Captopril administration reduces thrombus formation and surface expressionof platelet glycoprotein IIb IIIa in early postmyocardial infarction stage

Long-term administration of the angiotensin-converting enzyme inhibitor cap topril in survivors of myocardial infarction (MI) reduces the risk of cardi ovascular death, recurrence of MI, and unstable angina, suggesting that cap topril may posses antithrombotic properties that have not been clearly eluc idated. We assessed the short-term antithrombotic effects of captopril on p latelet aggregation, platelet-subendothelium interaction, and the expressio n of major glycoproteins on platelet surface. A double-blind study was carr ied out in 25 patients with MI. Blood samples were taken before (baseline) and 12 days after treatment in both the control and captopril groups. Plate let aggregation was tested by conventional aggregometry using common activa ting agents. Platelet interaction with deeply damaged subendothelial surfac e was evaluated in a perfusion model, with blood maintained under flow cond itions. Deposition of platelets was quantified by using computer-assisted m orphometric techniques on histological sections, and it was expressed as a percentage of total Vessel surface covered by platelets (CS) and as a ratio between large aggregates (T) and surface covered by platelets (100xT/CS), Glycoprotein expression was measured using flow cytometric techniques. Aggr egometric responses showed no significant variations; however, in the capto pril group, 100xT/CS decreased after 12 days of treatment (100xT/CS: 36+/-1 2.1% captopril versus 64+/-8.0% baseline; P=0.05). This parameter was also significantly decreased from that found in control group patients (100xT/CS : 67+/-4.5%; P=0.008). Flow cytometry showed a 30% reduction in glycoprotei n IIb/IIIa expression (P=0.02). Captopril reduced the formation of large ag gregates in a perfusion system, which might be related to a down-regulation of glycoprotein IIb/IIIa complex on the platelet surface. These results su ggest that captopril exerts an antiplatelet effect that may contribute to i ts beneficial action in MI.