1、Introduction to Cardiovascular Pathology-Fred Clayton Systemic Pathology of Congestive Heart Failure Pathology of Myocarditis Pathology of Cardiomyopathy Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Restrictive CardiomyopathyCongestive Heart Failure Cardiac output insufficient for metabolic re
2、quirements of the body Systolic dysfunction decreased myocardial contractility Diastolic dysfunction insufficient expansion for ventricular volume Problems are accentuated by increased demand high output heart failureCHF Bodys Compensation Tachycardia Frank-Starling increased End Diastolic Volume My
3、ocardial hypertrophy Renin-angiotensin-aldosterone system Catecholamines positive inotropic effect Adrenergic redistribution of blood flow Increase oxygen extraction from hemoglobinLungs Pulmonary edema Dyspnea breathlessness Orthopnea dyspnea lying down Paroxysmal nocturnal dyspnea extreme dyspneaL
4、ung Pulmonary Edema pale pink edema fluid filling alveoliLung alveolar hemorrhage,heme-filledmacrophages“heart failure cells”,with iron stain to rightKidneys reduced perfusion Ischemic tubular necrosis/ATN Prerenal azotemiaKidney-ATNBrain in CHF cerebral hypoxia Irritability Loss of attention span R
5、estlessness Stupor ComaRight-sided heart failure Pure cor pulmonale Consequence of left-sided failure Myocardial myocarditis,cardiomyopathy,constrictive pericarditisRight failure-systemic effects Liver chronic passive congestion Spleen congestive splenomegaly Kidneys congestion and hypoxia Sub-Q per
6、ipheral edema and anasarca Pleural space effusions Brain venous congestion and hypoxia Portal-ascitesLiver chronic passive congestion blood pools near the central veinsLiver chronic passive congestion Liver chronic passive congestion blood pools near the central veinsLiver chronic passive congestion
7、 red cell pooling near central veins and pericentral necrosis of the hepatocytesCHF final pathway to death Ischemic heart disease Hypertensive heart disease Valvular heart disease Cardiomyopathy Myocarditis Specific heart muscle diseasesMyocarditis Etiology Viral Coxsackie A,ECHO,Influenza Chlamydia
8、 and Rickettsia psittaci&typhi Bacteria diphtheria,TB,Strep Fungal&Protozoa Trypanosomes,Toxo Hypersensitivity SLE,RHD,drugs Physical Agents Radiation Idiopathic Giant cell myocarditisMyocarditis Morphology Gross dilated,flabby heart,pale patches with hemorrhage Microscopic interstitial inflammatory
9、 infiltrate with myocyte necrosis,fibrosis Mononuclear cells idiopathic or viral Neutrophils bacterial Eosinophils hypersensitivity or protozoa Granulomatous TB or sarcoidDilated,globoid heart in myocarditisMyocarditis meets Dallas criteria of a T lymphocyte infiltrate and myocyte necrosis or dropou
10、t.This is usually either viral or of unknown cause.Diphtheria myocarditis due to a toxin rather than bacterial invasion.There is some inflammation,myocyte changes(see the big nucleolus).Myocyte necrosis(not shown)also happens.Bacterial colony in myocarditisToxoplasmosisChagas diseaseGiant Cell Myoca
11、rditis Myocyte necrosis Multinucleated giant cells Lymphocytes,plasma cells,macrophages,eosinophils,and neutrophils Often fulminant,rapid progression to death Differential diagnosis cardiac sarcoidosisGiant Cell MyocarditisGiant Cell MyocarditisCardiomyopathiesDilated Cardiomyopathy Gross increased
12、weight,dilatation,endocardial fibrosis,normal valves and coronary arteries Microscopic myocyte hypertrophy,myofibrillar loss and interstitial fibrosis Etiology viral,genetic,toxins Clinical significance heart failure&deathDilated cardiomyopathyCardiomyopathy loss of myofibrilsCardiomyopathy trichrom
13、e stain showing extensive fibrosis(blue)betweenthe myocytes.The myocytes also vary in size,and some have partial loss of myofibrils.Normal Heart-EMLoss of fibrils in cardiomyopathy.The myocyte at lower left is about normal;the others have an extensive loss of myofibrils.Cardiomyopathy loss of fibril
14、s and a small contraction band in the top center.Hypertrophic Cardiomyopathy Hypertrophy of ventricular septum(95%)Disarray of myofibers(100%)Volume reduction of ventricles(90%)Endocardial thickening of LV(75%)Mitral valve leaflet thickening(75%)Dilated atria(100%)Abnormal intramural coronaries(50%)
15、Hypertrophic cardiomyopathyHypertrophic cardiomyopathyHypertrophic cardiomyopathyHypertrophic cardiomyopathy myofiber dysarray not all fibers are pulling the same direction.Thus the contraction is ineffective.However,the cardiac conduction system can have these same problems,which might cause the ar
16、rhythmias and sudden death these patients tend to die of.Hypertrophic Cardiomyopathy Etiology hereditary,mostly autosomal dominant,can appear sporadically Clinical significance syncope,arrhythmias and sudden death with a risk of 2-6%per year Cannot equate with hypertrophy alone!There is variation in
17、 heart size without disease.Large hearts correlate with endurance(Secretariat,Lance Armstrong).Restrictive Cardiomyopathy Amyloidosis Endomyocardial fibrosis subendocardial fibrosis Loefflers endocarditis eosinophilic infiltrate Endocardial fibroelastosisAmyloidosis notice the pink material between
18、the myocytes.Amyloidosis Congo Red is very,very positive.Amyloidosis this heart is thickened,pale,and has a rubbery consistency that interferes with cardiac expansion during diastole.Endomyocardial fibrosis fibrosis under the endocardium and in the the inner third of the myocardium.Endomyocardial fi
19、brosis of a ventricular wall.When extensive,this would cause restrictive heart failure too.Endocardial fibroelastosis elastic stain(black)is very positive.This disease,which occurred in young children and was once 1:5,000 births,now is almost never seen.Etiology is not known(?viral such as mumps).En
20、docardial fibroelastosisSpecific Heart Muscle Diseases Toxic alcohol,catecholamines,cocaine,Adriamycin Metabolic hemochromatosis,hyperthyroidism Neuromuscular muscular dystrophy Storage disease glycogen,Fabrys disease Infiltrative-sarcoidosisHeart-Beckers muscular dystrophy looks like idiopathic dil
21、ated cardiomyopathy.Note the fibrosis and loss of myofibrils in some cells.By electron microscopy,this was Adriamycin toxicity.See the clear vacuoles(theyare dilated sarcoplastic reticulum)and severe loss of myofibrils.Cocaine heart necrosis with contraction bands.This could happen with any severe c
22、hronic stimulation such as too much pressors in a failing heart or a pheochromocytoma.Cardiac Sarcoidosis well defined granuloma with giant cells.Dosent infiltrate&destroy myocardium like giant cell myocarditis.Eosinophils are less common in sarcoidosis than in giant cell myocarditis.Hemochromatosis
23、-note the brown perinuclear deposits of hemosiderin.It is,however,the soluble iron,not the hemosiderin,that is considered toxic.Hemochromatosis iron stain(iron is blue).Rheumatic fever Aschoff body A collection of cells,often near a vessel,with afew multinucleate cells and some vesicular nuclei with big nucleoli(Aschoff cells).Anichkov myocytes(not shown)are myocytes with very elongated big nucleoli.This is a marker for rheumatic fever,but the serious damage is to the valves.
