ugly cut in his arm as he did so.
At this moment he heard the yells of the other two Shawanoes, and
driven to fury by his imminent peril, he concentrated all his strength
in the one mighty effort, and grasping his adversary around the
waist, he lifted him clear off his feet, and flung him like an infant over
the precipice.
Down, like a meteor, through the dizzy air, shot the Shawanoe, with
his arms clutching wildly at space, spinning from crag to crag, with
his awful cry coming up like the wail of some spirit!
The struggle occupied scarcely a fifth of the time taken in describing
it. Impelled by the most implacable hate on each side, the blows
were quick and fierce, and the termination speedy and tragic. A
shock when the two encountered, a few blows and strivings, another
struggle, more determined than the others, and it was ended.
Hezekiah had secured his knife before throwing the savage into the
ravine, and with this single weapon he confronted his two foes. They
were both about the same distance from him, and he was in doubt
whether to expect their united onset at the same moment, or whether
they were going to attack him singly. The latter proved to be the
case. One of the Indians seemed to be a sort of chief, or, at least,
higher in authority than the other; for waving his hand for him to keep
his distance, he advanced upon the white man, with the
determination of disposing of him without assistance from any one
else.
This savage was a much more formidable foe than the other, and
Hezekiah being considerably exhausted from his recent efforts, he
was in a poor condition to receive him. Nevertheless, there was no
help for him, and he showed an undaunted front. The Shawanoe
halted a moment, as if to decide upon the best method of attack, and
then, with a yell as demoniac as the other, sprang forward.
He had passed over half the space intervening between him and his
adversary, when he uttered another yell—a short, frenzied, agonized
one, and throwing his arms aloft, fell dead!
Hezekiah had caught the report of a rifle, and saw a red spot
suddenly appear on the forehead of the Shawanoe, so that he
understood at once that he had been shot. But who had come up
and fired his piece so opportunely? What friend had he in the Dark
and Bloody Ground? Why did his friend remain concealed?
The remaining redskin had halted upon seeing his companion fall by
the mysterious shot, but he evinced no disposition to flee. On the
contrary, he continued to approach, fully resolved that the foe should
not escape him.
"By thunder! you're the only one left, and I reckon as how I can
dispose of you," exclaimed Hezekiah, preparing to receive him.
"Though if there should happen to be another rifle around, it would
be mighty welcome just now."
The Shawanoe had learned caution from what he had witnessed,
and although as brave as a mortal could possibly be, he deemed it
best to use prudence in the case. His mode of attack was peculiar.
He commenced slowly circling around his adversary, his black,
snake-like eye fixed upon him while the latter kept turning, as if on a
pivot, so as to confront him.
In going in this circular manner, the Indian came to the very brink of
the precipice, so that his form stood out in relief upon it. More than
once when he was in this position, Hezekiah was upon the point of
springing forward and shoving him over. His heart throbbed painfully,
as he balanced himself for the leap, lest the risk was too great for
him to attempt it. He more than half suspected the Indian was
manœuvering for that purpose, and would succeed in throwing him
over instead.
All at once, with the inevitable whoop, the redskin bounded forward,
and struck at Hezekiah with his drawn knife. Singular as it may
seem, the two weapons encountered in precisely the same manner
as did those of the first two combatants, and both were as suddenly
deprived of all arms, except such as nature gave them.
As the two closed in with each other, it seemed to Hezekiah that this
Indian was much more powerful and difficult to manage than the
other, or possibly his own strength was failing. Remembering,
however, that he was the only foe which it was necessary to
overcome, and that a prolonged contest might bring some of his
companions to the scene, he summoned all his strength to this last
conflict.
He succeeded in throwing the Shawanoe, and falling heavily upon
him, but it required such an expenditure of strength that he doubted
whether this means of exhausting him would not first "use up"
himself. Furthermore, he found it impossible to hold his foe. Whether
his body was greased or not, he could not tell, but the redskin kept
up such a twisting and squirming that he glided from his grasp as
easily as an eel could have escaped him.
Concluding that it was vain to hope for any success by means of
wrestling, Hezekiah now bent his efforts toward drawing him to the
edge of the cliff with the determination of throwing him over. The
savage comprehended his intention, and probably believing he could
do the same thing with the white man, favored his efforts, and in a
few seconds both were upon the very brink of the precipice.
And now commenced the awful struggle. With sinews strained to
their utmost tension, with limbs braced and pressed against each
other, their chests heaving, with teeth set, and their eyes gleaming
with the most implacable hate, the combatants strove together!
