Inhibition of Human Endothelial Prostacyclin Synthesis by Different Aspirin Formulations

The availability of different formulations of low-dose aspirin for use as anti-thrombotic agents merits a comparison of their effects on vessel wall biochemistry. We compared the effect of ingestion of an enteric-coated slow-release aspirin (Astrix) with that of soluble aspirin (Cardiprin) on human endothelial prostacyclin synthesis. Patients undergoing varicose vein surgery (10 per group) ingested 100 mg aspirin per day as Astrix or Cardiprin for 7 days prior to surgery. A control group ingested no aspirin. Prostacyclin synthesis by the endothelial surface of the great saphenous vein was determined in vitro. Both aspirin formulations caused significant inhibition of endothelial prostacyclin synthesis compared with the control group. Using the median values, the enteric-coated slow-release aspirin caused 76% inhibition, whereas the soluble formulation caused significantly greater inhibition (95%). If differential inhibition of platelet thromboxane synthesis with 'sparing' of endothelial prostacyclin synthesis is necessary for an optimum anti-thrombotic effect of aspirin, the results suggest that a lower dose of soluble aspirin than enteric-coated slow-release aspirin may be preferred.