Cardiovascular Medicine

150591010

Cardiovascular MedicineAll New Content, Including 120 Multiple-Choice Questions

18 AMA PRA Category 1 Credits™

available until July 31, 2015.

Medical Knowledge Self -Assessment Program®

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Table of Contents

Heart FailureDiagnosis and Evaluation of Heart Failure . . . . . . . . . 30

Clinical Evaluation. . . . . . . . . . . . . . . . . . . . . . . . 30Diagnostic Testing. . . . . . . . . . . . . . . . . . . . . . . . 31Laboratory Evaluation . . . . . . . . . . . . . . . . . . . . . 32Evaluation for Ischemia . . . . . . . . . . . . . . . . . . . . 32

Medical Therapy for Systolic Heart Failure . . . . . . . . . 32ACE Inhibitors and Angiotensin Receptor Blockers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33β-Blockers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33Initiating and Managing ACE Inhibitor and β-Blocker Therapy. . . . . . . . . . . . . . . . . . . . . . . . 34Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34Digoxin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34Aldosterone Antagonists . . . . . . . . . . . . . . . . . . . 34Hydralazine and Isosorbide Dinitrate. . . . . . . . . . 34Calcium Channel Blockers . . . . . . . . . . . . . . . . . . 35

Heart Failure With Preserved Ejection Fraction . . . . . 35Device Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

Implantable Cardioverter-Defibrillator for Prevention of Sudden Cardiac Death . . . . . . . . . . 36Cardiac Resynchronization Therapy. . . . . . . . . . . 36

Follow-up Management of Chronic Heart Failure . . . 37Serial Assessment . . . . . . . . . . . . . . . . . . . . . . . . . 37Assessing Prognosis . . . . . . . . . . . . . . . . . . . . . . . 37

Inpatient Management of Heart Failure . . . . . . . . . . . 37Acute Decompensated Heart Failure . . . . . . . . . . 37Cardiogenic Shock. . . . . . . . . . . . . . . . . . . . . . . . 38Strategies to Prevent Readmission . . . . . . . . . . . . 39

Advanced Refractory Heart Failure . . . . . . . . . . . . . . . 39Mechanical Circulatory Support . . . . . . . . . . . . . 39Management of Posttransplant Patients . . . . . . . . 40

Specific Cardiomyopathies . . . . . . . . . . . . . . . . . . . . . 40Takotsubo Cardiomyopathy. . . . . . . . . . . . . . . . . 40Acute Myocarditis . . . . . . . . . . . . . . . . . . . . . . . . 40Tachycardia-Mediated Cardiomyopathy. . . . . . . . 41Giant Cell Myocarditis. . . . . . . . . . . . . . . . . . . . . 41

Myocardial DiseaseHypertrophic Cardiomyopathy . . . . . . . . . . . . . . . . . . 41

Clinical Presentation and Diagnosis . . . . . . . . . . . 41Clinical Course and Risk Stratification . . . . . . . . . 43Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

Restrictive Cardiomyopathy . . . . . . . . . . . . . . . . . . . . 46

Epidemiology of Cardiovascular DiseaseOverview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Ethnicity and Cardiovascular Disease . . . . . . . . . . . . . . 1Chronic Kidney Disease and Cardiovascular Disease . . . 2Systemic Inflammatory Conditions and CardiovascularDisease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2Quality Measures in Cardiovascular Disease . . . . . . . . . 3

Diagnostic Testing in CardiologyClinical History and Physical Examination . . . . . . . . . . 3Diagnostic Testing for Atherosclerotic Coronary Disease. . 3

Cardiac Stress Testing . . . . . . . . . . . . . . . . . . . . . . 3Viability Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . 8Visualization of the Coronary Anatomy . . . . . . . . . 8Coronary Artery Calcium Scoring . . . . . . . . . . . . . 8Risks of Coronary Diagnostic Testing . . . . . . . . . . 8

Diagnostic Testing for Structural Heart Disease . . . . . . 9Diagnostic Testing for Cardiac Arrhythmias . . . . . . . . 11

