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Disorders of Cardiac Function. Cardiac Pathology Outline. Blood Vessels Heart I Heart Failure Congenital Heart Disease Ischemic Heart Disease. Ischemic Heart Disease. Myocardial perfusion can ’ t meet demand
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Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure • Congenital Heart Disease • Ischemic Heart Disease
Ischemic Heart Disease • Myocardial perfusion can’t meet demand • Usually caused by decreased coronary artery blood flow (“coronary artery disease”) • Four syndromes: • angina pectoris • acute MI • chronic IHD • sudden cardiac death
Angina Pectoris • Intermittent chest pain caused by transient, reversible ischemia • Typical (stable) angina • pain on exertion • fixed narrowing of coronary artery • Prinzmetal (variant) angina • pain at rest • coronary artery spasm of unknown etiology • Unstable (pre-infarction) angina • increasing pain with less exertion • plaque disruption and thrombosis
Myocardial Infarction • Necrosis of heart muscle caused by ischemia • 1.5 million people get MIs each year • Most due to acute coronary artery thrombosis • sudden plaque disruption • platelets adhere • coagulation cascade activated • thrombus occludes lumen within minutes • irreversible injury/cell death in 20-40 minutes • Prompt reperfusion can salvage myocardium
Manifestations of ST-Segment Elevation Acute Myocardial Infarction • Abrupt onset • Severe and crushing pain, usually substernal, radiating to the left arm, neck, or jaw • Gastrointestinal complaints (nausea and vomiting) • Complaints of fatigue and weakness • Tachycardia, anxiety, restlessness, feelings of doom • Pale, cool, and moist skin
ST Segment • Abnormalities of the ST segment and the T wave represent abnormalities of ventricular repolarization.
Factors Determining the Extent of an Infarct • Location and extent of occlusion • Amount of heart tissue supplied by the vessel • Duration of the occlusion • Metabolic needs of the affected tissue • Extent of collateral circulation • Heart rate, blood pressure, and cardiac rhythm
Myocardial Infarction • Clinical features • Severe, crushing chest pain ± radiation • Not relieved by nitroglycerin, rest • Sweating, nausea, dyspnea • Sometimes no symptoms • Laboratory evaluation • Troponins increase within 2-4 hours, remain elevated for a week. • CK-MB increases within 2-4 hours, returns to normal within 72 hours.
Myocardial Infarction • Complications • contractile dysfunction • arrhythmias • rupture • chronic progressive heart failure • Prognosis • depends on remaining function and perfusion • overall 1 year mortality: 30% • 3-4% mortality per year thereafter
Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure • Congenital Heart Disease • Ischemic Heart Disease • Hypertensive Heart Disease
Hypertensive Heart Disease • Can affect either L or R ventricle • Corpulmonale is RV enlargement due to pulmonary hypertension caused by primary lung disorders • Result: myocyte hypertrophy • Reasons for heart failure in hypertension are poorly understood
Cardiac Pathology Outline • Blood Vessels • Heart I • Heart II
Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure • Congenital Heart Disease • Ischemic Heart Disease • Hypertensive Heart Disease
Cardiac Pathology Outline • Blood Vessels • Heart I • Heart II • Valvular Heart Disease • Cardiomyopathies • Pericardial Disease • Tumors
Cardiac Pathology Outline • Blood Vessels • Heart I • Heart II • Valvular Heart Disease
Valvular Heart Disease • Stenosis and/or insufficiency • Stenosis: failure to open • Insufficiency: failure to close • Murmurs • Outcome depends on severity and speed of development
Calcific Aortic Stenosis • Part of aging process • Can occur on normal or congenitally bicuspid valves • Results in increased LV pressure, LV hypertrophy, and relative ischemia • Angina, CHF, or fainting
Calcific aortic stenosis: normal (L) and bicuspid (R) valves