In reaching the edge of the ravine, the Shawanoe was on the inside
—that is, he was the nearest to it—and Hezekiah succeeded in
keeping him there. Gradually working him nigher and nigher to the
dread chasm, until he felt his strength going, the New Englander
gathered his knee to his breast, and summoning all his power, with
one mighty effort he kicked the savage from him and over the cliff!
But horror of horrors! in going over, the Shawanoe caught him with
both hands by the ankle, and Hezekiah felt himself following! He
clutched with the twigs and stones within his grasp, but they all
yielded and came with him, and he could not shake off the dreadful
incubus that was drawing him on to death. He screamed and
shouted, and blistered his hands in his efforts to stay himself, but it
was all useless.
Further, further, further—the Shawanoe's weight seems to increase
each second—the white man's outspread hands slide over the earth
and rock!—he is going, going, going!—his head slips over! and now
down like a meteor, through the dizzying air, with wild, ecstatic thrills
shooting through his brain—a second's delirium—an awful, stunning
shock—and all was dark! The lifeless forms of Hezekiah Smith and
the Shawanoe Indian lay side by side at the bottom of the gorge!
The reader will recollect that Luther Waring, in wandering through
the woods, suddenly came upon an unexpected scene, and rushed
forward in a state of great excitement. The sight that met his gaze
was Hezekiah Smith and the second Indian struggling together.
Without a moment's reflection he discharged his piece, killing the
savage as before related. He was about to rush forward to the
rescue of his friend, when he caught sight of the third Indian; and
believing that a party had just arrived, and that he could afford him
no assistance, and that he was in imminent danger of his own
capture, he turned and fled.
Running some distance, he was considerably surprised to find that
he was not pursued, and suspecting that, after all, he might have
been mistaken, he cautiously retraced his steps. He arrived at the
spot of the tragic scene we have just described, and looking over the
brink, descried the two inanimate forms lying below.
With a painfully throbbing heart he hurried through the forest, and by
a circuitous route entered the gorge. In a short time he came upon
the two Indians and his friend. All three were bruised and bleeding,
and as Waring looked above him at the height of the precipice, he
took a melancholy consolation in the thought that the death of
Hezekiah Smith had been speedy and almost painless.
"Would that I could give him a decent burial," he murmured; "but I
cannot. He shall not remain here, however, to rot beside those
fiendish savages. I will do what I can for him."
Taking him in his arms he carried him some distance to where there
was a mass of debris and stones at the side of the ravine. Here
depositing him carefully upon the ground, he first covered him over
with brush, and then stones, until his body was entirely hidden from
sight. The principal object in doing this was to secure his remains
against outrage from the savages.
"Farewell," said Waring, as he turned away. "I have known you but a
short time, and have learned but little of you, but I have learned
enough to know that you were a FRIEND; and now, a last adieu to
you, my FRIEND!"
With a saddened, mournful heart he turned away and walked slowly
through the ravine.
CHAPTER XIV.
AN UNEXPECTED MEETING.
Waring's meditations, as he walked through the gorge, were gloomy
and melancholy enough. Now, indeed, he felt he was alone. Two of
his companions had been slain, and the other two captured; and
what could he, single and unaided, accomplish against these
inhuman denizens of the wilderness? Absolutely nothing.
And yet he could not persuade himself to give up the hope of a final
rescue of Virginia Lander. That hope gone, life looked dark and
gloomy to him. Rather than never see her again, he felt that he could
willingly share captivity and death with her.
The plan which Waring at length decided upon, was to make his way
to the settlement, and seek the aid of the settlers. He could be no
great distance from it; and, as the Shawanoes seemed to linger in
the forest, there could be little difficulty in finding and following their
trail.
With his head bent, and with feelings saddened and thoughtful, from
the frightful scenes he had just witnessed, Waring walked slowly
forward until he had emerged from the gorge, and was again
threading the shadowy woods. At length he entered a portion where
the undergrowth became more tangled and dense, and where from
necessity he was compelled to recall his mind from its reverie, and
occupy it with his immediate duties.
He had penetrated, perhaps, a third of a mile into this undergrowth,
when, becoming exhausted, he threw himself upon the ground for a
few minutes' rest. He had scarcely seated himself when he was fairly
startled out of his senses by hearing the hum of voices! Listening
carefully, he soon distinguished the words:
"Begorrah, it's meself that's thinking this is the most delightful retrate
of my life, barring that it was a retrate from necessity. What do you
think of it, my leddy?"
"Oh! I am so thankful to be free from those loathsome Indians that
have persecuted us so long!"
"If we only had that long-legged Hezekiah Smith, and the handsome
young felly that ye calls Waring, how much more pleasant the retrate