Coronary Artery DiseaseRisk Factors for Coronary Artery Disease . . . . . . . . . . 12

Established Risk Factors. . . . . . . . . . . . . . . . . . . . 12Emerging Risk Factors. . . . . . . . . . . . . . . . . . . . . 13

Chronic Stable Angina . . . . . . . . . . . . . . . . . . . . . . . . 14Diagnosis and Evaluation. . . . . . . . . . . . . . . . . . . 14Medical Therapy . . . . . . . . . . . . . . . . . . . . . . . . . 14Coronary Revascularization . . . . . . . . . . . . . . . . . 17Follow-up Care . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Acute Coronary Syndromes . . . . . . . . . . . . . . . . . . . . 19Clinical Presentation and Classification. . . . . . . . . 19Non–ST-Elevation Myocardial Infarction and Unstable Angina . . . . . . . . . . . . . . . . . . . . . . . . . 20ST-Elevation Myocardial Infarction . . . . . . . . . . . 22

Coronary Artery Disease in Patients with Diabetes Mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

Diagnostic Issues . . . . . . . . . . . . . . . . . . . . . . . . . 28Invasive Approaches. . . . . . . . . . . . . . . . . . . . . . . 29Pharmacologic Treatment and Secondary Prevention. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

Women and Cardiovascular Disease . . . . . . . . . . . . . . 29Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 29Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 30Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30Risk Reduction . . . . . . . . . . . . . . . . . . . . . . . . . . 30

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Clinical Presentation and Evaluation . . . . . . . . . . 46Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

Cardiac Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47Tumor Types. . . . . . . . . . . . . . . . . . . . . . . . . . . . 47Clinical Presentation and Evaluation . . . . . . . . . . 47Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

ArrhythmiasApproach to the Patient with Bradycardia . . . . . . . . . . 48

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 48Sinus Bradycardia. . . . . . . . . . . . . . . . . . . . . . . . . 48Atrioventricular Block . . . . . . . . . . . . . . . . . . . . . 49Pacemakers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49

Approach to the Patient With Tachycardia . . . . . . . . . 50Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50Antiarrhythmic Medications. . . . . . . . . . . . . . . . . 51

Atrial Fibrillation and Atrial Flutter . . . . . . . . . . . . . . . 52Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 52Acute Management . . . . . . . . . . . . . . . . . . . . . . . 53Long-term Management . . . . . . . . . . . . . . . . . . . 53Atrial Flutter . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55

Supraventricular Tachycardias . . . . . . . . . . . . . . . . . . . 55Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 55Atrioventricular Nodal Reentrant Tachycardia . . . 56Atrioventricular Reciprocating Tachycardia . . . . . 56Premature Atrial Contractions and Atrial Tachycardia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57

Ventricular Arrhythmias . . . . . . . . . . . . . . . . . . . . . . . 57Premature Ventricular Contractions . . . . . . . . . . . 57Ventricular Tachycardia with Structural Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57Idiopathic Ventricular Tachycardia . . . . . . . . . . . . 57

Inherited Arrhythmia Syndromes . . . . . . . . . . . . . . . . 58Sudden Cardiac Arrest . . . . . . . . . . . . . . . . . . . . . . . . 60

Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 60Acute Management . . . . . . . . . . . . . . . . . . . . . . . 60Device Therapy for Prevention of Sudden Death . . 61

Device Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

Pericardial DiseasePericarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 61Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

Pericardial Effusion Without Cardiac Compression . . . 67Clinical Presentation and Evaluation . . . . . . . . . . 67Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68

Cardiac Tamponade . . . . . . . . . . . . . . . . . . . . . . . . . . 68Clinical Presentation and Evaluation . . . . . . . . . . 68Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68

Constrictive Pericarditis . . . . . . . . . . . . . . . . . . . . . . . 69Clinical Presentation and Evaluation . . . . . . . . . . 69Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70

Valvular Heart DiseasePathophysiology of Valvular Heart Disease . . . . . . . . . 70Diagnostic Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . 71

History and Physical Examination . . . . . . . . . . . . 71Laboratory and Imaging Tests . . . . . . . . . . . . . . . 71

