Normal Human Heart Weight 250-300 F. 300-350 gm M. Ventricular thickness: Rt 0.3-0.5 cm; Lt 1.3-1.5 cm. Increased thickness: hypertrophy. Enlarged chamber: dilatation. Cardiomegaly: increased heart size. Structure: three layers; Most important is myocardium composed of branching and anastomosing cardiac muscle. Cardiac muscle cell: Sarcolema, T tubules for impulse conduction, Sarcoplasmic reticulum, contractile elements, mitochondria, nucleus.
Normal Heart Structure Mitochondria are numerous. Sarcomere is the functional unit 1.6- 2.2 um, Z line demarcates the sarcomere. Cardiac muscle is more complex. Atrial muscle cells contain granules containing atrial natriuretic peptide- hypertension and CCF. Intercalated discs join individual myocytes. Gap junctions: clusters of plasma membrane channels that directly connect the cytoplasmic components of neighboring cells, facilitate synchronous myocyte contraction. Abnormalities in the spatial distribution of gap junctions and their respective proteins in IHD and myocardial disease contributes to electromechanical dysfunction called arrhythmias. Specialized excitatory and conducting myocytes are involved in regulation of rate and rhythm of the heart. AV node, bundle of his, Lt and Rt branches.
Blood Supply of Heart Heart is supplied by three coronary arteries. Rt coronary artery, Rt aortic sinus supplies Rt atrium and ventricle, interatrial septum, SA and AV nodes, part of Lt atrium and Lt ventricle. Lt coronary artery, Lt aortic sinus supplies Lt ventricle and atrium, interventricular septum, AV bundles. Epicardial coronary arteries. Blood supply is maximum during ventricular diastole. Although coronaries are end arteries, collateral exist between them which get functional if one of them is narrowed with resulting hypoperfusion.
Effects of Aging on Heart Increased Lt atrial chamber size. Decreased Lt ventricle cavity size. Sigmoid shape of interventricular septum. Calcification of aortic and mitral valves. Thickening of leaflets. Tortuosities of coronary arteries, increased lumina, calcifications and atherosclerotic plaques. Increased myocardial mass. Increased subepicardial fat. Brown atrophy. Lipofuscin deposition. Basophilic degeneration. Decreased myocytes, increased collagen.
Aortic Changes Dilated ascending aorta and rightward shift Tortuous thoracic aorta Elastic tissue fragmentation and deposition of collagen Atherosclerosis
Normal Myocardium Microscopic View Branching and anastomosing striated muscle fibres
Cardiac Dysfunction Failure of pump action. Obstruction to outflow. Regurgitation of the pumped blood. Cardiac conduction defects. Disruption of circulatory system.
Heart Failure Heart is unable to pump blood at a rate required for tissue metabolism. Compensatory mechanisms are frank starling phenomenon, hypertrophy, increased heart rate by norepinephrines, activation of renin angiotensin aldosterone system, release of atrial natriuretic peptide. Most instances of heart failure are consequences of progressive deterioration of myocardial contractile function as in IHD, volume overload or cardiomyopathies. Causes of heart failure are hypertension, IHD and pericarditis. Congestive heart failure; Diminished cardiac out put and damming back of blood in the venous system. In CCF, the morphologic changes are often distant from heart produced by the hypoxic and congestive effects of the failing circulation.
Failure and Cardiac Hypertrophy Initially both left and right heart failure may produce independent signs and symptoms, but as heart is a close circuit, one sided failure produces burden on other, ultimately leading to failure of both units. Causes are chronic hypertension and aortic stenosis. Thickness of the myocardium is increased and cavity decreases. Regurgitation: both hypertrophy and dilatation occurs. Total weight of the heart may be increased up to 3 times of normal. Hypertrophy may initially compensate for the decreased function, but of course, the hypertrophied heart is not normal because of deleterious structural, biochemical and molecular alterations in the myocardium. Sustained hypertrophy evolves into failure.