would seem! Eh, wouldn't it now?"
"I do indeed pray that they may rejoin us. Since my poor father has
fallen, I am lonely enough with him also gone. Who knows but that
he, too, is in their hands?"
"It's meself that understands yer feelings. I mind the time that I lost
Molly McMooney at the Tipperary fair, me heart was broken intirely
till I found her agin."
Could Waring believe his ears! Those surely were the voices of Pat
Mulroony and Virginia Lander, and, from their words they were
alone. Could it be they had escaped? Have the Shawanoes
voluntarily freed them? What could it all mean?
He arose and looked around him. Yes; but a few rods away he saw
the two seated by a small fire, as comfortably as if on some pleasure
excursion. The genial face of the Irishman was wreathed in smiles,
as he blinked through the smoke at the girl upon the opposite side.
The face of the latter was pale, and she wore a saddened, thoughtful
expression, for it was hard for her to smile at the witticisms of her
good-natured companion, when her terrible bereavement was so
recent.
Hardly able to restrain his emotions, Waring approached the two. As
he did so, the back of Virginia was turned toward him, while the
Irishman faced him. The latter immediately caught sight of him, and
signalling him to stop, said to Virginia:
"Did you ever hear, my leddy, that Pat Mulroony was a magician?"
She looked up as if she did not comprehend his question.
"A magician? What do you mean?" returned Virginia.
"A man who on account of his superior vartues is gifted with more
than mortal powers. One who can do anything."
Thinking the words of the Irishman to be nothing more than some
jest, intended to divert her attention from her grief, Virginia made no
reply.
"Whisht now! ye doesn't belave me, I see. S'pose I should call up
that young Waring that belongs to yees out of the ground, would you
then belave it?"
"I am in no mood for such trifling," said she, with a reproving look. "I
would prefer you not to disturb me."
"Whisht now, jist look."
Pat Mulroony's incantations to convince his fair companion of his
supernatural powers were as singular as they were characteristic.
Pitching forward, he came down upon his hands so as to invert
himself, where balancing himself for a moment, he kicked his feet in
the air several times with such vigor that one of his shoes flew off.
This accomplished, he came down again, replaced his shoe, and
danced what he termed the "Tipperary Reel," after which he
suddenly became rigid, and exclaimed:
"Look behind yees! Mr. Waring, appair!"
Virginia would not have obeyed him, had she not detected the laugh
of her lover as the Irishman spoke. Starting up and turning around,
she was the next instant clasped in his arms.
"Thank God! thank God!" exclaimed the young adventurer, fervently.
"Found at last! Oh! how rejoiced I am!"
Virginia could not speak; her joy was too great for words.
During this affecting scene, the Irishman pretended to be busily
occupied with the fire. He did not replenish it, but kept displacing the
embers, as if to make them burn better. The air being quite warm
and genial, it seemed strange that he should have kindled it; but the
cause was his excessive politeness and consideration for the fair
charge in his hands. Noticing that Waring's actions seemed
somewhat restrained, he said, encouragingly:
"Don't be scart, don't be scart. I isn't watching yees. It's point of
honor with Pat Mulroony niver to disturb a couple when engaged in
courting. Plase proceed."
"We have no disposition to do anything of the kind at present,"
replied Waring. "I am surprised, Pat, that you should have escaped
from the Indians with Virginia here, when, a short time since, you
were both prisoners in their hands. Pray, how came it to happen?"
"It didn't happen at all jist. Pat Mulroony is the boy that is up to them
same tricks. He is the one that understands the blackguard haythen
—he is."
"I do not doubt that; but let me hear the account of this exploit of
yours."
"Begorrah! where is the long-legged chap, Hizikiah, that ye had with
yees?"
Waring, in a few words, related what is already known to the reader;
and then repeated his request to the Irishman for an account of his
escape from the Shawanoes.
"Wal, ye saas, the way that it happened was this. I s'pose you know
how I was took on that ould flat-boat?"
"Yes; your own foolishness was the cause of it. You need not relate
that. Give us what happened subsequently."
"Wal, ye saas, the haythen had us pretty fast, and it was mighty
onsartain the way things looked. Whisht! what is that?"
The near report of a rifle suddenly broke the stillness of the woods,
and the two speakers instantly sat down where they were better
protected by the undergrowth from observation. All interest was
immediately centred upon the one thought of safety.
"I am afraid that we are still in imminent peril," whispered Waring.
"Those Shawanoes, without doubt, are upon your trail."
"No, be the powers! they ain't."
"Don't be too sure, my friend. Those lynx-eyed savages will follow
the lightest footsteps."
"Not if they're made in the water—eh, boy?"
Waring began to comprehend matters. Still he replied:
"You are some distance from the river, remember, and neither you
nor Virginia could get to this spot without leaving a trail which these
Indians could follow without the least difficulty."
"S'powse they didn't know where to look for the same."