General Principles of Management of Valvular Disease. . . 75Aortic Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

Pathophysiology and Natural History . . . . . . . . . 77Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

Aortic Regurgitation. . . . . . . . . . . . . . . . . . . . . . . . . . 78Pathophysiology and Natural History . . . . . . . . . 78Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

Bicuspid Aortic Valve . . . . . . . . . . . . . . . . . . . . . . . . . 78Mitral Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

Pathophysiology and Natural History . . . . . . . . . 79Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

Mitral Regurgitation . . . . . . . . . . . . . . . . . . . . . . . . . . 80Pathophysiology and Natural History . . . . . . . . . 80Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80

Tricuspid Valve Disease. . . . . . . . . . . . . . . . . . . . . . . . 80Infective Endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . 81

Diagnosis and Management. . . . . . . . . . . . . . . . . 81Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

Prosthetic Valves. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

Adult Congenital Heart DiseaseIntroduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83Patent Foramen Ovale . . . . . . . . . . . . . . . . . . . . . . . . 83Atrial Septal Defect . . . . . . . . . . . . . . . . . . . . . . . . . . . 84

Pathophysiology and Genetics . . . . . . . . . . . . . . . 84Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 84Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 84Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85Reproductive Considerations . . . . . . . . . . . . . . . . 85Follow-up After Atrial Septal Defect Closure . . . . 85

Ventricular Septal Defect. . . . . . . . . . . . . . . . . . . . . . . 85Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 85Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 87Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 87Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87Reproductive Considerations . . . . . . . . . . . . . . . . 87Follow-up After Ventricular Septal Defect Closure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

Patent Ductus Arteriosus . . . . . . . . . . . . . . . . . . . . . . 88Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 88Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 88

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Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 88Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88

Pulmonary Valve Stenosis . . . . . . . . . . . . . . . . . . . . . . 88Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 88Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 88Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 88Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89Reproductive Considerations . . . . . . . . . . . . . . . . 89

Aortic Coarctation . . . . . . . . . . . . . . . . . . . . . . . . . . . 89Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 89Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 89Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . 89Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90Reproductive Considerations . . . . . . . . . . . . . . . . 90Follow-up After Aortic Coarctation Repair . . . . . 90

Tetralogy of Fallot . . . . . . . . . . . . . . . . . . . . . . . . . . . 90Diagnostic Evaluation after Repair of Tetralogy of Fallot. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91Treatment of Tetralogy of Fallot Residua . . . . . . . 91

Adults with Cyanotic Congenital Heart Disease . . . . . 91General Management . . . . . . . . . . . . . . . . . . . . . 91Eisenmenger Syndrome . . . . . . . . . . . . . . . . . . . . 92

Diseases of the AortaIntroduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92Imaging of the Thoracic Aorta . . . . . . . . . . . . . . . . . . 92Thoracic Aortic Aneurysm . . . . . . . . . . . . . . . . . . . . . 93Acute Aortic Syndromes . . . . . . . . . . . . . . . . . . . . . . . 95

Diagnosis and Evaluation. . . . . . . . . . . . . . . . . . . 95Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95

Aortic Atheroma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96Abdominal Aortic Aneurysm . . . . . . . . . . . . . . . . . . . 96

Screening and Surveillance. . . . . . . . . . . . . . . . . . 96Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97

Peripheral Arterial DiseaseEpidemiology and Screening. . . . . . . . . . . . . . . . . . . . 97Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98

History and Physical Examination . . . . . . . . . . . . 98Diagnostic Testing. . . . . . . . . . . . . . . . . . . . . . . . 98

Medical Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99Cardiovascular Risk Reduction. . . . . . . . . . . . . . . 99Symptom Relief . . . . . . . . . . . . . . . . . . . . . . . . . 100

Interventional Therapy . . . . . . . . . . . . . . . . . . . . . . . 100Acute Limb Ischemia . . . . . . . . . . . . . . . . . . . . . . . . 101

Cardiovascular Disease in Cancer SurvivorsCardiotoxicity of Radiation Therapy to the Thorax . . 102

