cardiovascular medicine
Cardiovascular Medicine
Medical Knowledge Self-Assessment Program
Cardiovascular Medicine All New Content, Including 120 Multiple-Choice Questions
150591010
18 AMA PRA Category 1 Credits™ available until July 31, 2015.
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Table of Contents
Epidemiology of Cardiovascular Disease
Heart Failure
Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Ethnicity and Cardiovascular Disease . . . . . . . . . . . . . . 1 Chronic Kidney Disease and Cardiovascular Disease . . . 2 Systemic Inflammatory Conditions and Cardiovascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Quality Measures in Cardiovascular Disease . . . . . . . . . 3
Diagnosis and Evaluation of Heart Failure . . . . . . . . . 30 Clinical Evaluation. . . . . . . . . . . . . . . . . . . . . . . . 30 Diagnostic Testing. . . . . . . . . . . . . . . . . . . . . . . . 31 Laboratory Evaluation . . . . . . . . . . . . . . . . . . . . . 32 Evaluation for Ischemia . . . . . . . . . . . . . . . . . . . . 32 Medical Therapy for Systolic Heart Failure . . . . . . . . . 32 ACE Inhibitors and Angiotensin Receptor Blockers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 β-Blockers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Initiating and Managing ACE Inhibitor and β-Blocker Therapy. . . . . . . . . . . . . . . . . . . . . . . . 34 Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Digoxin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Aldosterone Antagonists . . . . . . . . . . . . . . . . . . . 34 Hydralazine and Isosorbide Dinitrate. . . . . . . . . . 34 Calcium Channel Blockers . . . . . . . . . . . . . . . . . . 35 Heart Failure With Preserved Ejection Fraction . . . . . 35 Device Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 Implantable Cardioverter-Defibrillator for Prevention of Sudden Cardiac Death . . . . . . . . . . 36 Cardiac Resynchronization Therapy. . . . . . . . . . . 36 Follow-up Management of Chronic Heart Failure . . . 37 Serial Assessment . . . . . . . . . . . . . . . . . . . . . . . . . 37 Assessing Prognosis . . . . . . . . . . . . . . . . . . . . . . . 37 Inpatient Management of Heart Failure . . . . . . . . . . . 37 Acute Decompensated Heart Failure . . . . . . . . . . 37 Cardiogenic Shock. . . . . . . . . . . . . . . . . . . . . . . . 38 Strategies to Prevent Readmission . . . . . . . . . . . . 39 Advanced Refractory Heart Failure . . . . . . . . . . . . . . . 39 Mechanical Circulatory Support . . . . . . . . . . . . . 39 Management of Posttransplant Patients . . . . . . . . 40 Specific Cardiomyopathies . . . . . . . . . . . . . . . . . . . . . 40 Takotsubo Cardiomyopathy. . . . . . . . . . . . . . . . . 40 Acute Myocarditis . . . . . . . . . . . . . . . . . . . . . . . . 40 Tachycardia-Mediated Cardiomyopathy . . . . . . . . 41 Giant Cell Myocarditis. . . . . . . . . . . . . . . . . . . . . 41
Diagnostic Testing in Cardiology Clinical History and Physical Examination . . . . . . . . . . 3 Diagnostic Testing for Atherosclerotic Coronary Disease. . 3 Cardiac Stress Testing . . . . . . . . . . . . . . . . . . . . . . 3 Viability Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Visualization of the Coronary Anatomy . . . . . . . . . 8 Coronary Artery Calcium Scoring . . . . . . . . . . . . . 8 Risks of Coronary Diagnostic Testing . . . . . . . . . . 8 Diagnostic Testing for Structural Heart Disease . . . . . . 9 Diagnostic Testing for Cardiac Arrhythmias . . . . . . . . 11
Coronary Artery Disease Risk Factors for Coronary Artery Disease . . . . . . . . . . 12 Established Risk Factors. . . . . . . . . . . . . . . . . . . . 12 Emerging Risk Factors. . . . . . . . . . . . . . . . . . . . . 13 Chronic Stable Angina . . . . . . . . . . . . . . . . . . . . . . . . 14 Diagnosis and Evaluation. . . . . . . . . . . . . . . . . . . 14 Medical Therapy . . . . . . . . . . . . . . . . . . . . . . . . . 14 Coronary Revascularization . . . . . . . . . . . . . . . . . 17 Follow-up Care . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Acute Coronary Syndromes . . . . . . . . . . . . . . . . . . . . 19 Clinical Presentation and Classification. . . . . . . . . 19 Non–ST-Elevation Myocardial Infarction and Unstable Angina . . . . . . . . . . . . . . . . . . . . . . . . . 20 ST-Elevation Myocardial Infarction . . . . . . . . . . . 22 Coronary Artery Disease in Patients with Diabetes Mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Diagnostic Issues . . . . . . . . . . . . . . . . . . . . . . . . . 28 Invasive Approaches. . . . . . . . . . . . . . . . . . . . . . . 29 Pharmacologic Treatment and Secondary Prevention. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 Women and Cardiovascular Disease . . . . . . . . . . . . . . 29 Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 30 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Risk Reduction . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Myocardial Disease Hypertrophic Cardiomyopathy . . . . . . . . . . . . . . . . . . 41 Clinical Presentation and Diagnosis . . . . . . . . . . . 41 Clinical Course and Risk Stratification . . . . . . . . . 43 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Restrictive Cardiomyopathy . . . . . . . . . . . . . . . . . . . . 46 ix
