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Pathology of the Heart 4/22/09 Dr. Winokur
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The Heart as a Pump Pump parts - Cardiac equivalent
Powersource - Blood supply/oxygen Motor - Myocardium Pump with valves - Cardiac valves Control circuit - Conducting system and neurohumoral control
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Pathologic consequences of pump failure
Blood vessels/Oxygen supply - Ischemic heart disease Myocardium - Cardiomyopathy Valves - Inadequate forward flow/Increased back pressure Conducting system - Arrythmias Neurohumoral system - Inadequate compensation for pathologic processes Failure of any of these components can result in inadequate oxygen delivery to peripheral tissues otherwise known as HEART FAILURE
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Case 1 65 yo man with past medical history significant for diabetes mellitus, hypertension, and hypercholesterolemia presents to the ED complaining of crushing substernal chest pain that radiates to the jaw.
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Physical Exam EKG Labs Tachycardia Diaphoretic Abnormal with Q-wave
Elevated troponin I and CK-MB
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DIAGNOSIS? Myocardial infarct
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Ischemic heart disease
Mismatch between oxygen supply and demand Typically results from atherosclerotic narrowing of the coronary arteries Other causes include vasculitis, intramyocardial coronary arteries Can result from unusual oxygen demand Thyrotoxicosis Tachycardia
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Presentation of ischemic heart disease
Chest pain with exertion - Angina pectoris Myocardial infarct Many MI s are the initial presentation Sudden death Cardiac failure-chronic disease Note that in women the presentation is frequently atypical ie decreased exercise tolerance rather than pain with exercise
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Epidemiology Typically occurs in men in their older than 60 and in women about 10 years later Risk factors Hyperlipidemia, especially LDL cholesterol High blood pressure Smoking Diabetes
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Coronary pathology of MI
Coronary arteries are partially to completely occluded by atherosclerosis Significant changes of blood flow occur with >75% narrowing of the arteries Plaques rupture resulting in thrombosis Complete occlusion Myocardial necrosis
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Pathology of myocardial infarction
Early changes occur in the 1st .5-1hr and are seen only at the ultrastructural level Early intervention with thrombolytics or angioplasty can save myocardium Over the ensuing half day irreversible necrosis occurs and can be identified by the light microscope By 24 hours there is clear necrosis and neutrophils begin to invade the infarct This is the first time the infarct is identifiable by gross examination.
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Serum enzymes in MI 72 hrs 24 hrs 48 hrs Troponin CK-MB
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Over the ensuing week the infarct is overrun by neutrophils, then the dead tissue is removed by macrophages The infarct is repaired by granulation tissue followed by fibrosis
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Complications of myocardial infarction
Cardiac arrhythmias Cardiac failure/cardiogenic shock Extension of infarct Thromboembolism Ventricular rupture Papillary muscle rupture Ventricular aneurysm Post MI pericarditis
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Other presentations of ischemic heart disease
Sudden death Frequently cause cannot be determined but there is a strong association with coronary atherosclerosis Chronic ischemia with heart failure Poor oxygenation results in myocardial atrophy and some myocyte loss resulting in poor cardiac performance Revascularization can help in large vessel disease
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Myocarditis/Myocardial Inflammation
Can be caused by infections Viral Bacterial Fungal May be secondary to infections resulting in an autoimmune inflammation of the myocardium Post viral Post bacterial- Rheumatic heart disease Autoimmune diseases-Lupus
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Motor failure/cardiomyopathy
The heart muscle can fail from primary or secondary causes Primary dysfunction is related to genetic diseases Secondary cardiomyopathies result from toxic, infectious and degenerative diseases
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Three types of cardiomyopathy
Cardiomyopathy is a primary disease of the heart muscle (excludes myocardial changes resulting from hypertension, valvular disease, ischemic disease and pericardial disease) Dilated The ventricular chamber is dilated and the myocardium is modestly thickened Hypertrophic The myocardium is markedly thickened especially the septum Restrictive The myocardium is can be of normal thickness but it is stiff and unable to relax in diastole
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Dilated cardiomyopathy
Causes include genetic, viral/autoimmune and toxic insults Many cases are idiopathic and are thought to be secondary to previous viral infections Alcohol is the most common toxic cause Patients frequently present in heart failure with huge hearts and poor contractility The prognosis of this condition is poor 5 year survival is <50% Patients die from heart failure and arrhythmias
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Hypertrophic cardiomyopathy
