Autologous low density lipoprotein enhances platelet aggregation in whole blood, as measured by in vitro filtragometry.

The influence of low density lipoprotein (LDL) on platelet aggregability was studied using filtragometry and conventional Born aggregometry in vitro. Three different concentrations of autologous LDL, obtained from 9 healthy male volunteers, were incubated for 20 min, at 37°C, with whole blood anticoagulated with low molecular weight heparin (filtragometry) or citrated platelet-rich plasma (PRP; Born aggregometry). The LDL-cholesterol concentration was increased from 1.7 ± 0.2 mmol/1 to 2.4 ± 0.2, 3.5 ± 0.3 and 5.3 ± 0.5 mmol/l, respectively. Adenosine diphospate (ADP)-induced platelet aggregation in whole blood was enhanced in a dose dependent manner by LDL, as assessed by filtragometry (ADP cone, range 0.1-0.3 μM). Platelet aggregability in PRP (Born) was not affected by LDL at the ED(50) for ADP-induced platelet aggregation (i.e. 1-4 μM ADP). The marked platelet activation caused by the high ADP concentrations used with conventional Born aggregometry may have masked a modest LDL-induced platelet activation as a slight increase in spontaneous platelet aggregation was observed in PRP at the intermediate LDL-concentration. The present findings indicate that low concentrations of LDL stimulate platelet aggregability in the physiological whole blood milieu. This adverse effect of LDL-cholesterol may be of clinical importance in patients with hypercholesterolaemia.