heart

HEART: 

HEART

Anatomy: 

Anatomy Weight Males 300-350 gm Females 250-300 gm Wall thickness Rt ventricle – 0.3 to 0.5 cm Lt ventricle – 1.3 to 1.5 cm Inc weight & wall thickness – hypertrophy Enlarged chamber size – dilation Inc weight & size - cardiomegaly

Pathology : 

Pathology Failure of pump Obstruction to flow Regurgitant flow Disorder of cardiac conduction Disruption of the continuity of the circulatory system

Heart failure: 

Heart failure Also k/a congestive heart failure Heart is unable to pump the blood according to the rate of requirement of different tissue Results in cardiac hypertrophy Pulmonary hypertension & IHD 350-600 gm Systemic HTN ,aortic stenosis,mitral regurgitation or dilated cardiomegaly 400-800 gm Aortic regurgitation ,hypertrophic cardiopathy 600-1000 gm

pathogenesis : 

pathogenesis Pressure overload – hypertrophy of ventricle Volume overload-ventricular dilation & inc. muscle mass & wall thickness Sustained cardiac hypertrophy Cardiac failure

Slide 6: 

HYPERTENSION Pressure overload VALVULAR DISEASE Pressure/volume overload MYOCARDIAL INFARCTION Regional dysfunction with Volume over load Inc cardiac work Inc wall stress Cell stretch HYPERTROPHY OR DIALATION Characterized by Inc heart size & mass Inc protein synthesis CARDIAC DYSFUNCTION Characterized by Heart failure Arrhythemia Neurohumoral stimulation

Left sided heart failure: 

Left sided heart failure Etiology IHD HTN Aortic & mitral valve disease Non ischemic myocardial disease

Pathogenesis : 

Pathogenesis Blood supply in pulmonary circulation increases Peripheral blood pressure & flow is decreased

Morphology : 

Morphology Heart Abnormalities of MI or vulvular deformity Hypertrophied & often dilated chamber Secondary enlargement of left atrium Brain Hypoxic encephalopathy

Slide 10: 

Kidney Prerenal azotemia Lungs Pulmonary congestion & edema Heavy wet lungs Perivascular & interstitial transudate Edematous widening of alveolar septae Accumulation of edema fluid in alveolar septae Heart failure cells in alveoli

Clinical manifestation: 

Clinical manifestation Dyspnea Orthopnea Paroxysmal nocturnal dyspnea

Right sided heart failure: 

Right sided heart failure Etiology Secondary consequence of left sided heart failure Chronic severe pulmonary HTN

Pathogenesis : 

Pathogenesis Pressure overload Hypertrophy & dilation in rt. Ventricle & atrium Bulging of ventricular septum Left ventricular dysfunction

Morphology : 

Morphology Liver & portal system Congestive hepatomegaly Centrilobular necrosis Sinusoidal congestion Cardiac cirrhosis Spleen congestive splenomegaly Sinusoidal dilation Ascitis

Slide 15: 

Kidney Congestion Azotemia Brain Venous congestion & hypoxia Pleura & pericardial space Accumulation of fluid Subcutaneous tissue Peripheral edema in dependent portion of body

Clinical manifestation: 

Clinical manifestation Pedal edema Pretibial edema

Heart disease: 

Heart disease Congenital Ischemic Hypertensive Valvular Non ischemic myocardial disease

Congenital heart disease: 

Congenital heart disease VSD ASD PS PDA Tetralogy of fallot Coarctation of aorta Atrioventricular septal defect Aortic stenosis Transposition of great arteries Truncus arteriosus Tricuspid atresia

Slide 19: 

Etiology – developmental abnormalities Clinical feature - Malformation CF Lt to rt shunt (ASD,VSD,PDA) Low BP Rt to lt shunt (TOF,TGA,PTA,TA ) Cyanosis obstruction

Left to right shunt: 

Left to right shunt Atrial septal defect Abnormal opening in atrial septum Usually asymptomatic Pulmonary HTN in < 10% cases Complication Heart failure Paradoxical embolization Pulmonary vascular disease

Slide 21: 

Ventricular septal defect Incomplete closure of ventricular septum Common disorder Rt ventricular hypertrophy & pulmonary HTN Sign of cardiac failure in longer defect Persistent ductus arteriosus Does not produce functional difficulties at birth

Right to left shunt : 