Right Sided Heart Failure Usually secondary consequence. Increased burden on right heart. Pure right failures occurs in severe pulmonary hypertension- cor pulmonale. Right ventricle hypertrophied and dilated. Findings are: 1- minimal pulmonary congestion, 2- engorged systemic and portal veins. Liver shows increased size and weight- congestive hepatomegaly.Liver lobules show red centres surrounded by pale peripheral regions.Hypoxia may produce centrilobular necrosis.Sinusoids are congested.Cardiac cirrhosis.
Rt Heart FailureCongestive splenomegaly, marked sinusoidal dilatation.Chronic intestinal oedema may result in malabsorption syndrome. Kidneys show congestion, fluid retention. Peripheral oedema and azotemia as terminal event. Brain shows hypoxia and increased congestion. Pleural and pericardial fluid accumulation. Dependent oedema and anasarca.
Left Sided Heart Failure Causes are IHD, hypertension, aortic and mitral valve disease, myocardial diseases. There is progressive damming of blood in the pulmonary circulation and diminished peripheral pressure and flow. Findings depend on cause; Left ventricle may hypertrophied and/or dilated, fibrosis of myocardium, left atrial enlargement and fibrillation, thrombosis, congested lungs which appear heavy and wet, kidneys and brain are congested due to retrograde pressure.
Microscopic findings: perivascular and interstitial transudates, Kerley B lines in lungs due to interlobular fluid. Progressive oedematous widening of alveolar septa, accumulation of fluid in the alveoli and later hemosiderin laden macrophages called heart failure cells, dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, cough with expectoration. Kidney activate renin angiotensin aldosterone mechanism due to decreased perfusion, retention of sodium and water, blood volume increases which aggravates pulmonary oedema, pre renal azotemia. Brain shows hypoxic encephalopathy.
Ischemic Heart Disease Results from imbalance between perfusion and demand; Result in decreased oxygen and nutrition supply and waste removal. Isolated hypoxemia e.g. cyanosis, congenital disease, anemia are not so damaging to heart as IHD. Aetiology: coronary obstruction most likely due to atherosclerosis, symptomatic after long periods. Aggravating factors: hypertrophy, low BP, hypoxemia, increased heart rate. Onset of symptoms not predictable on the basis of severity of atherosclerotic narrowing. Young man with modest narrowing may land with acute myocardial infarction. Erosions, ulcerations, fissuring, rupture, deep hemorrhage and superimposed thrombosis.
Syndromes of Myocardial Ischemia Myocardial infarction: death of myocardium Angina pectoris: stable, Prinzmetal, unstable Chronic ischemia leading to heart failure Sudden cardiac death
Epidemiology Leading cause of death in men and women all over the world. Recent decrease in death incidence may be due to preventive measures, therapeutic measures, various medications, angioplasty, coronary by pass operations, control of diabetes, administration of post menopausal estrogens in females, lipid lowering agents, aspirin and antioxidants.
Pathogenesis Vast majority result from atherosclerotic narrowing along with other interactions including vasospasms, thrombosis and platelet aggregates. More than 90% symptomatic cases show at least.75 % reduction in the coronary blood flow. Usually first a few cm (epicardial parts) of two or all the three vessels are significantly narrowed. In addition to fixed obstruction, plaque change may precipitate the onset of sudden ischemia. Vasoconstriction at the site of coronary obstruction may be stimulated by adrenergic agonists, decreased nitric oxide by endothelial cells and mediators from mast cells.
Angina Pectoris It is a symptom complex of IHD characterized by paroxysmal and usually by recurrent attacks of retrosternal chest pain precipitated by physical exertion, emotional excitement, relieved by rest or vasodilators like nitroglycerin.
Myocardial Infarction It is the most important form of IHD. Transmural vs. Subendocardial infarction. Most are transmural resulting from chronic coronary atherosclerosis with superimposed thrombosis. Subendocardium is the most vulnerable part. Transmural also starts as subendocardial.
Incidence and Risk Factors Increasing age, hypertension, smoking, diabetes, hypercholesterolemia. Males at any age are at increased risk. No race differences. In post menopausal women estrogen therapy may decrease the incidence.