"That may all be," replied Waring, somewhat petulantly, "and yet
what I say is true. They are constantly ranging through the wood,
and it is by no means improbable that the traces of your passage is
discovered. But let us cease talking for the present."
The two listened for several moments, when hearing nothing further,
the Irishman cautiously arose, and commenced peering around him.
Ere he had half turned his head, he suddenly dropped to the ground
again, with a suppressed exclamation:
"He's right out there!" he whispered.
"Where? Who is there? What do you mean?"
"A bloody big Shawanoe, in his war paint, leaning against a tree out
there."
Imitating the motion of Pat Mulroony, Waring descried the savage in
question, standing as he had remarked. His back was turned toward
the whites, so that it was impossible to discern his features. He was
rather tall in stature, and appeared to have his arms folded, as if he
were exhausted.
"Wait till I show yees a specimen of Pat Mulroony's shooting," said
the Irishman, reaching out for the gun of Waring. But the latter
refused it.
"It looks too much like murder."
"It's mighty little like murder their dailings with us luks, be the same
token."
"His death can do us no good," added Waring. "The report of our rifle
would attract the attention of the savages in the vicinity, and we
could not again escape their clutches."
"Ye talks now like a raisonable person," said the Irishman, somewhat
mollified at the explanation. "Hist a moment till I takes another look
at the gintleman."
Pat Mulroony's head commenced slowly rising, while, as his knees
gradually straightened, his arms were elbowed, and his hands kept
flapping like the flippers of a turtle—the instinctive admonition to the
lookers on to maintain a profound silence.
As his head rose to its full height, Waring saw, from the sudden light
that filled his eyes, that he had discovered something further.
Without removing his gaze, he motioned for his companion to look.
The latter did so, and descried the Shawanoe walking away in the
woods. In a few moments he had disappeared, and the three were
left alone.
Waring turned to Virginia, and assured her that the danger had
passed, and that she need feel no further alarm. They would not
move from their present position until nightfall, when the chance of
escape would amount almost to a certainty. After this, the young
adventurer again demanded of the Irishman an account of his flight
from the Shawanoes, and he, nothing loth, proceeded to give it.
We choose to relate it in our own words.
CHAPTER XV.
AN EXPLOIT OF PAT MULROONY'S.
During the captivity of Pat Mulroony and Virginia Lander, the
Shawanoes kept them sedulously apart. Although Pat ventured to
address her several times, he was compelled to do it in tones loud
enough for all to hear him, though whether they understood him or
not was altogether a different matter.
The Indians remained at their camp, where Waring had seen them
through the night. As he had supposed, the party had divided, one
division taking both the captives with them. The cause of this was,
the Shawanoes were upon the war-path, and the whole company,
numbering over twenty warriors, had set out to attack a small village
belonging to a hostile tribe. Having inflicted about all the injury that it
was possible for them to inflict against the whites, they were now
anxious to proceed with their expedition. As their prisoners could be
nothing more than an incumbrance to them, eight of their number
were detailed to conduct them to one of the Shawanoe towns in
southern Ohio.
The separation of the Shawanoes was made early in the evening,
and before it was fairly light, the two parties were proceeding in the
direction of their respective destinations. The main party proceeded
down the river on the Kentucky side, while the eight Indians
embarked in separate canoes with their captives.
Six Indians were in one of the boats, and two in the other, excluding
the captives. It was intended that the two parties should keep
company to prevent any chance of escape by the burly Irishman,
although in his present helpless condition, bound and secured as he
was, a boy could have taken care of him without assistance.
The grey morning mist was just lifting from the Ohio, as the two
canoes shot out from the Kentucky shore, and sped swiftly down the
river. The point at which they intended to land upon the other side,
was several miles further down, bringing them considerably nearer
their town than a direct passage across the stream would have done.
The Irishman, who understood a few words of the Shawanoe tongue,
had gathered this much from the conversation of the savages before
starting.
The two Indians who used the paddles were seated in the stern of
the canoe, scarcely a foot apart, while Virginia was near the centre,
and Pat Mulroony in the bow, his back being turned down stream,
and his face toward his captors. In this position, the captives were
constantly under the gaze of the lynx-eyed Shawanoes, and could
not converse, even in whispers, without being seen. Nevertheless,
the Irishman had no hesitation in attempting it.
"Miss Virginny, how is it ye faals jist now?"
"Sadly enough," she replied. "Our only hope is in Providence."
"If I only had my hands loose," whispered Pat, "I would smash them
two copper skins there in the stern, and run into shore, in spite of the
haythen in the other vissel."
