EFFECTS OF SELECTIVE LDL-APHERESIS AND PRAVASTATIN THERAPY ON PLATELET-FUNCTION IN FAMILIAL HYPERCHOLESTEROLEMIA

Platelet function was studied in 10 patients with familial hypercholes terolaemia, following lipid-lowering treatment with selective LDL-aphe resis and with the HMG-CoA reductase inhibitor pravastatin. Platelet f unction was assessed before, and 2, 5 and 14 days after LDL-apheresis, and before and after 4 weeks of pravastatin therapy. Both treatments significantly reduced total- and LDL-cholesterol, whereas LDL-apheresi s also reduced VLDL-cholesterol. Lp(a)-levels were reduced by LDL-aphe resis and elevated by pravastatin treatment. Pravastatin therapy signi ficantly enhanced platelet aggregability in vivo, as measured by ex vi vo filtragometry. Plasma serotonin levels also increased. Other marker s of in vivo activation of platelets, i.e. beta-thromboglobulin in pla sma and urine, and 11-dehydro-thromboxane B-2 in urine were unaltered. Adenosine diphosphate-induced platelet aggregation in vitro remained unchanged during pravastatin therapy, and the platelet volume distribu tion was not affected. LDL-apheresis reduced the mean platelet volume, as well as the percentage of large platelets, whereas the percentage of small platelets increased. Other measures of platelet function in v ivo or in vitro were, however, unaltered following LDL-apheresis. Thus , pravastatin therapy enhances certain aspects of platelet aggregabili ty in vivo, whereas a single treatment with selective LDL-apheresis do es not consistently affect platelet aggregability during resting condi tions. These results do not support the concept that reduction of LDL- cholesterol improves platelet function in hypercholesterolaemic patien ts, at least not in the short-term. However, the reduction of platelet volume after LDL-apheresis may be beneficial for patients receiving t his therapy regularly.