Right to left shunt Tetrology of fallot Four feature VSD Obstruction to rt ventricular outflow Aorta overrides The VSD Rt ventricular hypertrophy Clinical features Cardiomegaly Subpulmonary stenosis Aortic valve insufficieny

Obstructive anomalies: 

Obstructive anomalies Coarctation of aorta narrowing or constriction of aorta Pulmonary stenosis Obstuction of pulmonary valve Aortic stenosis Obstruction of aotic valve

Ischemic heart disease: 

Ischemic heart disease Angina pectoris Myocardial infarction Chronic ischemic heart diseases Sudden cardiac death

Etiology : 

Etiology Smoking Inc BP HTN Inc cholesterol level Sedentary lifestyle

Pathogenesis : 

Pathogenesis Decrease coronary perfusion relative to myocardial demand

Angina pectoris: 

Angina pectoris It is a symptom complex of IHD characterized by paroxysmal & usually recurrent attacks of substernal or precordial chest discomfort caused by transient myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction Types Stable Prinzmetal unstable

Stable : 

Stable Common Cause – dec coronary perfusion to a critical level by chronic stenosing coronary atherosclerosis

Slide 29: 

Physical activity Emotional excitement Increased demand Inc. cardiac workload Relieved by rest

Prinzmetal : 

Prinzmetal Uncommon Occurs at rest Cause – coronary artery stenosis Respond to vasodilators

Unstable type: 

Unstable type Also k/a crescendo angina occurs at rest Prolonged duration Cause – disruption of atherosclerotic plaque with superimposed partial thrombosis & embolization or vaso spasm

Myocardial infarction: 

Myocardial infarction HEART ATTACK- death of cardiac muscles resulting from ischemia Types Transmural Subendocardial

Gross acute MI: 

Gross acute MI

Transmural : 

Transmural Involve full thickness of ventricular wall Associated with Coronary atherosclerosis Acute plaque change Superimposed thrombus Coronary thrombosis Epicarditis

Subendocardial : 

Subendocardial Limited to inner 1/3 rd of ventricular wall Associated with Plaque disruption Coronary thrombus Severe dec of systemic BP Less frequent ,not associated with coronary thrombosis & epicarditis

Pathogenesis : 

Pathogenesis Coronary artery occlusion Coronary atherosclerosis Plaque rupture Superimposed platelet aggregation Thrombosis vasospasm Loss of blood supply to myocardium Biochemical consequences Functional consequences Morphological consequenses Inc.myocardial demand Worsens condition

Biochemical consequences: 

Biochemical consequences Cessation of aerobic glycolysis Lead to inadequate Production of ATP Accumulation of lactic acid Loss of contractility Ischemic cell death

Slide 39: 

Features Time Onset of ATP depletion Seconds Loss of contractility < 2 min ATP reduced To 50% of normal To 10% of normal 10 min 40 min Irreversible cell injury 20-40min Microvascular injury >1 hr

Morphological changes: 

Morphological changes Frequency of coronary artery occlusion LAD ( Anterior wall of LV, apex, anterior part of ventricular septum ) – 40-50% RCA ( post wall of ventricular septum) - 30-40% Lt circumflex coronary artery (lateral wall of LV) -15-20%

Slide 41: 

Time Gross feature Microscopic feature 0-1/2 hr - - ½ - 4hr - Waviness of fiber 4-12 hr Dark mottling Beginning of coagulation necrosis, hemorrhage,edema 12-24 hr Dark mottling Coagulation, necrosis,pyknosis of nuclei, neutrophillic infiltration 1-3 days Yellow infarct Coagulation necrosis, neutrophilic infiltration

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3-7 days Hyperemic border,central yellow tan softening Disintegration of dead myofibres, phagocytosis by macrophages 2 weeks Maximal yellow tan with red margin Granulation tissue

Acute MI < 1 day: 

Acute MI < 1 day

2-3 days: 

2-3 days

3-4 days: 

3-4 days

1 week: 

1 week

opic : 

opic

2-3 weeks: 

2-3 weeks

Clinical feature: 

Clinical feature Rapid weak pulse Sweating Dyspnea Edema Ducto pulmonary congestion

Laboratory diagnosis: 

Laboratory diagnosis ECG Changes ST segment elevation T wave inversion Wide deep Q wave Serum cardiac markers Creatine phosphokinase Inc CK-MB for cardiac muscle Isoenzyme CK-MB 1 – EXTRACARDIAC CK MB 2 – MYOCARDIAL FORM