Pathogenesis Coronary artery occlusion. Atherosclerosis. Disruption manifested by hemorrhage, erosion or ulcerations. Subendothelial exposure of collagen and necrotic plaque contents, platelet adhesion, aggregation, activation and release of potent aggregators. Activation of coagulation pathways. Thrombus suddenly occludes the lumen of coronary artery. In 10%, vasospasm, emboli, vasculitis, hemoglobinopathies and other diseases of intramural portions of coronaries.
Myocardial Response Coronary blood flow occlusion results in profound functional, biochemical and morphological consequences. Occlusion of a major coronary artery results in ischemia and cell death in the anatomic region supplied by the vessel esp. At risk is the subendothelial myocardium. Outcome depends on the severity and duration of flow deprivation. Within 60 sec, profound loss of contractility occurs. Biochemical changes; Cessation of aerobic glycolysis, decreased ATP and accumulation of lactic acid. Early ultrastructural changes following ischemia are reversible in 20 to 40 minutes. Myocardial ischemia also contributes to arrhythmias. Sudden death in cardiac ischemia may be due to ventricular fibrillation.
Time of Onset of Events in Ischemia Onset of ATP depletion occurs in seconds. Loss of contractility within 2 min. Marked reduction of ATP occurs in 10 to 40 min. Irreversible cell injury occurs in 20-40 min. Microvascular injury follows in more than 60 min.
Morphological Changes. Coagulative necrosis follows prolonged myocardial ischemia 6-12 hours. All transmural infarcts involve Lt ventricle and part of septum; In only 3 % cases Rt ventricle alone is involved. Transmural infarcts encompass the entire perfusion zone of the occluded artery with preservation of 0.1 cm of endocardial myocardium.
Macroscopic or Naked Eye Changes. 12-24 hours: dark mottling with nuclear pyknosis. 1-3 days: mottling with yellow tan infarct in the centre. 3-7 days: hyperemic border, central yellow tan softening. 7-10 days: yellow tan infarct, red tan margins. 2-8 weeks: Grey white scar. Areas of ischemic damage undergo a progressive sequence of changes consisting of coagulative necrosis followed by inflammation and repair. At autopsy the gross changes may be unapparent in 2-3 hours, so tissue slices are immersed in triphenyltetrazolium chloride which imparts, brick red colour to the surrounding viable myocardium with unstained infarct area.
Microscopic Changes. Routine tissue stains show detectable coagulative necrosis in 4-12 hours. Surrounding myocardial cells may show reversible cell injury especially in the subendocardial regions. The necrotic muscle elicits acute inflammation in 2-3 days. Macrophages remove the necrotic debris. Then damaged area is progressively replaced by ingrowth of highly vascularized granulation tissue. Fibrous tissue replaces the granulation tissue in 2-4 weeks time. Larger lesion may take longer times for final healing.
Coronary Artery Thrombosis With Cholesterol Clefts
Atheroma With Cholesterol Clefts and FoamyMacrophages
Atheroma Showing Calcification and Marked LumenNarrowing
Recent Myocardial Infarction Showing Hemorrhage andLoss of Nuclei and Contraction Bands
Microscopic Appearance of 3-4 Days Old InfarctShowing Necrosis and Acute Inflammation
Old Myocardial Infarction Showing Scar Formation
Old Myocardial Infarction Showing Scar Microscopic
Infarct Modification After Reperfusion Thrombolytic therapy, angioplasty or coronary bypass. Streptokinase or tissue type plasminogen activators are used as thrombolytic agents, which activate the human thrombolytic system. The artery may get recanalized partly thereby limiting the infarct size, with consequent improvement in both short and long term function and survival. To achieve the purpose, the time is very crucial. Reperfusion within 15-20 min can prevent necrosis but if longer times elapse, necrosis cannot be prevented but viable myocytes can be salvaged.
. A complete infarct after reperfusion may be hemorrhagic due to leaky vessels. Infarcted myocardium after reperfusion, microscopically shows necrosis with contraction bands which are intensely eosinophilic transverse bands composed of closely packed hypercontracted sarcomeres. After reperfusion, there is exaggerated contraction of myofibrils. Reperfusion injury may also be initiated by oxygen free radicals.Although most of the viable myocardium at the time of reperfusion ultimately recovers, some sort of biochemical and functional defect may remain for several days so called prolonged post ischemic ventricular dysfunction.Chronic silent myocardial ischemia may prevent the heart from a greater ischemic attack by pre conditioning.
