Effects of cholestyramine and acipimox on subf ractions of plasma low density lipoprotein. Studies in normolipidaemic and hypercholesterolaemic subjects

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Abstract
Two independent studies were designed to investigate the separate and combined effects of acipimox and cholestyramine on plasma low density lipoprotein subfractions. In the first study, normolipidaemic subjects were given cholestyramine (16 g day‐1, 4 weeks), followed, after an 8‐week wash‐out period, by acipimox (750mg day‐1, 4 weeks). In the second study, moderately hypercholesterolaemic subjects were prescribed acipimox (1250mg day‐1, 10 weeks), followed by acipimox in combination with low dose cholestyramine (12g day‐1) for a further 10 weeks. In the normal subjects, cholestyramine decreased total LDL mass (density (d)= 1.019–1.063g ml‐1) by selectively reducing the largest, least dense LDL‐I(d 1.025–1.034 gml‐1, P < 0.05) and LDL‐II (d 1.034–1.044 g ml‐1, P‐1) showed a variable response to the resin. In the same subjects acipimox produced no overall change in total LDL mass but showed a tendency to redistribute LDL towards LDL‐I (+10%) and LDL‐II (+10%) in a manner related to the changes in plasma triglyceride (TG) (TG vs. LDL‐III r= 0.75, P P <0.05; LDL‐III‐50%) without affecting total LDL mass. The addition of cholestyramine produced a significant decrease in total LDL mass which was again confined to the LDL‐I (‐28%) and LDL‐II (‐23%) subfractions. These consistent and complementary changes in discrete LDL subfractions may, in part, explain the hypolipidaemic potency of acipimox in combination with low dose cholestyramine. In view of the association between LDL subfrac‐tion profile and coronary heart disease risk, this particular combination of drugs may represent an effective regimen for the modification of an athero‐genic lipoprotein phenotype.