Slide 51: 

Lactic dehydrognase LDH-1 inc Ratio of LDH-1 : LDH-2 >1 Rise after 24 hr Peak at 3-6 days Return to normal after 14 days Myoglobin First cardiac marker to become elevated return to normal with in 24 hrs

Slide 52: 

Cardiac – specific troponins Contractile muscle protiens Cardiac troponin T Cardiac troponin I Value raised after 4-6 hrs Return to normal after Troponin I – 7-10 days Troonin T – 10-14 days

Complication of MI: 

Complication of MI Left ventricular failure Arrhythmias Sinus bradycardia Heart block Ventricular Tachycardia Ventricular fibrillation Myocardial rupture Pericardium Rt ventricular infarction Infarct expansion Mural thrombus Ventricular aneurysm Papillary muscle dysfunction Progressive left heart failure

Rupture of papillae: 

Rupture of papillae

Chronic ischemic heart disease: 

Chronic ischemic heart disease Progressive heart failure as a consequence of ischemic myocardial damage MORPHOLOGY Enlarged heart Hypertrophy & dilation lt ventricle Atherosclerosis of coronary artery Mural thrombi

Sudden cardiac death: 

Sudden cardiac death Unexpected death with in one hour Non atherosclerotic causes Congenital structural abnormalities Aortic valve stenosis Mitral valve prolapse Myocarditis Dilated & hypertrophic cardiomyopathies Pulmonary hypertension Abnormalities of cardiac conduction Arrhythmia

Hypertensive heart disease: 

Hypertensive heart disease Response of the heart to the increased demand induced by systemic HTN

Slide 58: 

Systemic (lt sided) hypertension Response to pressure overload Myocardial dysfunction Cardiac dilation CHF Sudden death

Slide 59: 

Ventricular hypertrophy Inc cardiac size Stiffness to ventricle wall Deffective diastolic filling Lt ventricular enlargement

Slide 60: 

Morphological feature Lt ventricular hypertrophy H/O hypertension Consequence Therapeutic control Progressive IHD Renal damage or cerebrovascular stroke Progressive heart failure

Right side heart failure: 

Right side heart failure Pulmonary ( rt sided ) hypertensive heart disease Rt ventricular hypertrophy ( cor pulmonale ) & dilation Predisposing factors of cor pulmonale

Slide 62: 

Morphology Dilation of rt ventricle with out hypertrophy in acute cor pulmonale Both dilation & hypertrophy in chronic

Valvular heart disease: 

Valvular heart disease

Slide 64: 

Stenosis - It is failure of a valve to open completely there by impeding forward flow. Insufficiency - failure of the valve to close completely there by allowing reversed flow

Etiology : 

Etiology CONGENITAL ACQUIRED Mitral valve disease Mitral stenosis Post inflammatory scarring Mitral regurgitation Abnormalities of leaflets Postinflammatory scarring Infective endocarditis Mitral valve prolapse Abnormalities of tensor apparatus Rupture of papillary muscle Papillary muscle dysfunction Rupture of chordae tendinae

Slide 66: 

Aortic valve disease Aortic stenosis Post inflammatory scarring ( RHD ) Senile calcific aortic stenosis Calcification of congenitally deformed valve Aortic regurgitation Intrinsic valvular disease Post inflammatory scarring ( RHD ) Infective endocaditis Aortic disease Degenerative aortic dilation Syphilitic aortitis Ankylosing spondylitis Rheumatoid arthritis Marfan syndrome

Calcific aortic stenosis: 

Calcific aortic stenosis Common Due to senile changes there is calcification Calcific stenosis of congenitally bicuspid aortic valve MORPHOLOGY – Heeped up calcified masses with in the aortic cusp Aortic valve sclerosis CLINICAL FEATURES Cardiac hypertrophy Angina pectoris Nodular masses of calcium

Mitral annular calcification: 

Mitral annular calcification Degenerative calcific deposits in annulus ( fibrous ring ) of mitral valve MORPHOLOGY Ulcerated nodule CLINICAL FEATURE Arrhythmia Sudden death occurs COMPLICATION Infective endocarditis Calcific nodule

Mitral annular calcification: 

Mitral annular calcification

Myxomatous degeneration of the mitral valve: 

