Diseases of the Heart Chapter 11

A. Angina Definition intermittent, transient, reversible ischemia Types Stable: periodic pain caused by exertion and stress Unstable: crescendo angina, pre-infarction event. More pain that lasts longer and needs less stimuli.

I. Congestive Heart Failure - symptoms: dsypnea, edema, orthopnea

Left ventricular failure : From: hypertension, valve disease, ischemic heart disease, myocardial disease Results: pulmonary congestion B. Myocardial Infarction: an area of myocardial necrosis. Stats Incidence: . 1-1.5m/year, 1/3 fatal. 45-55 years peak for males, 4-5X higher incidence than women under age 80. Costs: Venous congestion pulmonary congestion (dyspnea and orthopnea) anasarca/edema renin-angiotensin activation Heart failure cells hemosiderin laden macrophages in lung $5 billon/year Risks same as athersclerosis Features (See Table 11-2) gross vs. histologic Location of MI Coronary arteries left descending - 40-50% right - 30-40% left circumflex - 15-20%

Right ventricular failure: From: left sided failure, cor pulmonale, congenital heart disease Results: anasarca/edema

II. Ischemic Heart Disease Etiology atherosclerosis of coronary arteries Most at risk atherosclerosis risk factors (Chapter 10) Acute disease 50-70% occlusion with a spasm or thrombus Chronic disease gradual decreasing lumen diameter

Transmural vs. subendocardium transmural - through-and-through subendocardial - inner 1/3 of wall Complications weak wall (especially if papillary muscle tears off wall) 5% get wall rupture, 95% have arrhythmias, 60% have pulmonary edema, 10 % go into shock, and 15-50% have thromboembolism

Outcomes 10-20% uncomplicated recovery 25% die (cardiogenic shock) 80% will have one or more complications 10-25% will be asymptomatic Testing Enzymes are released into the circulation from dying myocardial cells. Creatine kinase: found in myocardium, brain and skeletal muscle. The CK-MB dimer found mainly in myocardium. Total CK activity begins to rise 2-4 hours of heart attack and peaks at 24 hours. Although a good measure of acute myocardial necrosis, CK levels are not specific to heart damage.

IV. Cor Pulmonale (See Table 11-3) Etiology pulmonary disease -> heart disease (right side), pulmonary hypertension right ventricle becomes dilated and enlarged. Acute pulmonary thrombosis (greater than 50% occlusion) Chronic COPD, pulmonary interstitial fibrosis, cystic fibrosis, obesity, hypoxia Outcome is right sided congestive heart failure.

Troponin I: More specific serum marker than CK-MB. In patients with unstable angina, elevated levels may predict an MI.

V. Valvular Diseases (See Table 11-4) Rheumatic fever Etiology group A, !"#$-hemolytic Strep (pyogenes) 5-15 year olds at most risk, antibodies to "M" protein cross reacts with heart muscle. 3% with strep throat get rheumatic fever if untreated. An immunologically mediated disease. Lesions Ashoff bodies Fig. 11-11. a granulomatous focus, fibrinoid necrosis, giant cells Valves mitral 95%, mitral and aortic about 25% of the time

C. Sudden Death : Coronary disease atherosclerosis and anomalies Myocardial disease cardiac myopathies Valvular disease mitral valve prolapse, aortic stenosis, SBE

Symptoms migratory arthritis (large joints) subcutaneous nodules (histologically rheumatoid nodules) Outcomes Chronic disease female more often than males valve stenosis and vegetations ("fish mouth"), regurgitation, heart failure

III. Hypertensive Heart Disease Classic model concentric left ventricular hypertrophy (> 2cm thick) with a history of hypertension Essentially, the cardiac manifestation of hypertension.

Predisposes to Infective endocarditis. Dramatic increase in risk for SBE Infective endocarditis - accounts for 10-20% of valve replacements/year Acute: commonly associated with Staph. Subacute: $%hemolytic Strep (viridans)

VII.Congenital Heart Disease (See Table 11-1) Etiology genetics - a few percent (e.g.Turner Syndrome) idiopathic - about 90%. Since the decline in incidence of rheumatic heart disease, it is the most common cause of heart disease in children. These 3 defects cause left-toright shunts. Cyanosis develops sometime after birth. 1. ASD (Atrial Septal Defect) develops 4-6 week gestation, most common congenital defect diagnosed in adults. Mitral Valve Prolapse: most common cause of mitral valve regurgitation. Population: 3-5% of the population. 20-40 year olds. Most people asymptomatic.

2. VSD (Ventricular Septal Defect) develops 4-8 weeks gestation, most at base of heart. May close spontaneously. The most common congenital heart defect but often goes undiagnosed.

VI. Myocardial Disease Myopathies: 3 forms. Dilated mostly sporadic, ages 20-60, alcohol abuse, viruses. Results in ineffective contractions. Clinical symptoms of congestive heart failure. Most common myopathy.

3. PDA (Patent Ductus Arteriosus) A normal communication between the pulmonary artery and aorta during fetal development. Normally closes 1-2 days after birth (fibrosis into a "ligament'), accounts for only ~10% of defects. Predisposes to infective endocarditis. L to R shunt causes pulmonary hypertension; therefore, congestive heart failure. Small ones cause no problems.

Hypertrophic Hypertrophy of left ventricle. Unable to fill left ventricle during diastole. Therefore, decreased outflow during systole. Restrictive decreases ventricular compliance (elasticity) Least common myopathy worldwide, produces fibrosis of the heart.

Right-to-left shunt - cyanotic from birth Tetralogy of Fallot (See Figure 11-4) ~ 5% of congenital defects. Most common cause of cyanotic congenital heart disease. 4 components: (1. VSD, 2. dextraposed aorta, 3. pulmonary stenosis (from obstruction of pulmonary artery), and 4. right ventricular hypertrophy) People at increased risk for developing infective endocarditis.