Clinical Presentation and Evaluation . . . . . . . . . . 46 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Cardiac Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Tumor Types. . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Clinical Presentation and Evaluation . . . . . . . . . . 47 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
Arrhythmias Approach to the Patient with Bradycardia . . . . . . . . . . 48 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 48 Sinus Bradycardia. . . . . . . . . . . . . . . . . . . . . . . . . 48 Atrioventricular Block . . . . . . . . . . . . . . . . . . . . . 49 Pacemakers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 Approach to the Patient With Tachycardia . . . . . . . . . 50 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50 Antiarrhythmic Medications. . . . . . . . . . . . . . . . . 51 Atrial Fibrillation and Atrial Flutter . . . . . . . . . . . . . . . 52 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 52 Acute Management . . . . . . . . . . . . . . . . . . . . . . . 53 Long-term Management . . . . . . . . . . . . . . . . . . . 53 Atrial Flutter . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 Supraventricular Tachycardias . . . . . . . . . . . . . . . . . . . 55 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 55 Atrioventricular Nodal Reentrant Tachycardia . . . 56 Atrioventricular Reciprocating Tachycardia . . . . . 56 Premature Atrial Contractions and Atrial Tachycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 Ventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . 57 Premature Ventricular Contractions . . . . . . . . . . . 57 Ventricular Tachycardia with Structural Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 Idiopathic Ventricular Tachycardia . . . . . . . . . . . . 57 Inherited Arrhythmia Syndromes . . . . . . . . . . . . . . . . 58 Sudden Cardiac Arrest . . . . . . . . . . . . . . . . . . . . . . . . 60 Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 60 Acute Management . . . . . . . . . . . . . . . . . . . . . . . 60 Device Therapy for Prevention of Sudden Death . . 61 Device Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Pericardial Disease Pericarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 61 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Pericardial Effusion Without Cardiac Compression . . . 67 Clinical Presentation and Evaluation . . . . . . . . . . 67 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68 Cardiac Tamponade . . . . . . . . . . . . . . . . . . . . . . . . . . 68 Clinical Presentation and Evaluation . . . . . . . . . . 68 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68 x
Constrictive Pericarditis . . . . . . . . . . . . . . . . . . . . . . . 69 Clinical Presentation and Evaluation . . . . . . . . . . 69 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
Valvular Heart Disease Pathophysiology of Valvular Heart Disease . . . . . . . . . 70 Diagnostic Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . 71 History and Physical Examination . . . . . . . . . . . . 71 Laboratory and Imaging Tests . . . . . . . . . . . . . . . 71 General Principles of Management of Valvular Disease. . . 75 Aortic Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Pathophysiology and Natural History . . . . . . . . . 77 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Aortic Regurgitation. . . . . . . . . . . . . . . . . . . . . . . . . . 78 Pathophysiology and Natural History . . . . . . . . . 78 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 Bicuspid Aortic Valve . . . . . . . . . . . . . . . . . . . . . . . . . 78 Mitral Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 Pathophysiology and Natural History . . . . . . . . . 79 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 Mitral Regurgitation . . . . . . . . . . . . . . . . . . . . . . . . . . 80 Pathophysiology and Natural History . . . . . . . . . 80 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 Tricuspid Valve Disease . . . . . . . . . . . . . . . . . . . . . . . . 80 Infective Endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . 81 Diagnosis and Management. . . . . . . . . . . . . . . . . 81 Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 Prosthetic Valves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
Adult Congenital Heart Disease Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 Patent Foramen Ovale . . . . . . . . . . . . . . . . . . . . . . . . 83 Atrial Septal Defect . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 Pathophysiology and Genetics . . . . . . . . . . . . . . . 84 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 84 Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 84 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 Reproductive Considerations . . . . . . . . . . . . . . . . 85 Follow-up After Atrial Septal Defect Closure . . . . 85 Ventricular Septal Defect. . . . . . . . . . . . . . . . . . . . . . . 85 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 85 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 87 Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 87 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Reproductive Considerations . . . . . . . . . . . . . . . . 87 Follow-up After Ventricular Septal Defect Closure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Patent Ductus Arteriosus . . . . . . . . . . . . . . . . . . . . . . 88 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 88 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 88
Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 88 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88 Pulmonary Valve Stenosis . . . . . . . . . . . . . . . . . . . . . . 88 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 88 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 88 Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 88 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89 Reproductive Considerations . . . . . . . . . . . . . . . . 89 Aortic Coarctation . . . . . . . . . . . . . . . . . . . . . . . . . . . 89 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 89 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 89 Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 89 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90 Reproductive Considerations . . . . . . . . . . . . . . . . 90 Follow-up After Aortic Coarctation Repair . . . . . 90 Tetralogy of Fallot . . . . . . . . . . . . . . . . . . . . . . . . . . . 90 Diagnostic Evaluation after Repair of Tetralogy of Fallot. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 Treatment of Tetralogy of Fallot Residua . . . . . . . 91 Adults with Cyanotic Congenital Heart Disease . . . . . 91 General Management . . . . . . . . . . . . . . . . . . . . . 91 Eisenmenger Syndrome . . . . . . . . . . . . . . . . . . . . 92
Peripheral Arterial Disease
Diseases of the Aorta
Pregnancy and Cardiovascular Disease
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92 Imaging of the Thoracic Aorta . . . . . . . . . . . . . . . . . . 92 Thoracic Aortic Aneurysm . . . . . . . . . . . . . . . . . . . . . 93 Acute Aortic Syndromes . . . . . . . . . . . . . . . . . . . . . . . 95 Diagnosis and Evaluation. . . . . . . . . . . . . . . . . . . 95 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95 Aortic Atheroma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96 Abdominal Aortic Aneurysm . . . . . . . . . . . . . . . . . . . 96 Screening and Surveillance. . . . . . . . . . . . . . . . . . 96 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
Cardiovascular Changes During Pregnancy. . . . . . . . 105 Prepregnancy Evaluation . . . . . . . . . . . . . . . . . . . . . 106 Management of Cardiovascular Disease During Pregnancy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 Peripartum Cardiomyopathy . . . . . . . . . . . . . . . 107 Medication Use During Pregnancy . . . . . . . . . . 107 Anticoagulation Therapy During Pregnancy . . . 108
Epidemiology and Screening. . . . . . . . . . . . . . . . . . . . 97 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 History and Physical Examination . . . . . . . . . . . . 98 Diagnostic Testing. . . . . . . . . . . . . . . . . . . . . . . . 98 Medical Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99 Cardiovascular Risk Reduction. . . . . . . . . . . . . . . 99 Symptom Relief . . . . . . . . . . . . . . . . . . . . . . . . . 100 Interventional Therapy . . . . . . . . . . . . . . . . . . . . . . . 100 Acute Limb Ischemia . . . . . . . . . . . . . . . . . . . . . . . . 101
Cardiovascular Disease in Cancer Survivors Cardiotoxicity of Radiation Therapy to the Thorax . . 102 Manifestations and Monitoring of Cardiotoxicity After Completion of Radiation Therapy . . . . . . . 102 Management of Radiation-Induced Coronary Artery Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 102 Cardiotoxicity of Chemotherapy . . . . . . . . . . . . . . . . 103 Manifestations and Monitoring of Cardiotoxicity After Completion of Chemotherapy. . . . . . . . . . 103 Management of Chemotherapy-Induced Cardiotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . 105
Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111 Self-Assessment Test . . . . . . . . . . . . . . . . . . . . . 117 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
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Cardiovascular Medicine
Epidemiology of Cardiovascular Disease Overview Cardiovascular disease comprises several conditions that affect the cardiovascular system, including coronary artery disease (CAD), acute myocardial infarction (MI) and angina pectoris, hypertension, stroke, heart failure, atrial fibrillation, peripheral arterial disease, valvular heart disease, and congenital heart disease. More than 81 million adult Americans (1 in 3) have one or more types of cardiovascular disease. Cardiovascular disease accounts for 1 of every 2.8 deaths in the United States while CAD caused 1 of every 5 deaths in the United States in 2004. Data from the Framingham Heart Study indicate the lifetime risk for cardiovascular disease is 2 in 3 for men and 1 in 2 for women. The percentage of deaths attributable to