[Comparative study on the sclerotic changes of cardiac valve and blood vessel].

BACKGROUND Recently, there is an increase in number of surgical treatments for the aortic stenosis caused by valvular sclerosis with aging. Whether valvular sclerosis are related to aortic atherosclerosis, the prevention therapy of arteriosclerosis may benefit the clinical treatment of the valvular dysfunction due to aging. MATERIALS AND METHODS Gross, histological and immunohistochemical studies were made on 159 autopsy cases (97 men, 62 women, mean age 65.1 years old). The degree of sclerotic change in aortic valve (AV), mitral valve (MV), aorta (Ao) and coronary artery (CA) was classified by gross examination to none, mild, moderate, and severe, scored as 0 to 3, respectively. The data were statistically analyzed by the correlation test. To observe the expression of bone related proteins in valve calcification, indirect immunostaining procedures were applied with antibodies to osteocalcin, osteopontin and osteonectin. RESULTS Grossly, there was a significant correlation in sclerotic change between Ao and AV, Ao and MV, AV and MV, CA and AV, and CA and MV, respectively (p<0.01). Also, the degree of sclerotic change in each tissue was correlated with patients'age. However, the grade of sclerotic change of each tissue was variant in each case. On gross observation, all valvular sclerosis showed yellowish thickening and/or calcification. Microscopically, hyalinous change of the fibrosa was observed in the yellowish lesion of the valves. Accumulations of foamy macrophages were found focally at the surface area of the fibrosa, but no atheromatous change was observed in the valves. Calcified deposits, if present, were found in the fibrous valvular ring or fibrosa with hyalinous degeneration. In MV, calcification was usually localized in the fibrous ring. However, in AV, valvular calcification extended diffusely in the fibrosa and caused stenosis in some cases. These lesions were similar to calcified area in the intima with fibrous thickening of Ao and/or CA, but were different from atheromatous lesion of these tissues. Immunohistochemically, calcified areas of valves showed stronger reaction for osteocalcin than that of vessels. CONCLUSION Among sclerotic change of cardiac valves and arteriosclerosis, statistical correlations were found, but pathological features were different. Main causes of these differences are thought to be 1) not only the shear stress, but also intramural pressure and mechanical stress with opening and closing may interfere the sclerotic change of cardiac valves, and 2) mechanism of valvular sclerosis may be different from arteriosclerosis because medial smooth muscle cells are absent in the valves.