Signs and Symptoms Sudden severe retrosternal pain, sweating, weak rapid pulse, breathlessness, may be asymptomatic in 15% cases, esp. among diabetics and very old persons.. Laboratory findings are based on measurements of various macromolecules released in to the circulation from injured myocytes. Creatine kinase (CK) is an enzymes present in myocardium, skeletal muscle and brain. Its isoenzymes are CK MM, CK BB and CK MB. CK MB is concentrated in the myocardium. Total CK levels begins to rise within first 2-4 hours, peak at 18 and begin to fall after 72 hours time after onset of acute MI. Measurement of CK MB activity is more specific because, CK may also come from skeletal muscle injury.
Clinical Features Cont. Other laboratory investigations include measurement of AST and LDH activities. LDH is released more slowly; Therefore it may not be as useful as early markers of acute attack. Another cardiac specific marker is estimation of protein troponins (troponin 1 and troponin T) which are not detectable normally. After acute MI, levels are detectable at the same time as CK MB. The levels remain elevated for 7-10 days. Other diagnostic tools include electrocardiography, radionucleotide angiography, perfusion scintigraphy and MRI.
Complications of MI Death rate from acute MI has decreased from 30 to 15 % on accounts of impressive management and reperfusion therapy. Half of these deaths occur within 1 hour, and these individuals never reach the hospital. Factors associated with poor prognosis include; old age,female gender, diabetes and history of previous attacks of MI. Complications include; Cardiogenic shock: have 70% mortality. Arrhythmias: bradycardia, tachycardia, ventricular fibrillation and asystole.
Complications Cont. Myocardial Rupture; of wall and papillary muscle and rupture of septum. Pericarditis: fibrinous or fibrinohemorrhagic develops after 2-3 days of transmural infarct which is self limited. Right ventricular infarction leads to serious functional complications; although pure right sided disease is rare. Infarct extension. Infarct expansion. Mural thrombus: due to endocardial injury and loss of myocardial contractility and stasis.
Complications Ventricular aneurysms: late complication. Papillary muscle dysfunction: mitral regurgitation. Progressive heart failure: Prognosis and development of complications depends on: infarct size and transmural extent. Large transmural infarcts develop cardiogenic shock, arrhythmias and congestive cardiac failure. Anterior transmural infarcts develop rupture, expansion, mural thrombi and aneurysms; thus have the poor prognosis. Posterior transmural infarcts can be complicated by conduction defects and right ventricular failure.
Long Term Prognosis Depends on residual left ventricular function and extent of coronary obstruction in the viable myocardium. The overall total mortality is around 30% within one year; 3-4% mortality among the survivors with each passing year. Attempts to prevent the mortality among such persons is called secondary prevention.
Chronic Ischemic Heart Disease Mostly elderly people that develop progressive heart failure following ischemic damage. Usually constitutes post infarction cardiac decompensation; In other cases severe obstructive coronary disease may be present without acute or healed infarction but with diffuse myocardial dysfunction. Congestive cardiomyopathy may be used by clinicians who develop congestive cardiac failure with past episodes of MI or anginal attacks.
Sudden Cardiac Death Defined as unexpected death from cardiac causes early within 1 hour after or without the onset of symptoms. Non atherosclerotic causes include: congenital structural abnormalities, aortic valve stenosis, prolapse of mitral valve, myocarditis, hypertrophic cardiomyopathy, pulmonary hypertension, abnormalities in conduction system.
Hypertensive Heart Disease, Left Sided Response of the heart to increased pressure in the systemic circulation. Concentric hypertrophy develops as a compensatory phenomenon which may lead to cardiac dilatation, CCF and other cardiac dysfunctions. Morphology: initially there may be circumferential hypertrophy without increase in heart size, may exceed above 2 cm, weight may increase > 500 gm. Microscopically: increased transverse myocyte diameter, followed by increased size variation and interstitial fibrosis.
Clinical Aspects Compensated hypertension may be asymptomatic, detected only on ECG or echocardiography. At times patient may present with atrial fibrillation or congestive cardiac failure. Other complications include atherosclerosis with associated MI and CVA.