cardiovascular disease increases with age. In 2006, 19% of deaths in adults between the ages of 35 and 44 years were from cardiovascular disease, compared with 45% among persons aged 85 years and older. CAD is the leading cause of death in Americans aged 65 years and older and is second only to cancer for Americans between the ages of 45 and 64 years. Approximately one in six hospital stays in the United States result from cardiovascular disease, accounting for more than 30 million days of inpatient hospital care in 2006. The total inpatient hospital cost for cardiovascular disease was $71.2 billion, about one fourth the total cost of inpatient care in the United States. In 2010, the costs of cardiovascular disease were projected to be $503.2 billion, representing $324 billion in direct and more than $160 billion in indirect costs. By comparison, the estimated cost of all cancers in 2008 was $228 billion. One in five men and women who are aged 40 years or older will develop heart failure during the course of their lifetime. The average 1-year mortality rate for heart failure is approximately 20%. Survival is lower in men than in women. The number of hospital admissions for heart failure has increased markedly over the past decade, with more than 1.1 million Americans hospitalized for heart failure in 2006. Although the number of hospitalizations has gone up, the case fatality rate for these hospitalizations has declined over the same period. The estimated direct and indirect cost from heart failure in the United States for 2010 is almost $40 billion. Epidemiologic data from heart failure can be difficult to interpret because heart failure is the end stage of many processes, including CAD and hypertension.
Ethnicity and Cardiovascular Disease Prevalence data from the National Health Interview Survey (NHIS) and the National Center for Health Statistics (NCHS) indicate that in the United States, 12.1% of whites have CAD, compared with 10.2% of blacks or African Americans, 8.1% of Hispanics or Latinos, 5.2% of Asians, and 12.1% of American Indians or Alaska Natives. Death rates for cardiovascular disease are higher for blacks than for whites (for males and females) and are higher for American Indians and Hispanics than for Asian Americans. Different population risk factors around the world have been established by the INTERHEART study, a study of 30,000 persons conducted in 52 countries around the world. For example, South Asians are, as a group, at overall higher cardiovascular risk than other groups. This has been attributed to several mechanisms, including different distribution of body fat with greater central obesity, higher waist-to-hip circumference ratio, and a greater likelihood of insulin resistance in the South Asian population. Waist circumference and waistto-hip ratio are indicators of abdominal adiposity and are positively related to coronary heart disease in men and women independently of body mass index and conventional coronary heart disease risk factors. Mexican Americans have higher rates of CAD, attributable mainly to higher obesity rates and lower levels of physical activity. Blacks in the United States have a greater cardiovascular risk than persons of African or Caribbean descent living in the United Kingdom, a fact that might relate to greater levels of obesity, poorer socioeconomic status, and poorer access to health care among black Americans. American Indians are at higher risk of cardiovascular disease as well, although a subgroup, the Pima Indians of Arizona, have a low prevalence of CAD despite high rates of diabetes mellitus. This relatively low rate of CAD is attributed to lower cholesterol levels and the rarity of heavy smoking. The Japanese have traditionally had low rates of CAD, but now have increased rates of obesity with the adoption of a Western-style diet. This increased obesity, coupled with higher smoking rates, may result in a significant increase in CAD rates in this population. KEY POINT
• Death rates for cardiovascular disease are higher for blacks in the United States than for whites and are higher for American Indians and Hispanics than for Asian Americans. 1
Epidemiology of Cardiovascular Disease
Chronic Kidney Disease and Cardiovascular Disease Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Cardiovascular disease mortality is 5 to 30 times higher in dialysis patients than in the general population. Many traditional cardiovascular disease risk factors are also risk factors for CKD, including age, hypertension, diabetes, dyslipidemia, and smoking. Any degree of albuminuria is an independent risk factor for cardiovascular events, heart failure hospitalizations, and allcause mortality. Although a number of consensus statements have suggested that persons with CKD be considered part of the highest risk group for developing cardiovascular disease as well as for all-cause mortality, shared risk factors between cardiovascular disease and CKD may be responsible for much of the association. KEY POINT
• Any degree of albuminuria is an independent risk factor for cardiovascular events, heart failure hospitalizations, and all-cause mortality.
