Fig. 11.21 Infectiveendocarditis.(A)SubacuteendocarditiscausedbyStreptococcus viridans onapreviouslymyxomatousmitralvalve.Thelarge,friablevegetationsaredenotedbyarrows. (B)AcuteendocarditiscausedbyStaphylococcus aureus onacongenitallybicuspidaorticvalvewithextensivecuspaldestructionandringabscess(arrow).
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Fig. 11.22 Nonbacterialthromboticendocarditis(NBTE).(A)Smallthromboticvegetationsalongthelineofclosureofthemitralvalveleaflets(arrows).
(B)PhotomicrographofNBTElesion,showingblandthrombus,withvirtuallynoinflammationinthevalvecusp(C) orthethromboticdeposit(t).Thethrombusisonlylooselyattachedtothecusp(arrow).
Endocarditis in Systemic Lupus Erythematosus: Libman-Sacks Endocarditis
Libman-Sacks endocarditis is characterized by the presence of sterile vegetations on the valves of patients with systemic lupus erythematosus. It occurs in about 10% of patients with SLE. The lesions probably develop as a consequence of immune complex deposition and thus exhibit associated inflammation, often with fibrinoid necrosis of the valve adjacent to the vegetation; subsequent fibrosis and serious deformity can result in lesions that resemble chronic rheumatic heart disease. These can occur anywhere on the valve surface, on the cords, or even on the atrial or ventricular endocardium (see
Fig. 11.20 ). Similar lesions can occur in the setting of anti-phospholipid antibody syndrome (Chapter 4).
•Valvepathologycanleadtoocclusion(stenosis) and/orregurgitation(insufficiency); acquiredaorticormitralvalvestenosisaccountsforapproximatelytwothirdsofallvalvedisease.
Valvecalcificationtypicallyresultsinstenosis;abnormalmatrixsynthesisandturnoverleadstomyxomatousdegenerationandinsufficiency.
Inflammatoryvalvediseasescausepostinflammatoryneovascularizationandscarring.Rheumaticheartdiseaseresultsfromanti-streptococcalantibodiesthatcross-reactwithcardiactissues;itmostcommonlyaffectsthemitralvalveandisresponsibleforalmostallcasesofacquiredmitralstenosis.
Infectiveendocarditiscanrapidlydestroynormalvalves,orcanbeindolentandminimallydestructiveofpreviouslyabnormalvalves.Systemicembolizationcanproducesepticinfarcts.
Nonbacterialthromboticendocarditisoccursonpreviouslynormalvalvesasaresultofhypercoagulablestates;embolizationisanimportantcomplication.
Cardiac diseases due to intrinsic myocardial dysfunction are termed cardiomyopathies (literally, “heart muscle diseases”); these can be primary—that is, principally confined to the myocardium—or secondary presenting as the cardiac manifestation of a systemic disorder. Cardiomyopathies are thus a diverse group that includes inflammatory disorders (e.g., myocarditis), immunologic diseases (e.g., sarcoidosis), systemic metabolic disorders (e.g., hemochromatosis), muscular dystrophies, and genetic disorders of myocardial fibers. In many cases, the cardiomyopathy is of unknown etiology and thus is termed idiopathic; however, a number of previously “idiopathic” cardiomyopathies have been shown to be the consequence of specific genetic abnormalities in cardiac energy metabolism or in structural and contractile proteins.