"Perhaps they would loosen your hands if you requested them to do
so."
"Begorrah! but they won't though."
"You might try it, Pat; make believe your bonds hurt you, and I have
no doubt they will loosen them."
After a moment's thought, Pat determined to try the artifice which his
fair companion had recommended. Accordingly he began groaning
and twisting his face into all manner of contortions, in order to enlist
their sympathy for his suffering. It was little sympathy the savages
felt for him, but his moans and struggles were so persistent and
annoying that the foremost Indian, with one blow of his knife, freed
his arms, refusing, however, all his entreaties to do the same thing
for his feet.
"Ugh! keep still—kill with knife—don't," said he, threateningly.
Pat Mulroony had succeeded far better than he had dared to hope.
He felt considerably elated thereby, and, rising up in his seat,
commenced "joking" with his grim captors.
"Ye handles them paddles as if yees was used to 'em. Be the same
token, maybe ye is. How is it?"
But the stoical Shawanoes deigned not to notice him, and Pat
continued:
"Begorrah, but yer mothers must be proud of sich boys as yees, that
is if ye has ary mothers. Do you mind that haythen there in the starn,
Virginny? Wal, now, ef I had to make a guess about him, I should say
he was a cross between an Irish chimney swaap and a monkey from
the South Saas. It must be swate for a gal to be hugged by yees."
The canoes were now rather close to the Kentucky shore, and
constantly approaching nigher, although Pat Mulroony, who had his
eyes about him, was at a loss to conjecture the cause of this
movement. The other canoe was considerably in advance—its
inmates finding it difficult to time their velocity to the tardy
movements of their two companions.
Of course the remarks of the Irishman were not comprehended by
either of the Shawanoes, although they now and then caught a word.
But it was easy to see from his pleasant eye, his broad grin, and the
rollicking expression of his face, that he was in the best of spirits.
Despite the stern, gloomy exterior of the foremost savage, there was
a spice of waggery in his composition, and his black, snake-like eyes
softened somewhat in expression as he looked upon the jovial
Irishman.
"Paddle 'um canoe!" suddenly remarked this Indian, handing his
paddle to him.
"Of course I will," replied Pat, eagerly taking the proffered paddle.
He dipped it deep into the water, and attempted to make a powerful
sweep with it; but it turned in his hand, cutting through the water like
a knife, and with such velocity as nearly to throw him overboard.
Both savages laughed at his awkward movements, while the
Irishman worked all the harder.
"Get in the bow of the boat," he whispered to Virginia, as he kept
hard at work. The girl arose and exchanged places with him, the
savages looking upon her movement as a voluntary one upon her
part, to be safe from the erratic blows of the toiling captive. By and
by these became so amusing, that the remaining Shawanoe ceased
working in order to watch him.
There were three noticeable facts which entirely escaped the
observation of the savages. The first was that the other canoe was a
considerable distance in advance of them—much further than they
would have been willing to allow, had their attention been called to it.
The second was that a few hundred yards down stream, a large
creek put in from the Kentucky shore; and the last, and certainly
most important one, was that in spite of the awkward, vimless efforts
of the Irishman, the canoe was approaching slowly but surely the
mouth of this creek. The latter fact might possibly have been merely
accidental, but a suspicious observer would not have believed thus.
Virginia, too, noticed an expression in the eyes of Pat Mulroony, that
made her heart beat faster.
Nearer and nearer approached the canoe to the eddying mouth of
the creek. The Indians, grinning and unsuspicious, did not notice it
until they were fairly within it. Then one of them reached forward to
take the oar.
"Ugh! turn back!"
The Shawanoe suddenly dropped back, having received a stunning
blow upon the head from the heaviest end of the oar. So violent was
it, that, striking the edge of the canoe, he rolled over as helplessly as
a log.
"Begorrah, but I axes yer pardon!" exclaimed Pat, to the struggling
savage. "But I handles the paddle so awkwardly, that—holy virgin! if I
haven't hit the other haythen a crack, too, and he's gone overboard!
What's got into me paws?"
The second savage had sprang up, as his companion went into the
water, but, as quick as lightning, he dropped back in his seat,
catching the sides of the canoe so firmly, that he did not go out of it.
The Irishman's blows being "sidewinders,"—that is, on the side of the
head, their natural result was to send the recipients overboard, and
the Shawanoe in question saved himself so narrowly, that Pat was
mistaken in supposing that he was following his comrade.
"That was another awkward piece of business. Let me tip ye another
iligant whack with me shillaleh, in the true style of Pat Mulroony, from
Tipperary."
Ere the second blow caught the savage, he gave vent to a
screeching yell, loud enough to wake the dead. But it did not save
him from whisking over the canoe like a frog, and going down out of
sight.
The first Indian had by this time arisen, and was endeavoring to
climb into the canoe. His hideous face, painted and agleam with the