Systemic Inflammatory Conditions and Cardiovascular Disease Systemic inflammatory diseases are inflammatory conditions that are associated with more than one organ system. These
TA B L E 1 .
conditions can have various cardiac presentations, including pericarditis, myocarditis, myocardial fibrosis, coronary arteritis, endocardial disease with valvular involvement, pulmonary hypertension due to concomitant lung disease, rhythm disturbances (including both bradyarrhythmias and tachyarrhythmias), and systemic hypertension (Table 1). Not all conditions that present with these manifestations are systemic inflammatory diseases—the broad differential also includes infections, toxins (cocaine, amphetamines), drug-induced hypersensitivity reactions, and infiltrative processes. In a patient with a systemic inflammatory disease presenting with a cardiac condition, it is important to consider such causes in the differential diagnosis. Atherosclerosis is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE) as well as other inflammatory conditions, including rheumatoid arthritis. In SLE, accelerated atherosclerosis is attributed to both an increased prevalence of traditional risk factors in this population as well as the inflammatory effect of SLE itself. The risk of MI is increased by up to 50-fold in women aged 35 to 44 years with SLE compared with agematched Framingham controls. This premature atherosclerosis has led to evaluation of subclinical markers, including coronary artery calcification and carotid atherosclerosis in risk assessment for SLE. Notably, the recently published LAPS trial (Lupus Atherosclerosis Prevention Study) failed to show benefit of statin therapy on either progression of coronary artery calcification, carotid intima media thickness, or carotid plaque over a 2-year period in patients with SLE in comparison with placebo.
Systemic Inflammatory Conditions and Associated Cardiovascular Diseases
Systemic Inflammatory Condition
Cardiac Involvement and Prevalence
Systemic lupus erythematosus
Pericarditis (25%-50%), noninfective endocarditis (22%-61%), moderate or severe valvular regurgitation (up to 20%), premature coronary artery disease
Rheumatoid arthritis
Pericardial effusion (30%-40%), coronary artery disease, leaflet fibrosis (up to 30%), left ventricular diastolic dysfunction (up to 15%)
Ankylosing spondylitis
Proximal aortitis/valvulitis (25%-60%), moderate or severe aortic regurgitation (up to 40%), conduction system disease (2%-20%), left ventricular diastolic dysfunction
Systemic sclerosis
Systemic hypertension, including scleroderma renal crisis; pulmonary arterial hypertension; myocardial fibrosis; pericardial disease
Takayasu arteritis
Arteritis, predominantly aortic (aneurysms, stenosis, occlusion); coronary arteritis (15%-25%); aortic regurgitation; pulmonary arterial stenosis or aneurysm; malignant hypertension due to renovascular involvement
Giant cell arteritis
Peripheral arterial disease, stroke, myocardial infarction
Polyarteritis nodosa
Cardiomyopathy
Kawasaki disease
Coronary artery aneurysms, occlusion
Behçet syndrome
Aortic valve regurgitation, myocarditis, pericarditis, conduction abnormalities
Sarcoidosis
Cardiomyopathy (dilated or restrictive); conduction abnormalities; ventricular arrhythmias, including sudden death
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This self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefully before answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choice questions. The American College of Physicians is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The American College of Physicians designates MKSAP 16 Cardiovascular Medicine for a maximum of 18 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Earn “Same-Day” CME Credits Online For the first time, print subscribers can enter their answers online to earn CME credits in 24 hours or less. You can submit your answers using online answer sheets that are provided at mksap.acponline.org, where a record of your MKSAP 16 credits will be available. To earn CME credits, you need to answer all of the questions in a test and earn a score of at least 50% correct (number of correct answers divided by the total number of questions). Take any of the following approaches: ➢ Use the printed answer sheet at the back of this book to record your answers. Go to mksap.acponline.org, access the appropriate online answer sheet, transcribe your answers, and submit your test for same-day CME credits. There is no additional fee for this service. ➢ Go to mksap.acponline.org, access