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The histopathology of endocardial sclerosis
W E Stehbens1, B Delahunt, J M Zuccollo
1Departments of Pathology and Molecular Medicine and Obstetrics and Gynaecology, Wellington South, New Zealand. wstehbens@wnmeds.ac.nz
Insights
Endocardial thickening in human hearts, from fetus to old age, is driven by local blood flow, not aging. This process, similar to blood vessel atherosclerosis, affects cardiac valves and is worsened by hypertension.
Area of Science:
- Cardiovascular Histology
- Pathology
- Hemodynamics
Background:
- Endocardial thickening is observed in human hearts across all age groups.
- The composition of this thickening includes collagen, elastin, and smooth muscle cells.
Purpose of the Study:
- To investigate the factors influencing endocardial thickening.
- To compare endocardial changes with vascular intimal proliferation and atherosclerotic processes.
- To propose a classification for these chronic degenerative changes.
Main Methods:
- Histological examination of human heart tissues from fetal to old age.
- Analysis of proliferation patterns and composition.
- Comparison with cardiac valve and blood vessel histology.
Main Results:
- Endocardial proliferation in fetal, neonatal, and infant hearts mirrors adult hearts in composition.
- Severity and localization are determined by local blood flow conditions, not age.
- Chronic changes in old age and rheumatic heart disease show similarities to atherosclerosis, including hyalinization and lipid accumulation.
Conclusions:
- Endocardial thickening is a hemodynamically induced process.
- These changes, particularly in cardiac valves, should be termed 'endocardial atherosclerosis'.
- Severity is exacerbated by hypertension, cardiac malformations, and other disease-related dysfunctions.
Abstract:
This histological study of endocardial thickening in human hearts revealed that as in adult hearts, the proliferation in fetal, neonatal, and infant hearts 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 conditions 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 disease the proliferation exhibited hyalinization, cell depletion, loss and fragmentation of elastin, lipid accumulation, and thrombosis, indicative of a similar pathogenesis to atherosclerotic changes in valvular endocardium and blood vessels. It was concluded that these chronic hemodynamically induced degenerative changes in the endocardium, including cardiac valves, should be classified as endocardial atherosclerosis analogous to that in arteries and veins and that severity is aggravated by high blood pressure, cardiac malformations, and dysfunction or damage caused by other disease processes.