Primarily a genetic disease and may persist subclinically Patients present with dyspnea, syncope or sometimes with sudden death Echocardiography is the best diagnostic modality but may be detected on ECG and physical exam Pathology- marked hypertrophy of the left ventricle with septal thickening Septal hypertrophy causes outflow tract obstruction These patients can frequently be successfully managed
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Restrictive cardiomyopathy
Fibrosis or infiltration of the myocardium causes marked stiffness and poor relaxation Causes include fibrosis, amyloid deposition, sarcoidosis, hemochromatosis, storage diseases Cardiac filling is impaired and patients present with diastolic heart failure Poor prognosis unless the underlying cause can be treated
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Cardiac hypertrophy There are two patterns of hypertrophy
Concentric hypertrophy Caused by pressure overload ie hypertension, valvular stenosis Results in marked wall thickening with a smaller chamber Good contractility but poor relaxation Eccentric hypertrophy Caused by volume overload ie valve regurgitation or septal defects Results in wall thickening with dilation of the chamber Good contractility and acceptable relaxation
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Cell length New sarcomeres added lengthwise
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Cor Pulmonale Right sided hypertrophy secondary to pulmonary hypertension followed by dilatation and right heart failure Acute - 2° to pulmonary thromboembolism Chronic - Secondary to primary pulmonary hypertension or chronic obstructive pulmonary disease (COPD)
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Valvular disease All of the four valves are subject to disease
Left sided valves are more commonly affected and produce more problems Diseases include degenerative, infectious and autoimmune
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Infectious endocarditis
Damage to the valve surface provides a site for bacterial adherence Chronic valve disease Prosthetic valves Bacteria in the blood stream adhere to the surface and proliferate Bacteria can be derived from oral cavity, other bacterial infections or the GI tract during procedures Bacteria can be injected by IV drug abusers and result in right sided endocarditis
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Infection can be indolent growth of bacterial colonies or highly destructive infection with valve destruction and incompetence Strep viridans typically results in an indolent infection Staph aureus is highly destructive Prosthetic valves are frequently infected by coagulase negative Staph species Aggressive and indolent bacteria can embolize and produce peripheral abcesses including the CNS
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Non bacterial thrombotic endocarditis (NBTE)
Small vegetations usually occuring at the valve closure lines Associated with other diseases especially adenocarcinomas and cachexia Usually asymptomatic and discovered incidentally Can undergo bacterial colonization leading to infectious endocarditis
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Rheumatic fever An acute, immunologically mediated, multisystem inflammatory disease that follows an untreated episode of group A streptococcal pharyngitis after an interval of a few weeks Relatively rare in developed countries Peak incidence is 5-15 yo. Inflammatory infiltrates may occur in a wide range of sites including the heart
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Acute Rheumatic Carditis
Inflammatory changes in all three layers of the heart Pericardium – fibrinous pericarditis; effusions Myocardium – heart failure Endocardium – valvular damage
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Rheumatic endocarditis
Repeated episodes of damage eventually damage the valve and associated apparatus Results in valve stenosis with or without regurgitation Mitral and aortic valves are most affected 99% of mitral stenosis is secondary to rhd Virtually the only cause of simultaneous mitral and aortic stenosis Can be the substrate for infectious endocarditis
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Calcific aortic stenosis
Most common cause of aortic stenosis Irregular calcium deposits behind valve cusps Congenitally bicuspid valves Normal valves as an age-related degenerative change
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Mitral valve prolapse Most frequent valvular lesion (7%) Young women
Stretching of posterior mitral valve leaflet Systolic murmur with midsystolic click Can result in mitral insufficiency Predisposes to infective endocarditis
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Arrythmias Normal cardiac automaticity requires coordination of the SA node, AV node and the intervening myocardium Disruption of any players can result in arrythmias Common causes of arrythmias include infarcts, alter chamber geometry (dilation and hypertrophy), viral infections affecting the pacemakers
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Congenital Heart Disease
Left to Right Shunts ASD VSD PDA Right to Left Shunts Tetralogy of Fallot Transposition of the Great Arteries Obstruction Coarctation of the aorta
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Right to Left Shunts Cyanosis at or near birth
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Pericardial Diseases Pericarditis – inflammation of pericardium
Primary – viruses Secondary Acute MI, cardiac surgery, uremia, acute rheumatic fever Pericardial Effusions Serous – heart failure Serosanguinous – trauma, malignancy Chylous Hemopericardium Cardiac tamponade
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Pericarditis
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Cardiac Tumors Metastatic neoplasms Primary neoplasms Lung and breast
Myxomas Cardiac rhabdomyomas
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Myxoma
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