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The majority of coronary thrombi (∼75%) is caused by plaque rupture .1,2 Prototype of the rupture-prone plaque contains a large, soft, lipid-rich necrotic core with a thin and inflamed fibrous cap, so-called thin-cap fibroatheroma (TCFA) ( Figure 1 ).3,4 Other common features include expansive remodelling, large plaque size, plaque haemorrhage, neovascularization, adventitial inflammation, and ‘spotty’ calcifications.4 Thin-cap fibroatheroma caps are usually

Decreased plasma low density lipoproteins (LDL) cholesterol and apolipoprotein B (apo B) levels are observed in heavy alcohol drinkers. LDL composition was determined in 16 alcohol addicts immediately after a period of alcohol abuse. Cholesterol to apo B ratio in the LDL fraction was significantly higher in the alcoholic group when compared with controls. In half of them the ratio exceeded 1.75. LDL subfractionation showed that in all subjects with atypically high LDL cholesterol to apolipoprotein B ratio, most of the LDL was in the form of a light subfraction. Acetylation in vitro showed that the heavy LDL subfraction was modified to a greater extent than the light subfraction. This suggests that the low apo B levels often observed after heavy drinking may arise from enhanced removal of the heavy LDL subfraction from the bloodstream.

Groups of rabbits were fed for six weeks various diets: standard died + ethanol, high-cholesterol diet and a high-cholesterol + ethanol one. During the next six weeks every diet was supplemented with a fresh vegetable (carrot). Cholesterol and triglycerides were determined in the whole serum and in lipoprotein fractions. In rabbits fed standard diet ethanol caused a moderate elevation of VLDL cholesterol and triglyceride and LDL cholesterol levels. In animals on high-cholesterol diet cholesterol and triglyceride concentrations in these fractions were very high. Simultaneous consumption of large amounts of cholesterol and of ethanol resulted in a greater rise of cholesterol concentration in the whole serum and in VLDL and LDL fraction than did high-cholesterol diet alone. Addition of carrot caused a pronounced reduction of serum cholesterol concentration in animals fed all kinds of diets. The reduction concerned mainly VLDL.

The purpose of this study was an assessment of the relative proportions of apolipoprotein C subfractions in the VLDL fraction, which could contribute to explaining the development of metabolic disturbances in hyper-pre-beta-lipoproteinaemias. The study was carried out in 21 patients with hyperlipoproteinaemia type IIa, IIb, III, IV and in 8 subjects without lipid metabolism disturbances. Apolipoproteins C were separated in disc electrophoresis on polyacrylamide gel (PAGE) with added 8-M of urea. After the electrophoresis three main subfractions were obtained and were identified according to their electrophoretic mobility as Apo CII, Apo CIII1 and Apo CIII2. The relative per cent proportions of apolipoproteins C were determined by densitometry. A correlation was found between triglyceride concentration in the VLDL fraction and the relative amounts of Apo CII and Apo CIII1. Moreover, a raised ratio of the lipoprotein lipase inhibitor (Apo CIII1) to the activator of this enzyme (Apo CII) was demonstrated in hyperlipoproteinaemias type IIb, III and IV, which may suggest decreased susceptibility of these lipoproteins to the action of lipoprotein lipase.

Current evidence indicates that the non-selective beta-blocker propranolol reduces the severity of experimental atherosclerosis in animal model. We studied the effect of propranolol on cholesterol ester synthesis and storage in mouse peritoneal macrophages in vitro. Propranolol in concentrations found in the plasma of patients treated with it (150 ng/ml) decreased by 20-30% beta-VLDL-stimulated synthesis of cholesterol esters with (14C)-oleate. A similar effect was observed also on this synthesis stimulated by acetyl-LDL. In a similar degree the accumulation of cholesteryl esters in the cells was decreased during the 48-hour incubation with lipoproteins in the presence of propranolol. No effect of the drug was observed on the uptake and degradation of beta-VLDL or acetyl-LDL. These observations suggest that propranolol may inhibit cholesteryl ester accumulation in macrophages at the point subsequent to lipoprotein uptake. This may have an impact on the treatment or prevention of atherosclerosis.