Pulmonary Hypertension Also called cor pulmonale, constitutes right ventricular hypertrophy, dilatation and failure secondary to lung diseases or of pulmonary vasculature. Acute cor pulmonale develops following massive pulmonary embolism. Chronic is secondary to obstruction of pulmonary arteries or arterioles or compression of septal capillaries like in emphysema.
Morphology Acute: marked right ventricular dilatation without hypertrophy. Chronic: ventricular wall thickness may be up to 1 cm. Sometimes there may be tricuspid regurgitation with fibrous thickening of the valve.
Valvular Heart Disease May cause stenosis or incompetence. These abnormalities may be pure or mixed. Defect may involve single valve (isolated disease) or multiple (combined). Functional regurgitation results when ventricle dilates due to any disease. Valvular dysfunction may be slight or severe, that may be rapidly fatal e.G. Infective endocarditis may destroy aortic valve, resulting in rapidly progressing cardiac failure; In contrast, rheumatic heart disease may be well tolerated due to insidious onset. Depending on degree, duration and cause, secondary changes in heart, blood vessels and other organs may develop.
Causes of Acquired Valvular Dysfunctions Mitral stenosis: rheumatic heart disease. Mitral regurgitation. Abnormalities of leaflets and commissures e.g. postinflammatory scarring, infective endocarditis, mitral valve prolapse. Abnormalities of tensor apparatus e.g. Rupture of papillary muscle or of chordae tendineae. Abnormalities of left ventricular cavity and/or annulus e.g. Left ventricle enlargement and calcification of mitral valve. Aortic stenosis. Post inflammatory scarring e.g. Rheumatic heart disease. Senile calcific aortic stenosis.
Causes Cont. Aortic regurgitation Intrinsic valvular disease e.g. Postinflammatory scarring and infective endocarditis Aortic disease e.g. Degenerative aortic dilatation, syphilitic aortitis, ankylosing spondylitis, rheumatoid arthritis and Marfans syndrome.
Calcific Aortic Stenosis Patients present in their 70’s or 80’s, as they had congenitally normal valves. Morphologic hall mark of non rheumatic calcific aortic stenosis is heaped up calcified masses within aortic cusps, preventing the opening of the valve. Calcification involves the bases of the cusps. Early process that is not important hemodynamically, is called aortic valve sclerosis. Mitral valve is not affected simultaneously, in contrast to rheumatic heart disease.
Clinical Features of Aortic Stenosis. It is the most common of all the valvular abnormalities. Due to obstruction to out flow pressure gradient may exceed well above between left ventricle and aorta, which results in hypertrophy of left ventricle. Patient may present with angina or syncope, mechanism is not known. Onset of symptoms heralds the failure of compensatory mechanism. Death may result from left sided heart failure within 3 years if untreated.
Myxomatous Degeneration of Mitral Valve Affects 3% of adults usually young women. One or both leaflets are enlarged, hooded, redundant or floppy and prolapse back in to left atrium. Serious complications develop in a minority of cases. Morphology: affected leaflets are thick and rubbery, tendinous cords are elongated, thinned and may be ruptured, annular dilatation is characteristic. Concomitant tricuspid involvement is 20-40%. Histologically, attenuation of fibrosa layer of the valve, on which the structural integrity of valve depends along with focally marked thickening of the spongiosa layer with deposition of mucoid material.
Morphology Cont. Secondary changes include fibrous thickening of valves esp. of rubbing surfaces, linear fibrous thickening of left ventricular endocardium, thickening of left atrial endocardium as a result of prolapsing valves, thrombi on atrial surfaces of leaflets and focal calcifications.
Pathogenesis and Clinical Features. Developmental abnormality of connective tissue because in Marfans syndrome, involvement of other systems is also seen, caused by mutations in gene encoding fibrillin. Subtle defects in structural proteins may predispose to damage by long standing hemodynamic stress. Most patients remain asymptomatic, there may be mid diastolic click due to tensing of everted cusp, there may be holosystolic murmur if regurgitation occurs. Echocardiography reveals valve prolapse. Chest pain, dyspnoea, fatigue, psychiatric disorders like depression and personality disorders. Serious complications include: infective endocarditis, mitral insufficiency, thrombo embolism and arrhythmias.