Myxomatous degeneration of the mitral valve MITRAL VALVE PROPLAPSE Mitral leaflets are floppy & prolapse or balloon back in left atrium during systole MORPHOLOGY Leaflets of valve enlarged thick & rubbery Elongated tendinous cord can rupture Annular dilation also seen in mitral insufficiency Fibrosis in valve Linear fibrous thickening in left ventricular endocardium

Slide 71: 

Mural endocardium thickened of left ventricle or atrium Thrombi & myxomatous degeneration Associated with marfans syndrome CLINICAL FEATURES Usually asymptomatic Late systole Murmurs Chest pain Prolapsed mitral leaflet

Ballooning of the mitral leaflet: 

Ballooning of the mitral leaflet

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COMPLICATIONS Endocarditis Mitral insufficiency Stroke Arrhythmia

Rheumatic fever & rheumatic heart diseases: 

Rheumatic fever & rheumatic heart diseases Acute immune mediated multisystem inflammatory disease occurs few weeks following an episode of group A streptococcal pharyngitis Imp. Consequences – chronic valvular deformities Characterized by - fibrotic valvular disease ( mitral stenosis ) Common age – 5 – 15 yr

Morphology (acute rheumatic fever): 

Morphology (acute rheumatic fever) Focal inflammatory lesion Aschoff bodies Swollen eosinophilic edges Surrounded by lymphocyte, Plasma cells & macrophages Anitschkow cells vegetation vegetation

Rheumatic fever verrucous vegetation: 

Rheumatic fever verrucous vegetation

Fish mouth appearence: 

Fish mouth appearence

Shortened and thickened chordi: 

Shortened and thickened chordi

Mural thrombus & left atrial enlargement: 

Mural thrombus & left atrial enlargement

Slide 80: 

Anitschkow cells Abundant cytoplasm Central round to oval nucleus Wavy ribbon like chromatin (caterpillar cells) Aschoff giant cells Multinucleated cells

RHD collection of mononuclear cells: 

RHD collection of mononuclear cells

Aschoff nodule at higher magnification: 

Aschoff nodule at higher magnification

Anitschkow cell: 

Anitschkow cell

Pancarditis : 

Pancarditis PERICARDIUM – inflammation Serofibrinous pericardial exudate MYOCARDIUM – inflammation Scattered Aschoff bodies Often perivascular ENDOCARDIUM – inflammation Fibrinoid necrosis in the form of small vegetation along the line of closure ( verrucae bodies ) Maccallum plaques Subendocardial lesion ( left atrium ) Irregular thickening

Chronic rheumatic heart disease: 

Chronic rheumatic heart disease Acute inflammation with fibrosis & neovascularization Aschoff bodies replaced by fibrosis Valvular leaflets – thickened & retracted Leaflet thickening Commissural fusion Shortening & thickening & fusion of tendinous cords

Pathogenesis : 

Pathogenesis Antibodies directed against the M protien of certain strain of streptococci cross react glycoprotien antigen in the heart , joints

Pathogenesis : 

Pathogenesis

Jones criteria : 

Jones criteria MAJOR CRITERIA Carditis Arthritis Subcutaneous nodules Chorea Erythema marginatum MINOR CRITERIA CLINICAL Fever Arthralgia Previous rheumatic fever ESSENTIAL CRITERIA Evidence for recent streptococcal infection ( inc antistreptolysin O titre,positive throat culture,recent scarlet fever) LABORATORY Acute phase reactant (leukocytois,elevated ESR, inc C-reactive protien) Prolonged PR interval

Slide 89: 

CRITERIA FOR DIAGNOSIS Two major One major + two minor CLINICAL MANIFESTATION FEVER-10 days to 6 wks after pharyngitis ARTHRITIS – common in adults swollen joints CARDITIS – pericardial friction rub , weak heart sound , tachycardia, arrhythmia CHRONIC RHEUMATIC CARDITIS – manifests for years

Slide 90: 

COMPLICATIONS Mitral stenosis Aortic stenosis Fish mouth or buttonhole stenosis

Infective endocarditis: 

Infective endocarditis Colonization or invasion of the heart valves or mural endocardium by microbe leading to bulky friable vegetation composed of thrombotic debris & organism associated with destruction of cardiac tissue ORGANISM – streptococcus viridians - streptococcus aureus Hacek group

Infective endocarditis Gross: 

Infective endocarditis Gross

Etiology : 

