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Biomedical subjects

L Gherasim

Publications and source records attributed to L Gherasim.

36 records · Page 2Linked to original sources

A morphological quantitative study of small vessels in diabetic cardiomyopathy.

In 25 adult diabetic patients, tissue fragments from myocardium were removed at necropsy and processed routinely. The morphometrical analysis was made using eye-piece ocular micrometer on a definite microscopic area. The arteriolar wall thickness increased from 5.10 mu +/- 1.71 in control group to 7.37 mu +/- 1.98 in the diabetic heart. The arterioles number decreased from 5.82/mm2 +/- 0.54 in the nondiabetics to 2.51/mm2 +/- 0.65 in the diabetic heart. The mean arteriolar diameter increased from 24.61 mu +/- 7.7 in the control group to 29.45 mu +/- 8.25 in the diabetic myocardium. The mean capillary diameter increased from 4.09 mu +/- 0.63 to 5.69 mu +/- 1.34 in diabetics. The capillaries number/mm2 decreased from 6.98 +/- 1.55 in the nondiabetics to 4.39 +/- 1.54 in diabetic patients. All differences, less the mean arteriolar diameter, are statistically significant. The following microscopical aspects were found in the small intramural coronary arteries: proliferation of endothelial cells with focal protuberances leading to partial narrowing of the lumen; increased thickness of the arteriolar wall due to fibrosis and accumulation of neutral mucopolysaccharides; alterations of elastic fibers. Frequently small areas of perivascular fibrosis and isolated foci of myocytolysis were found as well. These results suggest that the arteriolar impairment, especially the thickening of the arteriolar wall, could play a role in the pathogenesis of diabetic cardiomyopathy.

Cardiovascular Diseases↗

Correlated biochemical modifications of plasma lipoproteins in coronary heart disease: an accelerating pathologic factor.

We investigated the presence of biochemically modified plasma lipoproteins as pathologic factor for coronary heart disease in 15 patients with angina pectoris (CHD-P) vs 20 normal subjects (N). Decreased HDL were the most significant pathological feature present in P over 66 years old, while, P under 66 had, in addition to low HDL-Cholesterol (HDL-C), high levels of plasma cholesterol (C), LDL-Cholesterol (LDL-C), and lipid peroxides (TBARS), together with the presence of desialylated LDL and VLDL. We demonstrated by statistic analysis that these risk factors are correlated: high plasma C with a more pronounced imbalance between LDL and HDL, which, in turn, is associated with high TBARS levels, and also with circulating desialylated VLDL; high plasma TBARS values with desialylated LDL. We detected an increased level of autoantibodies towards autologous LDL and VLDL, in P vs N. The level of autoantibodies anti-LDL correlated with LDL-C level and with LDL desialylation, thus modified circulating LDL being most probably atherogenic. Circulating anti-LDL autoantibodies together with the low level of HDL might contribute to acceleration and aggravation of the atherosclerotic process.

Adult↗