Mitral Valve Prolapse • Common (5% of adults in US, F>M) • Ballooning of mitral leaflets • Myxoid/mucoid change within leaflet • Pathogenesis unknown • Most patients asymptomatic
Rheumatic Valvular Disease • Rheumatic fever: systemic inflammatory disease occurring a few weeks after strep throat • Valves (esp. mitral) become scarred • Consequence: stenosis (± regurgitation)
Rheumatic Fever • Body makes antibody to strep bug that cross-reacts with antigens in heart and joints • 2-3 weeks after strep throat, patient gets: • migratory polyarthritis • pericardial friction rub, arrhythmias • Chronic disease can reappear decades later • mitral stenosis, left atrial enlargement, thrombi • increased risk of infective endocarditis • Long term prognosis variable
Strep throat Antibody production Antibody cross-reaction with heart vegetations Aschoff body pericarditis
Infective Endocarditis • Microbial invasion of heart valves, endocardium • Acute endocarditis • highly virulent bug attacks normal valve • half of patients dead within days to weeks • Subacuteendocarditis • low virulence bug colonizes abnormal valve • slow onset, long course, most recover • Symptoms: fever, flu-like symptoms • Complications: septicemia, arrhythmias, renal failure, systemic emboli
Infective Endocarditis • Invasion of the heart valves and endocardium by a microbial agent • Formation of bulky, friable vegetations and destruction of underlying cardiac tissues • Systemic manifestations • Streptocococci • Enterococci • Haemophilussp. • Actinobacillusactinomycetemcomitans • Cardiobacteriumhominis • Eikenellacorrodens • Kingellakingae • Gram-negative bacilli • Fungi
Cardiac Pathology Outline • Blood Vessels • Heart I • Heart II • Valvular Heart Disease • Cardiomyopathies
Myocardial Diseases • Myocarditis • Inflammation of the heart muscle and conduction system without evidence of myocardial infarction • Primary cardiomyopathies • Heart muscle diseases of unknown origin • Secondary cardiomyopathies • Conditions in which the cardiac abnormality results from another cardiovascular disease, such as myocardial infarction
Cardiomyopathies • Diverse group of disorders in which there is intrinsic myocardial dysfunction • Lots of causes; some idiopathic • Three groups • dilated cardiomyopathy • hypertrophic cardiomyopathy • restrictive cardiomyopathy
Dilated Cardiomyopathy • Heart dilates, enlarges, and can’t contract well • Causes • viral • alcohol/toxin • genetic abnormalities • peripartum • Slowly progressing CHF • 70% of patients dead within 5 years
Restrictive Cardiomyopathy • Heart wall is stiff; can’t fill during diastole • Cause: Idiopathic or secondary to systemic disease (amyloidosis, hemochromatosis, sarcoidosis) • Symptoms: shortness of breath, peripheral edema • Treatment: not often helpful • 70% of patients dead within 5 years
Hypertrophic Cardiomyopathy • Massively hypertrophied L ventricle can’t fill • Cause: mutation in a sarcomereprotein gene • Symptoms: atrial fibrillation, CHF, arrhythmia, sudden death • Treatment: drugs to promote ventricular relaxation or surgical excision of part of septum • Prognosis: about 4% of patients die each year
Treatment of Cardiomyopathy • Treatment depends on the type • Medication • Implanted pacemakers • Defribillators • Ventricular assist devices • Ablation • The goal of treatment is often symptom relief, and some patients may eventually require a heart transplant.
Cardiac Pathology Outline • Blood Vessels • Heart I • Heart II • Valvular Heart Disease • Cardiomyopathies • Pericardial Disease
Pericardial Disease • Pericarditis • secondary (MI, radiation, pneumonia) or primary (infectious) • atypical chest pain • dangers: tamponade, chronic fibrosis • Pericardial effusion • serous (CHF), serosanguinous (aortic dissection), chylous (lymphatic obstruction) • outcome depends on stretchiness of pericardial sac • slow = asymptomatic; sudden = catastrophic