TREATMENT EFFECTS ON SERUM-LIPOPROTEIN LIPIDS, APOLIPOPROTEINS AND LOW-DENSITY-LIPOPROTEIN PARTICLE-SIZE AND RELATIONSHIPS OF LIPOPROTEIN VARIABLES TO PROGRESSION OF CORONARY-ARTERY DISEASE IN THE BEZAFIBRATE CORONARY ATHEROSCLEROSIS INTERVENTION TRIAL (BECAIT)

Objectives. To investigate the mechanisms by which bezafibrate retarde d the progression of coronary lesions in the Bezafibrate Coronary Athe rosclerosis Intervention Trial (BECAIT), we examined the relationships of on-trial lipoproteins and lipoprotein subfractions to the angiogra phic outcome measurements. Background. BECAIT, the first double-blind, placebo-controlled, randomized serial angiographic trial of a fibrate compound, showed that progression of focal coronary atherosclerosis i n young survivors of myocardial infarction could be retarded by bezafi brate treatment. Methods. A total of 92 dyslipoproteinemic men who had survived a first myocardial infarction before the age of 45 years wer e randomly assigned to treatment for 5 gears with bezafibrate (200 mg three times daily) or placebo; 81 patients underwent baseline and at l east one post-treatment coronary angiography. Results. In addition to the decrease in very low density lipoprotein (VLDL) cholesterol (-53%) and triglyceride (-46%) and plasma apolipoprotein (apo) B (-9%) level s, bezafibrate treatment resulted in a significant increase in high de nsity lipoprotein-3 (HDL3) cholesterol (+9%) level and a shift in the low density lipoprotein (LDL) subclass distribution toward larger part icle species (peak particle diameter +0.32 nm). The on-trial HDL3 chol esterol and plasma apo B concentrations were found to be independent p redictors of the changes in mean minimum lumen diameter (r = -0.23, p < 0.05), and percent (%) stenosis (r = 0.30, p < 0.01), respectively. Decreases in small dense LDL and/or VLDL lipid concentrations were unr elated to disease progression. Conclusions. Our results suggest that t he effect of bezafibrate on progression of focal coronary atherosclero sis could be at least partly attributed to a rise in HDL, cholesterol and a decrease in the total number of apo B containing lipoproteins. ( J Am Coll Cardiol 1998;32:1648-56) (C)1998 by the American College of Cardiology.