Key result
Ticlopidine reduces post-exercise platelet aggregation ~35% and increases exercise tolerance in ischemic heart disease.
Why the study?
Platelet aggregation during exercise is a key mechanism for acute myocardial infarction, and the effect of ticlopidine on exercise-induced platelet aggregation in ischemic heart disease patients was evaluated.
Does ticlopidine reduce exercise-induced platelet aggregation and improve exercise tolerance time in patients with ischemic heart disease?
Does ticlopidine reduce exercise-induced platelet aggregation and improve exercise tolerance time in patients with ischemic heart disease?
Ticlopidine suppresses exercise-induced platelet aggregation and increases exercise-tolerance time in patients with ischemic heart disease.
Answers are grounded in this paper and cite their sources.
May attenuate exercise-induced platelet aggregation in IHD; leaves open clinical benefit and need for prospective trials.
Platelet aggregation is one of the most important mechanisms for acute myocardial infarction during exercise. We sought to evaluate the effect of ticlopidine (TP) on platelet aggregation (PA) during exercise in patients with ischemic heart disease (IHD). We studied 38 patients with IHD, 26 patients with effort angina pectoris, and 12 patients with a previous myocardial infarction. In protocol I, subjects were divided into two groups. Drugs altering platelet aggregation were withheld 2-4 weeks before the study in 25 patients (control group). TP (200 mg/day) was administered for 7 days in 13 patients (ticlopidine group). A symptom-limited modified Bruce protocol treadmill exercise test was performed. PA was measured at rest and after exercise by using optical densitometry induced by adenosine diphosphate (ADP). PA ratio (percentage of maximum) was compared. In protocol II, in 12 patients, treadmill exercise test and PA measurement were performed with and without TP. PA significantly increased after exercise in control (from 51.7+/-23.3% to 64.4+/-27.7%, p < 0.01) and ticlopidine (from 31.9+/-10.5% to 42.0+/-20.4%, p < .01) groups; however, its grade was lower in the ticlopidine group than in the control group. After exercise, PA was lower in the ticlopidine group than in control group (42.0+/-20.4% vs. 64.4+/-27.7%; p < 0.01). In the same patients, PA was lower with TP than without TP after exercise. Treadmill exercise-tolerance time was greater in the ticlopidine group than in the control group, but not statistically significant (762.3+/-139.2 vs. 711.6+/-169.6 s; NS). Exercise-tolerance time was significantly greater with TP than without TP in same patient (791.7+/-98.9 vs. 733.3+/-152.8 s; p < .05). TP suppressed the increase of PA during exercise and increased the exercise-tolerance time in patients with IHD.
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Tsuruta et al. (1999) studied Ischemic heart disease (n=38). Ticlopidine vs. Control (no drugs altering platelet aggregation) was evaluated on Platelet aggregation after exercise (p=<0.01). Ticlopidine significantly reduced platelet aggregation after exercise compared to control (42.0% vs 64.4%; p<0.01) and increased exercise-tolerance time in patients with ischemic heart disease.
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