Objectives. To investigate the mechanisms by which bezafibrate retarded the progression of coronary lesions in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT), we examined the relationships of on-trial lipoproteins and lipoprotein subfractions to the angiographic 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 in young survivors of myocardial infarction could be retarded by bezafibrate treatment.

Methods. A total of 92 dyslipoproteinemic men who had survived a first myocardial infarction before the age of 45 years were randomly assigned to treatment for 5 years with bezafibrate (200 mg three times daily) or placebo; 81 patients underwent baseline and at least 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%) levels, bezafibrate treatment resulted in a significant increase in high density lipoprotein-3 (HDL₃) cholesterol (+9%) level and a shift in the low density lipoprotein (LDL) subclass distribution toward larger particle species (peak particle diameter +0.32 nm). The on-trial HDL₃cholesterol and plasma apo B concentrations were found to be independent predictors 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 unrelated to disease progression.

Conclusions. Our results suggest that the effect of bezafibrate on progression of focal coronary atherosclerosis could be at least partly attributed to a rise in HDL₃cholesterol and a decrease in the total number of apo B-containing lipoproteins.