Manifestations and Monitoring of CardiotoxicityAfter Completion of Radiation Therapy . . . . . . . 102Management of Radiation-Induced Coronary Artery Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 102

Cardiotoxicity of Chemotherapy . . . . . . . . . . . . . . . . 103Manifestations and Monitoring of Cardiotoxicity After Completion of Chemotherapy. . . . . . . . . . 103Management of Chemotherapy-Induced Cardiotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . 105

Pregnancy and Cardiovascular DiseaseCardiovascular Changes During Pregnancy. . . . . . . . 105Prepregnancy Evaluation . . . . . . . . . . . . . . . . . . . . . 106Management of Cardiovascular Disease During Pregnancy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107

Peripartum Cardiomyopathy . . . . . . . . . . . . . . . 107Medication Use During Pregnancy . . . . . . . . . . 107Anticoagulation Therapy During Pregnancy . . . 108

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111

Self-Assessment Test . . . . . . . . . . . . . . . . . . . . . 117

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215

Cardiovascular Medicine

Ethnicity and CardiovascularDiseasePrevalence 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 whiteshave CAD, compared with 10.2% of blacks or AfricanAmericans, 8.1% of Hispanics or Latinos, 5.2% of Asians, and12.1% of American Indians or Alaska Natives. Death rates forcardiovascular disease are higher for blacks than for whites (formales and females) and are higher for American Indians andHispanics than for Asian Americans.

Different population risk factors around the world havebeen established by the INTERHEART study, a study of30,000 persons conducted in 52 countries around the world.For example, South Asians are, as a group, at overall highercardiovascular risk than other groups. This has been attributedto several mechanisms, including different distribution ofbody fat with greater central obesity, higher waist-to-hip cir-cumference ratio, and a greater likelihood of insulin resistancein the South Asian population. Waist circumference and waist-to-hip ratio are indicators of abdominal adiposity and are pos-itively related to coronary heart disease in men and womenindependently of body mass index and conventional coronaryheart disease risk factors.

Mexican Americans have higher rates of CAD, attribut-able mainly to higher obesity rates and lower levels of physi-cal activity. Blacks in the United States have a greater cardio-vascular risk than persons of African or Caribbean descentliving in the United Kingdom, a fact that might relate togreater levels of obesity, poorer socioeconomic status, andpoorer access to health care among black Americans.American Indians are at higher risk of cardiovascular diseaseas well, although a subgroup, the Pima Indians of Arizona,have a low prevalence of CAD despite high rates of diabetesmellitus. This relatively low rate of CAD is attributed tolower cholesterol levels and the rarity of heavy smoking. TheJapanese have traditionally had low rates of CAD, but nowhave increased rates of obesity with the adoption of aWestern-style diet. This increased obesity, coupled withhigher smoking rates, may result in a significant increase inCAD rates in this population.

K E Y P O I N T

• Death rates for cardiovascular disease are higher forblacks in the United States than for whites and arehigher for American Indians and Hispanics than forAsian Americans.

Epidemiology ofCardiovascular DiseaseOverviewCardiovascular disease comprises several conditions thataffect the cardiovascular system, including coronary arterydisease (CAD), acute myocardial infarction (MI) and anginapectoris, hypertension, stroke, heart failure, atrial fibrillation,peripheral arterial disease, valvular heart disease, and con-genital 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 inthe United States while CAD caused 1 of every 5 deaths inthe United States in 2004. Data from the Framingham HeartStudy indicate the lifetime risk for cardiovascular disease is 2in 3 for men and 1 in 2 for women.

The percentage of deaths attributable to cardiovasculardisease increases with age. In 2006, 19% of deaths in adultsbetween the ages of 35 and 44 years were from cardiovascu-lar disease, compared with 45% among persons aged 85 yearsand older. CAD is the leading cause of death in Americansaged 65 years and older and is second only to cancer forAmericans between the ages of 45 and 64 years.