the appropriate online answer sheet, directly enter your answers, and submit your test for same-day CME credits. There is no additional fee for this service. ➢ Pay a $10 processing fee per answer sheet and submit the printed answer sheet at the back of this book by mail or fax, as instructed on the answer sheet. Make sure you calculate your score and fax the answer sheet to 215-351-2799 or mail the answer sheet to Member and Customer Service, American College of Physicians, 190 N. Independence Mall West, Philadelphia, PA 19106-1572, using the courtesy envelope provided in your MKSAP 16 slipcase. You will need your 10-digit order number and 8-digit ACP ID number, which are printed on your packing slip. Please allow 4 to 6 weeks for your score report to be emailed back to you. Be sure to include your email address for a response. If you do not have a 10-digit order number and 8-digit ACP ID number or if you need help creating a username and password to access the MKSAP 16 online answer sheets, go to mksap.acponline.org or email custserv@ acponline.org. CME credit is available from the publication date of July 31, 2012, until July 31, 2015. You may submit your answer sheets at any time during this period.
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Self-Assessment Test
Cardiovascular Medicine Self-Assessment Test
Each of the numbered items is followed by lettered answers. Select the ONE lettered answer that is BEST in each case.
Item 1 A 60-year-old man is evaluated for chest pain of 4 months’ duration. He describes the pain as sharp, located in the left chest, with no radiation or associated symptoms, that occurs with walking one to two blocks and resolves with rest. Occasionally, the pain improves with continued walking or occurs during the evening hours. He has hypertension. Family history does not include cardiovascular disease in any first-degree relatives. His only medication is amlodipine. On physical examination, he is afebrile, blood pressure is 130/80 mm Hg, pulse rate is 72/min, and respiration rate is 12/min. BMI is 28. No carotid bruits are present, and a normal S1 and S2 with no murmurs are heard. Lung fields are clear, and distal pulses are normal. Electrocardiogram is shown. Which of the following is the most appropriate diagnostic test to perform next? (A) (B) (C) (D)
Adenosine nuclear perfusion stress test Coronary angiography Echocardiography Exercise treadmill stress test
Item 2 A 52-year-old man is evaluated in the office during a routine visit. Medical history is significant for type 2 diabetes mellitus, hypertension, hypercholesterolemia, and obesity. Medications are lisinopril, insulin glargine, insulin aspart, aspirin, and pravastatin (20 mg/d).
On physical examination, he is afebrile, blood pressure is 128/80 mm Hg, pulse rate is 73/min, and respiration rate is 18/min. BMI is 35. The lungs are clear to auscultation, and no murmurs are heard. Laboratory studies: 7.2% Hemoglobin A1c Total cholesterol 168 mg/dL (4.35 mmol/L) LDL cholesterol 109 mg/dL (2.82 mmol/L) HDL cholesterol 40 mg/dL (1.04 mmol/L) Triglycerides 95 mg/dL (1.07 mmol/L) Which of the following is the most appropriate management? (A) (B) (C) (D)
Increase statin dose Start bile acid sequestrant Start fibrate Start niacin
Item 3 A 38-year-old man is evaluated during a routine health examination. He exercises 2 or 3 days each week by jogging for 30 minutes without shortness of breath or chest discomfort. During stressful emotional situations, he occasionally feels “skipped heart beats” but has not had prolonged palpitations, presyncope, or syncope. He generally feels in good health. He has no history of medical problems and takes no medications. He has not had fever or chills. Physical examination shows normal temperature, blood pressure is 124/68 mm Hg, pulse rate is 64/min and regular, and respiration rate is 14/min. BMI is 23. Cardiac examination
ITEM 1
119
Self-Assessment Test
Directions
Answers and Critiques Answer:
D