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SECTION 1 CARDIOVASCULAR DISEASE: PAST, PRESENT, AND FUTURE

SECTION 2 FOUNDATIONS OF CARDIOVASCULAR MEDICINE

CHAPTER 4 Functional Anatomy of the Heart

SECTION 3 EVALUATION OF THE PATIENT

CHAPTER 11 The History, Physical Examination, and Cardiac Auscultation

SECTION 4 SYSTEMIC ARTERIAL HYPERTENSION

CHAPTER 23 Epidemiology of Hypertension

SECTION 5 METABOLIC DISORDERS AND CARDIOVASCULAR DISEASE

CHAPTER 26 The Metabolic Syndrome

SECTION 6 CIGARETTE SMOKING AND CARDIOVASCULAR DISEASE

CHAPTER 30 Epidemiology of Smoking and Pathophysiology of Cardiovascular Damage

SECTION 7 ATHEROSCLEROSIS AND CORONARY HEART DISEASE

CHAPTER 32 Atherothrombosis: Disease Burden, Activity, and Vulnerability

SECTION 8 VALVULAR HEART DISEASE

CHAPTER 46 Acute Rheumatic Fever

SECTION 9 CONGENITAL HEART DISEASE

CHAPTER 55 Mendelian Basis of Congenital and Other Cardiovascular Diseases

SECTION 10 MYOCARDIAL, PERICARDIAL, AND ENDOCARDIAL DISEASES

CHAPTER 57 Classification of Cardiomyopathies

SECTION 11 HEART FAILURE

CHAPTER 68 Pathophysiology of Heart Failure

SECTION 12 CARDIOPULMONARY DISEASE

CHAPTER 74 Pulmonary Hypertension

SECTION 13 RHYTHM AND CONDUCTION DISORDERS

CHAPTER 78 Electrophysiologic Anatomy

CHAPTER 93 Diseases of the Aorta

SECTION 15 MISCELLANEOUS CONDITIONS AND CARDIOVASCULAR DISEASE

CHAPTER 98 Perioperative Evaluation for Noncardiac Surgery

SECTION 16 POPULATIONS AND SOCIAL DETERMINANTS OF CARDIOVASCULAR DISEASE

CHAPTER 107 Social Determinants of Cardiovascular Disease

EMMANUEL E. EGOM, MD, MSc, PHD

INNA ERMEICHOUK, MSc

CAROLINE FRANCK, MSc

SARAH B. WINDLE, MPH

Chapter 9: Figure 9-1.

Chapter 5: Figure 5-1.

Cardiovascular Disease: Past, Present, and Future

DIRECTIONS: Choose the one best response to each question.

1-4. Who performed the first cardiac catheterization in a human?

1-5. From which Latin word is the term angina appropriated?

1-7. Who first described audible heart murmurs?

1-10. Which of the following statements about hypertension is false?

DIRECTIONS: Choose the one best response to each question.

2-6. What is the most common complication of infective endocarditis?

DIRECTIONS: Choose the one best response to each question.

3-7. What is the specific function of clinical data standards?

Foundations of Cardiovascular Medicine

DIRECTIONS: Choose the one best response to each question.

4-1. Which of the following statements is false?

4-3. Regarding Figure 4-1, select the statement that is false:

4-7. All of the following are true statements except:

DIRECTIONS: Choose the one best response to each question.