Approximately one in six hospital stays in the UnitedStates result from cardiovascular disease, accounting for morethan 30 million days of inpatient hospital care in 2006. Thetotal inpatient hospital cost for cardiovascular disease was$71.2 billion, about one fourth the total cost of inpatient carein the United States. In 2010, the costs of cardiovascular dis-ease were projected to be $503.2 billion, representing $324billion 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 orolder will develop heart failure during the course of their life-time. The average 1-year mortality rate for heart failure isapproximately 20%. Survival is lower in men than in women.The number of hospital admissions for heart failure hasincreased markedly over the past decade, with more than 1.1million Americans hospitalized for heart failure in 2006.Although the number of hospitalizations has gone up, the casefatality rate for these hospitalizations has declined over thesame period. The estimated direct and indirect cost from heartfailure in the United States for 2010 is almost $40 billion.Epidemiologic data from heart failure can be difficult to inter-pret because heart failure is the end stage of many processes,including CAD and hypertension.

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Chronic Kidney Disease andCardiovascular DiseaseCardiovascular disease is the leading cause of death inpatients with chronic kidney disease (CKD). Cardiovasculardisease mortality is 5 to 30 times higher in dialysis patientsthan in the general population. Many traditional cardiovas-cular disease risk factors are also risk factors for CKD, includ-ing age, hypertension, diabetes, dyslipidemia, and smoking.Any degree of albuminuria is an independent risk factor forcardiovascular events, heart failure hospitalizations, and all-cause mortality. Although a number of consensus statementshave suggested that persons with CKD be considered part ofthe highest risk group for developing cardiovascular diseaseas well as for all-cause mortality, shared risk factors betweencardiovascular disease and CKD may be responsible formuch of the association.

K E Y P O I N T

• Any degree of albuminuria is an independent risk fac-tor for cardiovascular events, heart failure hospitaliza-tions, and all-cause mortality.

Systemic InflammatoryConditions and CardiovascularDiseaseSystemic inflammatory diseases are inflammatory conditionsthat are associated with more than one organ system. These

Epidemiology of Cardiovascular Disease

conditions can have various cardiac presentations, includingpericarditis, myocarditis, myocardial fibrosis, coronary arteri-tis, endocardial disease with valvular involvement, pulmonaryhypertension due to concomitant lung disease, rhythm dis-turbances (including both bradyarrhythmias and tach-yarrhythmias), and systemic hypertension (Table 1). Not allconditions that present with these manifestations are systemicinflammatory diseases—the broad differential also includesinfections, toxins (cocaine, amphetamines), drug-inducedhypersensitivity reactions, and infiltrative processes. In apatient with a systemic inflammatory disease presenting witha cardiac condition, it is important to consider such causes inthe differential diagnosis.

Atherosclerosis is a major cause of morbidity and mor-tality in patients with systemic lupus erythematosus (SLE) aswell as other inflammatory conditions, including rheuma-toid arthritis. In SLE, accelerated atherosclerosis is attrib-uted to both an increased prevalence of traditional risk fac-tors in this population as well as the inflammatory effect ofSLE itself. The risk of MI is increased by up to 50-fold inwomen aged 35 to 44 years with SLE compared with age-matched Framingham controls. This premature atheroscle-rosis has led to evaluation of subclinical markers, includingcoronary artery calcification and carotid atherosclerosis inrisk assessment for SLE. Notably, the recently publishedLAPS trial (Lupus Atherosclerosis Prevention Study) failedto show benefit of statin therapy on either progression ofcoronary artery calcification, carotid intima media thickness,or carotid plaque over a 2-year period in patients with SLEin comparison with placebo.

TABLE 1 . Systemic Inflammatory Conditions and Associated Cardiovascular Diseases

Systemic Cardiac Involvement and PrevalenceInflammatory Condition

Systemic lupus Pericarditis (25%-50%), noninfective endocarditis (22%-61%), moderate or severe valvular regurgitation erythematosus (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

Self-

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Cardiovascular Medicine Self-Assessment TestThis self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefullybefore answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choicequestions. The American College of Physicians is accredited by the Accreditation Council for Continuing Med-ical Education (ACCME) to provide continuing medical education for physicians.