Educational Objective: Evaluate chest pain in a patient with an intermediate pretest probability of coronary artery disease. The most appropriate test to establish a diagnosis of coronary artery disease (CAD) in this patient is an exercise treadmill stress test. The description of chest pain has both typical and atypical features. Based on the patient’s age and sex, the pretest likelihood that his symptoms represent angina are increased, giving him an intermediate pretest probability for CAD. The patient is able to exercise and has a normal baseline electrocardiogram (ECG). In this setting, an exercise treadmill stress test is the most appropriate noninvasive imaging study. A pharmacologic stress test such as an adenosine nuclear perfusion stress test is useful when a patient cannot exercise because of physical limitations such as arthritis, physical deconditioning, or advanced lung disease and in the setting of an abnormal baseline ECG. Pharmacologic stress agents include dobutamine, dipyridamole, and adenosine. Given that the patient has a normal baseline ECG and is able to exercise, a pharmacologic stress test would not be the correct choice. Coronary angiography has a small but inherent risk of vascular complications and is therefore usually not the initial diagnostic test used to evaluate a patient presenting with chest pain. For patients with lifestyle-limiting angina despite optimal medical therapy, high-risk criteria on noninvasive stress testing, or successful resuscitation from sudden cardiac death, coronary angiography may be useful. An echocardiogram would be useful to evaluate left ventricular systolic function (ejection fraction), assess for wall motion abnormalities (that may indicate a previous myocardial infarction), and exclude significant valvular heart disease. A normal echocardiogram, however, would not exclude the presence of underlying CAD and therefore would not be the best test to establish a diagnosis in this patient. KEY POINT
• For a patient who is able to exercise and has a normal baseline electrocardiogram, an exercise treadmill stress test is the most appropriate noninvasive study to evaluate for coronary artery disease. Bibliography Chou TM, Amidon TM. Evaluating coronary artery disease noninvasively–which test for whom? West J Med. 1994;161(2):173-180. [PMID: 7941543]
Item 2
Answer:
A
Educational Objective: Manage elevated cholesterol level in a patient with diabetes mellitus. The most appropriate modification of this patient’s treatment regimen is to increase the statin dose. The National Cholesterol Education Program (NCEP) Adult Treatment Panel III LDL cholesterol treatment target for all patients at high risk is below 100 mg/dL (2.59 mmol/L). High risk is defined as the presence of coronary heart disease (CHD) or CHD risk equivalents, which include peripheral arterial disease, abdominal aortic aneurysm, carotid artery disease, transient ischemic attacks or stroke of carotid origin or 50% obstruction of a carotid artery, diabetes mellitus, and 10-year risk for cardiovascular disease of 20% or greater. For patients in the very-high-risk category, such as those with coronary artery disease and diabetes mellitus, as well as in the setting of an acute coronary syndrome, an LDL cholesterol level below 70 mg/dL (1.81 mmol/L) is a therapeutic option. Patients with diabetes show similar relative risk reductions compared with those without diabetes, but as the absolute risk in these patients is higher, the number needed to treat (to prevent a cardiovascular event) is lower. Several studies have demonstrated the benefits of statin therapy. In ad hoc analyses involving patients with diabetes from the Scandinavian Simvastatin Survival Study, simvastatin therapy was associated with a 55% reduction in major coronary events. In analyses of the 8000 patients in the diabetic subgroup from the Heart Protection Study, there was a 22% reduction (20.2% vs. 25.1%) in major vascular events in the group receiving simvastatin. Statins remain the first-line therapy for the treatment of hyperlipidemia and for the primary and secondary prevention of CHD. Trials of nonstatin drugs in the primary prevention of CHD have been associated with reductions in coronary events but not mortality. In this patient, an increase from a low dose (20 mg) of pravastatin to a moderate dose (40 mg) is the best approach, both in terms of tolerability and effectiveness. KEY POINT
• The presence of diabetes mellitus is considered a cardiovascular disease risk equivalent in the assessment of cardiovascular risk. Bibliography Rydén L, Standl E, Bartnik M, et al; Task Force on Diabetes and Cardiovascular Diseases of the European Society of Cardiology (ESC); European Association for the Study of Diabetes (EASD). Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: executive summary. The Task Force on Diabetes and Cardiovascular Diseases of the European Society of Cardiology (ESC) and of the European Association for the Study of Diabetes (EASD). Eur Heart J. 2007;28(1):88-136. [PMID: 17220161]
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Answers and Critiques
Item 1