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Hypercholesterolemia does not affect the antiplatelet activity of clopidogrel.

In a recent article, Hohlfeld et al,’ showed that severe hypercholesterolemia in rabbits considerably attenuated the inhibition of adenosine 5’-diphosphate ( ADP)-induced platelet aggregation by ticlopidine. These authors suggested that this effect could be related to the stimulation of thromboxane A2 formation by ADP occurring during severe hypercholesterolemia. However, in these experiments, the total plasma cholesterol level was around 30 mM ( 12 g/1), a concentration which cannot be considered as relevant clinically. In order to investigate the effect of a severe but relevant hypercholesterolemia (less than 4 g/1) on the antiplatelet activity of clopidogrel,2 a chemical analogue of ticlopidine, the following experiments were performed: male New Zealand rabbits were randomly divided into four groups of six animals. Rabbits were fed for 10 days with either a standard diet or a diet supplemented with 0.5% cholesterol. One control group and one cholesterol fed-group received clopidogrel (5 mg/kg/day, PO). The total plasma cholesterol concentration was monitored during the experiment using an assay kit and platelet aggregation was measured by the turbimetric method of Born.3 Ten days after the beginning of the cholesterol-rich diet, the total plasma cholesterol concentration increased from 0.3 f0.07 g/1 to 3.7 f 0.4 g/l. As shown in Figure 1, the oral treatment with clopidogrel (5 mg/kg/day) reduced ADPinduced aggregation of platelets prepared from