The American College of Physicians designates MKSAP 16 Cardiovascular Medicine for a maximum of 18 AMAPRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their partic-ipation in the activity.

Earn “Same-Day” CME Credits OnlineFor the first time, print subscribers can enter their answers online to earn CME credits in 24 hours or less. You cansubmit your answers using online answer sheets that are provided at mksap.acponline.org, where a record of yourMKSAP 16 credits will be available. To earn CME credits, you need to answer all of the questions in a test andearn a score of at least 50% correct (number of correct answers divided by the total number of questions). Takeany 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 CMEcredits. There is no additional fee for this service.

➢ Go to mksap.acponline.org, access the appropriate online answer sheet, directly enter your answers, andsubmit 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 bymail or fax, as instructed on the answer sheet. Make sure you calculate your score and fax the answer sheetto 215-351-2799 or mail the answer sheet to Member and Customer Service, American College of Physi-cians, 190 N. Independence Mall West, Philadelphia, PA 19106-1572, using the courtesy envelope pro-vided 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 backto 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 usernameand 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 youranswer sheets at any time during this period.

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Item 1A 60-year-old man is evaluated for chest pain of 4 months’duration. He describes the pain as sharp, located in the leftchest, with no radiation or associated symptoms, that occurswith walking one to two blocks and resolves with rest.Occasionally, the pain improves with continued walking oroccurs during the evening hours. He has hypertension.Family history does not include cardiovascular disease in anyfirst-degree relatives. His only medication is amlodipine.

On physical examination, he is afebrile, blood pressureis 130/80 mm Hg, pulse rate is 72/min, and respirationrate is 12/min. BMI is 28. No carotid bruits are present,and a normal S1 and S2 with no murmurs are heard. Lungfields are clear, and distal pulses are normal.

Electrocardiogram is shown.

Which of the following is the most appropriate diag-nostic test to perform next?

(A) Adenosine nuclear perfusion stress test(B) Coronary angiography(C) Echocardiography(D) Exercise treadmill stress test

Item 2A 52-year-old man is evaluated in the office during a rou-tine visit. Medical history is significant for type 2 diabetesmellitus, hypertension, hypercholesterolemia, and obesity.Medications are lisinopril, insulin glargine, insulin aspart,aspirin, and pravastatin (20 mg/d).

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Each of the numbered items is followed by lettered answers. Select the ONE lettered answer that is BEST in each case.

On physical examination, he is afebrile, blood pressureis 128/80 mm Hg, pulse rate is 73/min, and respirationrate is 18/min. BMI is 35. The lungs are clear to ausculta-tion, and no murmurs are heard.Laboratory studies:Hemoglobin A1c 7.2%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 man-agement?

(A) Increase statin dose(B) Start bile acid sequestrant(C) Start fibrate(D) Start niacin

Item 3A 38-year-old man is evaluated during a routine healthexamination. He exercises 2 or 3 days each week by joggingfor 30 minutes without shortness of breath or chest dis-comfort. During stressful emotional situations, he occasion-ally feels “skipped heart beats” but has not had prolongedpalpitations, presyncope, or syncope. He generally feels ingood health. He has no history of medical problems andtakes no medications. He has not had fever or chills.

Physical examination shows normal temperature, bloodpressure is 124/68 mm Hg, pulse rate is 64/min and regular,and respiration rate is 14/min. BMI is 23. Cardiac examination

I T E M 1

Item 1 Answer: DEducational Objective: Evaluate chest pain in apatient with an intermediate pretest probability ofcoronary artery disease.

The most appropriate test to establish a diagnosis of coro-nary artery disease (CAD) in this patient is an exercisetreadmill stress test. The description of chest pain has bothtypical and atypical features. Based on the patient’s age andsex, the pretest likelihood that his symptoms representangina are increased, giving him an intermediate pretestprobability for CAD. The patient is able to exercise and hasa normal baseline electrocardiogram (ECG). In this setting,an exercise treadmill stress test is the most appropriate non-invasive imaging study.

