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Shows lovastatin predominantly increases HDL2 subfractions in patients with peripheral vascular disease, suggesting a higher circulating HDL particle count.
The effects of lovastatin treatment on high-density lipoprotein subfractions (HDL2 and HLD3) were investigated in 34 patients with severe peripheral vascular disease and type IIa or type IIb hyperlipoproteinemia by use of a density gradient ultracentrifugation method. Lovastatin therapy caused greater percentage changes in HDL2 than in HDL3. In HDL2 the increases of cholesterol, total lipid, apolipoprotein AI (apoAI) and apolipoprotein AII (apoAII) concentrations were 23% (p < 0.05), 28% (p < 0.01), 24% (p < 0.01) and 11% (p < 0.01), respectively, in subjects with the type IIa phenotype. In patients with the type IIb phenotype the corresponding increases were 42% (p < 0.01), 44% (p < 0.01), 38% (p < 0.01) and 21% (p < 0.05), respectively. The apoAI/apoAII weight ratio in HDL2 rose by 11% and by 13% in type IIa and type IIb patients, respectively. The present results suggest that during lovastatin treatment the slight increase in serum HDL-cholesterol concentration was due, not to cholesterol enrichment by high-density lipoproteins, but more probably to an increase of the number of HDL particles. The observed changes were more pronounced in type IIb than in type IIa patients.
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Tilly-Kiesi et al. (1993) studied this question.
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