Key result
On-trial HDL3 and apo B independently predict coronary angiographic progression during bezafibrate therapy.
Why the study?
Does bezafibrate improve lipid profiles and retard angiographic progression of coronary atherosclerosis in young male survivors of myocardial infarction?
RCT (n=92)
double-blind
randomly assigned
Does bezafibrate improve lipid profiles and retard angiographic progression of coronary atherosclerosis in young male survivors of myocardial infarction?
Answers are grounded in this paper and cite their sources.
Bezafibrate retards the progression of focal coronary atherosclerosis in young male MI survivors, an effect that is independently predicted by increases in HDL3 cholesterol and decreases in apo B concentrations.
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 +032 nm). The on-trial HDL3 cholesterol 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 HDL3 cholesterol and a decrease in the total number of apo B-containing lipoproteins.
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Ruotolo et al. (1998) conducted an RCT in dyslipoproteinemia and prior myocardial infarction (n=92). bezafibrate vs. placebo was evaluated on relationships of on-trial lipoproteins and lipoprotein subfractions to angiographic outcome measurements (mean minimum lumen diameter and percent stenosis). Bezafibrate altered lipoprotein profiles, with on-trial HDL3 and apo B independently predicting changes in mean minimum lumen diameter (r=-0.23, p<0.05) and percent stenosis (r=0.30, p<0.01).
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