A. Broijersen et al., GEMFIBROZIL ENHANCES PLATELET ACTIVITY IN PATIENTS WITH COMBINED HYPERLIPOPROTEINEMIA, Arteriosclerosis, thrombosis, and vascular biology, 15(1), 1995, pp. 121-127
A placebo-controlled crossover study was conducted to evaluate whether
lipid-lowering with gemfibrozil (10 to 12 weeks) affects platelet fun
ction in vivo at rest and during mental stress in 21 men with combined
hyperlipoproteinemia. Gemfibrozil lowered plasma triglycerides and to
tal and VLDL cholesterol (P<.001 for all), whereas HDL cholesterol inc
reased (P<.001). Gemfibrozil increased platelet counts by 18% (P<.001)
and, according to filtragometry measurements, enhanced overall (means
of rest and stress values) platelet aggregability in vivo (P=.014); t
his effect was more evident during mental stress (P=.027) than at rest
(P=.18). Moreover, the urinary excretion of 11-dehydro-thromboxane-B-
2 was 54% higher during treatment with gemfibrozil (P<.001), whereas t
he excretion of beta-thromboglobulin in urine was unaltered. Plasma be
ta-thromboglobulin tended to be slightly elevated during active treatm
ent (P=.15). Mental stress increased heart rate and catecholamine leve
ls and elevated all cholesterol fractions (P<.01) and plasma beta-thro
mboglobulin (during placebo, P=.02), but platelet aggregability did no
t increase significantly. A positive correlation was found between 11-
dehydrothromboxane-B-2 excretion and LDL cholesterol levels during pla
cebo (r=.62, P=.0057). In conclusion, gemfibrozil has beneficial effec
ts on plasma lipoprotein levels but enhances several aspects of platel
et activity in vivo and increases platelet counts. These changes might
be prothrombotic and thus adverse for the hyperlipidemic patient. Pri
mary preventive effects of gemfibrozil might be enhanced if a platelet
inhibitor such as aspirin is administered with gemfibrozil.