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.

[Sudden death in acute myocardial infarct in hospitalized patients: a clinical and anatomicopathological study over a 10.5-year period]. / Moartea subita în faza acuta a infarctului de miocard la bolnavi spitalizati: studiu clinic si anatomopatologic pe o perioada de 10.5 ani.

The paper reports on the study of 1457 patients with acute myocardial infarct (Ami) admitted in the word of the cardiac intensive care of the clinic for 10.5 years. The general mortality was of 21.2% and the sudden death (defined as such when appeared suddenly within less than 1 hour from the onset of the acute symptoms, but after 24 hours from the onset of AMI in a patient apparently equilibrated) appeared in 114 patients who were examined postmortem (43.3% of the total of the deaths). The main causes of the SD was rupture of the myocardium (28.8% of the general mortality), primary ventricular fibrillation (22.0%) and thromboembolic phenomena (17.8%). The sudden death by rupture of the myocardium appeared in a first AMI, usually large and was not helped by the anticoagulant treatment or by other therapy. Primary ventricular fibrillation appeared during the first week from the onset and was favoured by the ventricular hyperexcitability and active myocardial ischemia (which were not specific). Xyline (only more than 2 mg/min) and amiodarone gave a good protection. The sudden death by systemic thromboembolization appeared almost only in the antero-lateral myocardial infarcts, 5-8 days after the onset. The appearance of a small flow syndrome "sine materia" with or without association of some recurrent arrhythmias was suggested. Efficient anticoagulation prevented systemic thromboembolization and, to a smaller extent to pulmonary thromboembolization.

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.