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Ticlopidine in Acute Myocardial Infarction Improves pl atelet survival and reduces infarct size In a double-blind trial, 43 patients with acute myocardial infarction randomly received either liclopidine 250mg bid or placebo for 3 months, There was no significant difference between the 2 groups with respect to age, incidence 01 previous infarclion or durat ion of symptoms (mean 3.8 hrs in both groups). Peak serum creatine kinase-MB level was significantly lower in the ticlopidine than in the placebo group. Platelet survival was significantly reduced in the placebo group compared with the ticlopidine group 24-36 hours after infarction, but was similar in the 2 groups 3 mon ths after infarction. In the ticlopidine group, adenosine diphosphate (ADP)-induced platelet aggregation and ADP- and collagen·induced seroton in release were significantly in hibited throughout the study, compared with baseline and placebo. Ticlopidine treatment had no significant effect compared with placebo on platelet count, factor VIII activity or associated antigen, fibrinogen or fibrin monomers, or spontaneous or stasis·induced fibrinolytic activity. In conclusion, ticlopidine appears to prolong shortened platelet survival, and reduce infarct size by improving microcirculation in the marginal infarction area through decreased formation of platelet aggregates and th rombi. Knudsen. J.B.; K;a ller. E.. SIlage<>. K. and Gofmsen. J: 'Thrombosis and HacmmJlasis 53: 332-336 (.}un 1985) 0156·270Jj85jl005-{IQ17/0$J)1.00/0 ® AOIS Press INPHAAMA'" 26 Ocl 1985 17

Ticlopidine in Acute Myocardial Infarction

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Page 1: Ticlopidine in Acute Myocardial Infarction

Ticlopidine in Acute Myocardial Infarction Improves platelet survival and reduces infarct size

In a double-blind trial, 43 patients with acute myocardial infarction randomly received either liclopidine 250mg bid or placebo for 3 months, There was no significant difference between the 2 groups with respect to age, incidence 01 previous infarcl ion or duration of symptoms (mean 3.8 hrs in both groups). Peak serum creatine kinase-MB level was significantly lower in the ticlopidine than in the placebo group.

Platelet survival was significantly reduced in the placebo group compared with the ticlopidine group 24-36 hours after infarction, but was similar in the 2 groups 3 months after infarction. In the t iclopidine group, adenosine diphosphate (ADP)-induced platelet aggregation and ADP- and collagen·induced serotonin release were significantly inhibited throughout the study, compared with baseline and placebo. Ticlopidine treatment had no significant effect compared with placebo on platelet count , factor VIII activity or associated antigen, fibrinogen or fibrin monomers, or spontaneous or stasis·induced fibrinolytic activity.

In conclusion, ticlopidine appears to prolong shortened platelet survival, and reduce infarct size by improving microcirculation in the marginal infarction area through decreased formation of platelet aggregates and thrombi. Knudsen. J.B.; K;aller. E.. SIlage<>. K. and Gofmsen. J: 'Thrombosis and HacmmJlasis 53: 332-336 (.}un 1985)

0156·270Jj85jl005-{IQ17/0$J)1.00/0 ® AOIS Press INPHAAMA'" 26 Ocl 1985 17