Rheumatic Heart Disease Rheumatic fever: acute immunologically mediated multisystem inflammatory disease, a few weeks after acute episode of beta hemolytic streptococcal infection (throat). Acute rheumatic carditis may progress to chronic valvular deformities. Recently there is significant decrease in the complications of this disease on account of raised socioeconomic standards, better diagnostic facilities and early treatment of pharyngitis. Only 3% of group A beta streptococci develop this serious complication.
Morphological Features Acute rheumatic fever: disseminated but focal lesions esp. in heart called Aschoff bodies, fibrinoid degeneration surrounded by lymphocytes, plasma cells and plump macrophages called Anitschkow cells or caterpillar cells, some times multinucleated giant cells may also form. During acute attack, all the three layers of heart may be involved- called pancarditis. In pericardium, serofibrinous or fibrinous pericarditis. Myocardium: scattered Aschoff bodies, called myocarditis within interstitial connective tissue.
Morphology Cont. Involvement of endocardium and left sided valves by inflammatory foci comprises of fibrinoid necrosis within cusps or along the tendinous cords on which small vegetations called verrucae along the lines of closure of valves. Warty projections are due to precipitation of fibrin at the sites of erosions related to underlying inflammation and degenerations. These changes in acute fever cause no disturbances to valvular functions.
Morphology Cont. Subendocardial lesions in left atrium are called MacCallum plaques. Chronic rheumatic heart disease: organization of acute inflammation and deforming fibrosis e.G. Thickening and retracted valve with fusion of leaflets causing permanent deformity and narrowing, shortening, thickening and fusion of tendinous cords; Mitral and aortic valves are most important. Microscopically: diffuse fibrosis and neovascularization replacing the original avascular leaflets, Aschoff bodies not present in ch. Disease.
Morphology Cont. Rheumatic heart disease is the most frequent cause of mitral stenosis. Mitral valve alone is involved in 65-70% cases of rheumatic disease. Tricuspid valve is involved less frequently and with much less severity. If there is calcification or formation of fibrous bridges across the valvular commissures, buttonhole or fish mouth stenosis. Lt atrial hypertrophy, dilatation, pulmonary congestion, pulmonary hypertension and right ventricular hypertrophy. Normal left ventricle in pure mitral valve stenosis.
Pathogenesis and Clinical Features. Hypersensitivity reaction induced by group A streptococci. Antibodies directed against M proteins of certain strains cross react with tissue glycoproteins in heart, joints and other tissues. Genetic susceptibility regulates the hypersensitivity reaction because minority of patients develop this complication. Children 5-15 yrs. By the time fever develops, throat cultures are negative but antibodies to streptolysin o and anti DNAse are usually detectable in sera.
Clinical Features Cont. Arthritis and carditis predominant clinical features. Arthritis is migratory polyarthritis, with fever, mostly large joints are involved. Features of carditis include: pericardial friction rub, weak heart sounds, tachycardia and arrhythmias. Usually no mortality in acute disease. After initial attack, there is increased vulnerability to reactivation of disease with subsequent pharyngitis. Carditis worsens with each attack and damage is cumulative. Other hazards are embolism and infective endocarditis.
Clinical Features Cont. Chronic rheumatic carditis is not manifested clinically for years of decades after initial acute attack. Signs and symptoms depend upon the valves involved. Cardiac murmurs, cardiac hypertrophy and dilatation, heart failure, arrhythmias like atrial fibrillation, thrombo embolic phenomenon and infective endocarditis. Replacement of mitral valve with prosthetic devices has greatly improved the prognosis.
Infective Endocarditis Serious disease characterized by colonization of cardiac valves, endocardium and other cardiovascular sites by a microorganism. Bulky friable vegetations composed of thrombotic debris along with organisms with destruction of underlying cardiac tissues. Aorta, aneurysmal sacs, other blood vessels and prosthetic valves may be infected. Microorganisms are bacterial, fungi, rickettsiae and chlamydia. Most important are bacteria-bacterial endocarditis.
