RANDOMIZED TRIAL OF RIDOGREL, A COMBINED THROMBOXANE A(2) SYNTHASE INHIBITOR AND THROMBOXANE A(2) PROSTAGLANDIN ENDOPEROXIDE RECEPTOR ANTAGONIST, VERSUS ASPIRIN AS ADJUNCT TO THROMBOLYSIS IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION - THE RIDOGREL VERSUS ASPIRIN PATENCY TRIAL (RAPT)/

Background Aspirin, by nonselectively blocking cyclooxygenase both in platelets and in endothelial cells, not only inhibits the thromboxane A(2) pathway of platelet activation but at the same time also the gene ration of vasodilating and platelet-inhibitory prostanoids, such as pr ostacyclin, by the endothelial cells. Ridogrel, by inhibiting thrombox ane A(2) synthase and blocking the thromboxane A(2)/prostaglandin endo peroxide receptors, is a more potent antiplatelet agent than aspirin a nd might offer an advantage over aspirin as an adjunct to thrombolysis . This study was performed to compare the efficacy and safety of ridog rel with that of aspirin as conjunctive therapy for thrombolysis in pa tients with acute myocardial infarction. Methods and Results A total o f 907 patients with acute myocardial infarction were randomized betwee n aspirin and ridogrel given in addition to streptokinase (1.5 MU over a period of 1 hour). The primary end point was coronary patency (TIMI flow grades 2 and 3) at predischarge angiography to be performed betw een 7 and 14 days after admission. A patent infarct-related vessel was found in similar proportions of patients in the two treatment groups: 72.2% in the ridogrel and 75.5% in the aspirin group. The presence of clinical markers of reperfusion at 2 hours and the incidence of major clinical events during hospital stay were also similar in both groups . However, in a post hoc analysis, a lower incidence of new ischemic e vents (reinfarction, recurrent angina, ischemic stroke) was observed w ith ridogrel: 13% versus 19% in the aspirin group (a 32% reduction; P< .025). No excess of serious bleeding complications, including hemorrha gic stroke, was found. Conclusions Ridogrel is not superior to aspirin in enhancing the fibrinolytic efficacy of streptokinase but might be more effective in preventing new ischemic events.