[Anti-ischemic effects of SIN-1, a molsidomine metabolite, during coronary angioplasty and antiplatelet effects in humans].

The effects of SIN-1, the biologically active metabolite of molsidomine, on tolerance of ischaemia during percutaneous transluminal coronary angioplasty were studied in 12 patients. Following an intracoronary injection of SIN-1 0.5 mg, the time required for the ST segment to be depressed by at least 0.2 mV was significantly prolonged from 44 to 55-62 seconds. Simultaneously, SIN-1 reduced the significant rise in left ventricular end-diastolic pressure observed during dilatation. One minute after SIN-1 was injected, no effect was noted or on the increase in left ventricular volume indices or on the reduction of ejection fraction associated with dilatation. The maximum anti-ischaemic effect of SIN-1 was obtained 5 minutes after the injection. As regards the mechanism of action of the drug, a decrease in parietal tension through reduction of left ventricular preload should be considered. In addition, strong inhibition of platelet aggregation and adenosine triphosphate secretion was demonstrated in high platelet content plasma and whole blood 2 hours after an oral 16 mg dose of molsidomine. The antiplatelet effect of molsidomine may contribute to its anti-ischaemic effect by reducing both platelet adherence at the site of dilatation and the release of vasoconstrictor and pro-aggregant mediators.