Classification Clinically divided in to acute and subacute depending on virulence of the causative organisms and presence of underlying cardiac disease. Acute: destructive infection of a previously normal heart valves by a highly virulent organism, that can lead to death of around 50% of the patients within days to weeks in spite of intensive management. Subacute: caused by organisms of low virulence affecting previously abnormal heart, particularly deformed valves. The disease runs protracted course and may settle with appropriate treatment.
However both clinical and morphologic patterns suggest, possibility of a spectrum rather than a clear cut demarcation between acute and subacute.
Pathogenesis Usually cardiac and vascular abnormalities predispose to this form of infection. Previously rheumatic heart disease was major contributor but recently, myxomatous mitral, degenerative calcific valvular stenosis, biscuspid aortic valve, prosthetic valves and vascular grafts are more common. Predisposing host factors include: neutropenia, immunodeficiency, therapeutic immunosuppressive drugs, diabetes and alcohol and intravenous drug abuse. Indwelling cardiac or vascular catheters may also cause infective endocarditis.
In 50-60% of the cases, the causative organisms are alpha hemolytic streptococci called viridans streptococci. 10-20% cases are caused by staphylococcus aureus, being major offenders in intravenous drug abusers. Other bacteria include: enterococci, Haemophilus, Acinetobacteria, Cardiobacterium; Commensals of oral cavity. Prosthetic valve carditis is most often caused by coagulase negative staphylococci. Other agents: gram negative bacilli and fungi.
In 10% cases no offending agent can be isolated called culture negative endocarditis, may due to previous antimicrobial treatment. Portal of entry of microorganisms may be an obvious focus of infection such as a dental or other surgical procedure that causes a bacteremia, intravenous injection of bacteria by I/V drug users, or from an occult source from GIT, oral cavity or trivial injuries.
Morphologic Features. Both acute and subacute develop friable, bulky vegetations, containing fibrin, inflammatory cells and bacteria, most commonly on heart valves, most often mitral and aortic. Right sided valves may be involved in I/V drug abusers. Vegetations may be single or more often multiple. Vegetations are often destructive to underlying myocardium producing abscess cavity. Fungal vegetations are usually larger. In subacute form, vegetations are smaller and less destructive.
Morphology Cont. Systemic embolism may occur at any time because of friability of the vegetations; Infarcts in brain, kidneys, myocardium etc, septic infarcts may cause abscesses in the above said tissues. Microscopically vegetations consist of granulation tissue at their bases; With the passage of time, fibrosis, calcifications and chronic inflammatory infiltrate may develop.
Clinical Features Fever most important feature, may be absent in elderly. Non specific fatigue, loss of weight and flu like state. Murmurs in 90% cases. Features like petechial rashes, subungual hemorrhages and Roth spots in eyes have become less common because of effective antimicrobials. Acute disease has stormy course, high grade fever with chills, weakness and lassitude. Cardiac complications: stenosis or insufficiency, myocardial ring abscesses and suppurative pericarditis.
Embolic complications: cerebral infarcts, meningitis, myocardial infarction,kidney abscesses, lung infarcts and abscesses, pneumonia. Focal and diffuse glomerulonephritis leading to hematuria, albuminuria and renal failure. Splinter hemorrhages in the nail beds.
Endocarditis Showing Vegetations Case of infective endocarditis, spreading from aortic valves to the endocardium and
Endocarditis With Vegetations on AorticValves Infective Endocarditis showing red vegetation on the aortic valve.
Non Infected Vegetations Non bacterial thrombotic endocarditis are characterized by deposition of small masses of fibrin, platelets and other blood components on the valvular leaflets in debilitated patients. The vegetations are sterile and loosely attached resulting in embolism.
Myocardial Diseases. Inflammatory disorders, immunologic diseases, systemic metabolic disorders, muscular dystrophies, genetic abnormalities of myocardial cells and diseases of unknown cause. Cardiomyopathies are a group of diseases resulting from a primary abnormality in the myocardium. Clinicopathologic patterns are: dilated cardiomyopathy, hypertrophic and restrictive cardiomyopathy. Of these dilated one is most common (90%). Each of these may be idiopathic or specific cause.