Etiology Aorta aneurysmal sac Prosthetic devices Fungi Rickettsiae Chlamydiae Bacterial Others RHD .mitral valve prolapse Calcific valvular stenosis .Bicuspid aortic valve Diabetes .Alcohol .Therapeutic immunosuppresion

Classification : 

Classification Features Acute Subacute Duration Organism Virulence of organisms Condition of valve Lesion on valve <6 wks Staph.aureus B-streptococci High Previously normal Invasion ,destructive,suppurative > 6 wks Streptococcus viridians Less Previously damaged Not invasive or suppurative

MORPHOLOGY: 

MORPHOLOGY Friable, bulky destructive vegetation containing fibrin inflammatory cells & bacterial colonies on the heart valve Commonly involve – aortic & mitral valve Ring abscess – vegetation erode myocardium Fungal endocarditis – larger vegetation

Slide 99: 

Friable vegetation

Microscopic : 

Microscopic

Complication : 

Complication Septic infarcts & emboli Subacute endocarditis – less destructive with granulation tissue & calcification CLINICAL FEATURE Fever Acute – rapid onset Can be accompanied by glomerulonephritis murmurs

Diagnostic criteria: 

Diagnostic criteria PATHOLOGIC CRITERIA Microorganism in a vegetation ,emboli from a vegetation or intracardiac abscess Histologic confirmation active endocarditis in vegetation or intracardiac abscess CLINICAL CRITERIA MAJOR Positive blood culture ECG findings New valvular regurgitation

Slide 103: 

MINOR Fever Predisposing heart lesion Vascular lesions ( arterial patechiae , subungal/splinter hemorrhages , emboli, septic infarcts, mycotic aneurysm , intracranial hemorrhage , janeway lesion Immunologic phenomena ,including glomerulonephritis, osler nodes, roth spots, rheumatoid factor Microbiologic evidence Diagnosis made on 2 major 1major + 3 minor 5 minor

Non infected endocarditis: 

Non infected endocarditis NBTE characterized by deposits of small masses of fibrin platelets & other blood components on the leaflets of cardiac valves Vulvular lesions are sterile ( i.e. do not contain microorganism ) MORPHOLOGY Nondestructive small vegetation (.1-.5mm) Along the line of closure of leaflets MICROSCOPICALLY – blind thrombus without inflammatory reaction with fibrous tissue

Non bacterial endocarditis: 

Non bacterial endocarditis

Slide 106: 

PATHOGENESIS Occurs with venous thrombosis or pulmonary embolism Associated with hypercoagulable state,DIC , carcinoma etc THROMBOTIC EMBOLISM BLAND THROMBUS

Libmann – sacks disease: 

Libmann – sacks disease Endocarditis of SLE Mitral & tricuspid valvulitis with small sterile vegetation Granular pink vegetation – 1-4 mm MICOSCOPICALLY granular fibrinous eosinophilic material with LE cells Fibrosis Can be associated with antiphospholipid syndrome thrombocytopenia

Libmans sacks gross: 

Libmans sacks gross

Slide 110: 

feature Rheumatic Libman sacks NBTE bacterial Valves affected Mitral,mitral+aortic Mitral,aortic Mitral , less often aortic & tricuspid Mitral,aortic, or mitral+aortic Location on valves Along line of closure Both surface Along line of closure On diseased valve-SABE ABE on normal Macroscopy Small multiple warty grey brown translucent firmly attached Medium sized multiple Small,single or multiple brownish,firm but more friable than of rheumatic Large grey towny to greenish, irregular,single or multiple typically friable

Slide 111: 

Microscopy Fibrin with superimposed platelet thrombi and no bacteria Endocardium -oedema,proliferation of capillaries & mononuclear inflammatory infiltrate Fibrinoid material with superimposed fibrin & no bacteria Endocardium- fibrinoid necrosis,acute & chronic inflammatory infiltrate Haematoxylin bodies Degenerated valvular tissue,fibrin platelets thrombi No bacteria Valve swelling of collagen,fibrinoid change Outer eosinophilic zone of fibrin & platelets Colonies of bacteria Endocardium ABE-ABSCESSES SABE-inflammatory granulation

Slide 112: 

RHD IE NBTE LSE

Carcinoid Heart disease: 

Carcinoid Heart disease Cardiac manifestation of the carcinoid tumor. Fibrous intimal thickening on the inside surface of the cardiac chamber & leaflets. Common site- right ventricle Thickening composed of smooth muscle cells and collagen fibers. CF-flushing of the skin,cramps,nausea,vomiting & diarrhea serotonin

Cardiomyopathies: 

Cardiomyopathies Dilated cardiomyopathies Hypertrophic Restrictive

Dilated Cardiomyopathies: 

Dilated Cardiomyopathies Progressive cardiac dilation with concomitants hypertrophy Systolic dysfunction k/a congestive cardiac myopathy. Etiology- toxicity,alcoholism, myocarditis,pegnancy associated nutritional deficiency.

