Presentation on theme: "Introduction to Cardiovascular Pathology - Fred Clayton Systemic Pathology of Congestive Heart Failure Pathology of Myocarditis Pathology of Cardiomyopathy."— Presentation transcript:
Introduction to Cardiovascular Pathology - Fred Clayton Systemic Pathology of Congestive Heart Failure Pathology of Myocarditis Pathology of Cardiomyopathy –Dilated Cardiomyopathy –Hypertrophic Cardiomyopathy –Restrictive Cardiomyopathy
Congestive Heart Failure Cardiac output insufficient for metabolic requirements of the body Systolic dysfunction – decreased myocardial contractility Diastolic dysfunction – insufficient expansion for ventricular volume Problems are accentuated by increased demand – high output heart failure
CHF – Body’s Compensation Tachycardia Frank-Starling – increased End Diastolic Volume Myocardial hypertrophy Renin-angiotensin-aldosterone system Catecholamines – positive inotropic effect Adrenergic redistribution of blood flow Increase oxygen extraction from hemoglobin
Myocarditis Morphology Gross –dilated, flabby heart, pale patches with hemorrhage Microscopic – interstitial inflammatory infiltrate with myocyte necrosis, fibrosis Mononuclear cells – idiopathic or viral Neutrophils – bacterial Eosinophils –hypersensitivity or protozoa Granulomatous – TB or sarcoid
Dilated, globoid heart in myocarditis
Myocarditis – meets Dallas criteria of a T lymphocyte infiltrate and myocyte necrosis or dropout. 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 myocarditis
Giant Cell Myocarditis Myocyte necrosis Multinucleated giant cells Lymphocytes, plasma cells, macrophages, eosinophils, and neutrophils Often fulminant, rapid progression to death Differential diagnosis – cardiac sarcoidosis
Giant Cell Myocarditis
Dilated Cardiomyopathy Gross – increased 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 & death
Cardiomyopathy – loss of myofibrils
Cardiomyopathy – trichrome stain showing extensive fibrosis (blue) between the myocytes. The myocytes also vary in size, and some have partial loss of myofibrils.
Normal Heart - EM
Loss of fibrils in cardiomyopathy. The myocyte at lower left is about normal; the others have an extensive loss of myofibrils.
Cardiomyopathy – loss of fibrils 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%)
Hypertrophic 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 arrhythmias 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 heart size without disease. Large hearts correlate with endurance (Secretariat, Lance Armstrong).
Amyloidosis – notice the pink material between 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 fibrosis 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).
Note the fibrosis and loss of myofibrils in some cells.
By electron microscopy, this was Adriamycin toxicity. See the clear vacuoles (they are dilated sarcoplastic reticulum) and severe loss of myofibrils.
Cocaine heart – necrosis with contraction bands. This could happen with any severe chronic stimulation such as too much pressors in a failing heart or a pheochromocytoma.
Cardiac Sarcoidosis – well defined granuloma with giant cells. Dosen’t infiltrate & destroy myocardium like giant cell myocarditis. Eosinophils are less common in sarcoidosis than in giant cell myocarditis.
Hemochromatosis - 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 a few 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.