The histopathology of endocardial sclerosis

This histological study of endocardial thickening in human hearts revealed that as in adult hearts, the proliferation in fetal, neonatal, and infant h earts consisted of collagen, elastin, and smooth muscle cells. Variation in severity from chamber to chamber and site to site indicated that severity is not an aging phenomenon and that predominantly local blood flow conditio ns determine localization and progression of proliferation. The similarity to endocardial thickening of cardiac valves and to intimal proliferation in blood vessels was remarkable. In old age and in chronic rheumatic heart di sease the proliferation exhibited hyalinization, cell depletion, loss and f ragmentation of elastin, lipid accumulation, and thrombosis, indicative of a similar pathogenesis to atherosclerotic changes in valvular endocardium a nd blood vessels. It was concluded that these chronic hemodynamically induc ed degenerative changes in the endocardium, including cardiac valves, shoul d be classified as endocardial atherosclerosis analogous to that in arterie s and veins and that severity is aggravated by high blood pressure, cardiac malformations, and dysfunction or damage caused by other disease processes . Cardiovasc Pathol 2000;9:161-173 (C) 2000 by Elsevier Science Inc.