A pharmacologic stress test such as an adenosinenuclear perfusion stress test is useful when a patient cannotexercise because of physical limitations such as arthritis,physical deconditioning, or advanced lung disease and inthe setting of an abnormal baseline ECG. Pharmacologicstress agents include dobutamine, dipyridamole, andadenosine. Given that the patient has a normal baselineECG and is able to exercise, a pharmacologic stress testwould not be the correct choice.

Coronary angiography has a small but inherent risk ofvascular complications and is therefore usually not the ini-tial diagnostic test used to evaluate a patient presenting withchest pain. For patients with lifestyle-limiting angina despiteoptimal medical therapy, high-risk criteria on noninvasivestress testing, or successful resuscitation from sudden car-diac death, coronary angiography may be useful.

An echocardiogram would be useful to evaluate leftventricular systolic function (ejection fraction), assess forwall motion abnormalities (that may indicate a previousmyocardial infarction), and exclude significant valvularheart disease. A normal echocardiogram, however, wouldnot exclude the presence of underlying CAD and thereforewould not be the best test to establish a diagnosis in thispatient.

K E Y P O I N T

• For a patient who is able to exercise and has anormal baseline electrocardiogram, an exercisetreadmill stress test is the most appropriatenoninvasive study to evaluate for coronaryartery disease.

BibliographyChou TM, Amidon TM. Evaluating coronary artery disease noninva-

sively–which test for whom? West J Med. 1994;161(2):173-180.[PMID: 7941543]

Item 2 Answer: AEducational Objective: Manage elevated choles-terol level in a patient with diabetes mellitus.

The most appropriate modification of this patient’s treatmentregimen is to increase the statin dose. The National Choles-terol Education Program (NCEP) Adult Treatment Panel IIILDL cholesterol treatment target for all patients at high riskis below 100 mg/dL (2.59 mmol/L). High risk is definedas the presence of coronary heart disease (CHD) or CHDrisk equivalents, which include peripheral arterial disease,abdominal aortic aneurysm, carotid artery disease, transientischemic attacks or stroke of carotid origin or 50% obstruc-tion of a carotid artery, diabetes mellitus, and 10-year risk forcardiovascular disease of 20% or greater. For patients in thevery-high-risk category, such as those with coronary arterydisease and diabetes mellitus, as well as in the setting of anacute coronary syndrome, an LDL cholesterol level below 70mg/dL (1.81 mmol/L) is a therapeutic option.

Patients with diabetes show similar relative risk reductionscompared with those without diabetes, but as the absolute riskin these patients is higher, the number needed to treat (to pre-vent a cardiovascular event) is lower. Several studies havedemonstrated the benefits of statin therapy. In ad hoc analysesinvolving patients with diabetes from the Scandinavian Sim-vastatin Survival Study, simvastatin therapy was associated witha 55% reduction in major coronary events. In analyses of the8000 patients in the diabetic subgroup from the Heart Pro-tection Study, there was a 22% reduction (20.2% vs. 25.1%) inmajor vascular events in the group receiving simvastatin.

Statins remain the first-line therapy for the treatmentof hyperlipidemia and for the primary and secondary pre-vention of CHD. Trials of nonstatin drugs in the primaryprevention of CHD have been associated with reductionsin coronary events but not mortality. In this patient, anincrease from a low dose (20 mg) of pravastatin to a mod-erate dose (40 mg) is the best approach, both in terms oftolerability and effectiveness.

K E Y P O I N T

• The presence of diabetes mellitus is considereda cardiovascular disease risk equivalent in theassessment of cardiovascular risk.

BibliographyRydén L, Standl E, Bartnik M, et al; Task Force on Diabetes and Car-

diovascular Diseases of the European Society of Cardiology (ESC);European Association for the Study of Diabetes (EASD). Guide-lines on diabetes, pre-diabetes, and cardiovascular diseases: execu-tive summary. The Task Force on Diabetes and Cardiovascular Dis-eases of the European Society of Cardiology (ESC) and of theEuropean Association for the Study of Diabetes (EASD). Eur HeartJ. 2007;28(1):88-136. [PMID: 17220161]

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