Presentation on theme: "Introduction to Cardiovascular Pathology - Fred Clayton"— Presentation transcript:
1 Introduction to Cardiovascular Pathology - Fred Clayton Systemic Pathology of Congestive Heart FailurePathology of MyocarditisPathology of CardiomyopathyDilated CardiomyopathyHypertrophic CardiomyopathyRestrictive Cardiomyopathy
2 Congestive Heart Failure Cardiac output insufficient for metabolic requirements of the bodySystolic dysfunction – decreased myocardial contractilityDiastolic dysfunction – insufficient expansion for ventricular volumeProblems are accentuated by increased demand – high output heart failure
3 CHF – Body’s Compensation TachycardiaFrank-Starling – increased End Diastolic VolumeMyocardial hypertrophyRenin-angiotensin-aldosterone systemCatecholamines – positive inotropic effectAdrenergic redistribution of blood flowIncrease oxygen extraction from hemoglobin
23 Myocarditis – meets Dallas criteria of a T lymphocyte infiltrate and myocyte necrosis or dropout. This is usually either viral or of unknown cause.
24 Diphtheria myocarditis – due to a toxin rather than bacterial invasion Diphtheria myocarditis – due to a toxin rather than bacterial invasion. There issome inflammation, myocyte changes (see the big nucleolus). Myocyte necrosis(not shown) also happens.
46 Hypertrophic cardiomyopathy – myofiber dysarray – not all fibers are pulling the same direction. Thus the contraction is ineffective. However, the cardiacconduction system can have these same problems, which might cause thearrhythmias and sudden death these patients tend to die of.
47 Hypertrophic Cardiomyopathy Etiology – hereditary, mostly autosomal dominant, can appear sporadicallyClinical significance – syncope, arrhythmias and sudden death with a risk of 2-6% per yearCannot equate with hypertrophy alone! There is variation in heart size without disease. Large hearts correlate with endurance (Secretariat, Lance Armstrong).
50 Amyloidosis – notice the pink material between the myocytes.
51 Amyloidosis – Congo Red is very, very positive.
52 Amyloidosis – this heart is thickened, pale, and has a rubbery consistency that interferes with cardiac expansion during diastole.
53 Endomyocardial fibrosis – fibrosis under the endocardium and in the the inner third of the myocardium.
54 Endomyocardial fibrosis of a ventricular wall Endomyocardial fibrosis of a ventricular wall. When extensive, this would causerestrictive heart failure too.
55 Endocardial fibroelastosis – elastic stain (black) is very positive 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).
59 Note the fibrosis and loss of myofibrils in some cells.
60 By electron microscopy, this was Adriamycin toxicity By electron microscopy, this was Adriamycin toxicity. See the clear vacuoles (theyare dilated sarcoplastic reticulum) and severe loss of myofibrils.
61 Cocaine heart – necrosis with contraction bands Cocaine heart – necrosis with contraction bands. This could happen with anysevere chronic stimulation such as too much pressors in a failing heart or apheochromocytoma.
62 Cardiac Sarcoidosis – well defined granuloma with giant cells 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.
63 Hemochromatosis - note the brown perinuclear deposits of hemosiderin Hemochromatosis - note the brown perinuclear deposits of hemosiderin. It is,however, the soluble iron, not the hemosiderin, that is considered toxic.
65 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.