Dilated cardiomyopathy microscopic: 

Dilated cardiomyopathy microscopic

: 

Large & flabby heart with dilated chambers. Histological-hypertrophied muscle with large nucleus, endocardial fibrosis Any age common 20-50 yrs. CF-shortness of breath, fatiguability & poor exertional capacity. Sudden death due to arrhythmia

Microscopic : 

Microscopic

Hypertrophic cardiomyopathy: 

Hypertrophic cardiomyopathy k/a idiopathic hypertrophic subaortic stenosis. Myocardial hypertrophy & diastolic filling abnormality Endocardial thickening, mural plaque, thickening of the mitral valve leaflet. Myocyte hypertrophy & fibrosis

Hypertrophic cardiomyopathy gross: 

Hypertrophic cardiomyopathy gross

Microscopic : 

Microscopic

Restrictive cardiomyopathy: 

Restrictive cardiomyopathy Decrease in the ventricular compliances resulting in the impaired ventricular filling during diastole. Idiopathic, radiation,amyloidosis,metastatic tumor. Slight ventricular enlargement,patchy interstitial fibrosis

Microscopic : 

Microscopic

Apple green birefregence Congo red: 

Apple green birefregence Congo red

Myocarditis: 

Myocarditis Etiology Infection Virus – coxackievirus,cmv, influenza, HIV Chlamydiae Rickettsiae Bacteria-c diptheriae,Neisseria,mengiococcus Fungi Protozoa- trypanosoma,toxoplasma Helminth

Slide 126: 

Immune mediated Postviral Rheumatic fever SLE Drug hypersensitivity Transplant rejection Unknown Giant cell myocarditis sarcoidosis

Myocarditis gross: 

Myocarditis gross

Slide 128: 

Morphological features Normal or dilated heart with flabby ventricular myocardium Interstitial mononuclear inflammation & focal necrosis CF systolic murmur arrhythmias & sudden death

Microscopic : 

Microscopic

Myocarditis – giant cell: 

Myocarditis – giant cell

Pericarditis: 

Pericarditis Types- Serous Serofibrinous Suppurative

Etiology : 

Etiology Infectious –virus,tuberculosis,fungi,parasite &pyogenic bacteria Immune mediated-RF,SLE,scleroderma Others-MI, uremia, following cardiac surgery, neoplasia, trauma radiation

Serous pericarditis : 

Serous pericarditis Noninfectious etiology-RF,SLE etc Less number of non-specific inflammation Volume of the fluid is less(50-200ml)

Fibrinous pericarditis: 

Fibrinous pericarditis Most frequent Dry surface of the pericardium with fine granular roughening More thick yellow fluid Leukocytes erythrocytes & fibrin

Gross : 

Gross

Microscopic : 

Microscopic

Suppurative pericarditis: 

Suppurative pericarditis Thin or thick pus 400ml-500ml Acute inflammatory reaction Complication- constrictive pericarditis-heart is enclosed in the fibrocalcific scar limit diastolic phase

Slide 139: 

Gross

Tuberculous pericarditis : 

Tuberculous pericarditis

Cardiac tumors: 

Cardiac tumors Primary Myxoma- location atria,adults, large sessile to pedenculated mass, with globular myxomatous cells, smooth muscle cells & some undifferentiated cells within mucopolysaccharide ground substance. Secondary

Cardiac myxoma: 

Cardiac myxoma

Miroscopic : 

Miroscopic Cardiac myxoma shows minimal cellularity shows only scattered spindle cells in loose myxoid stroma

Cardiac Rhabdomyoma: 

Cardiac Rhabdomyoma Rare primary tumor Still common in infants & children. Microscopic cells have spider like appearence

Slide 145: 

THANKS By: dr ravi jain