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Ticlopidine versus aspirin after myocardial infarction (STAMI) trial
D Scrutinio1, C Cimminiello, E Marubini
1Division of Cardiology, S. Maugeri Foundation, IRCCS, Institute of Rehabilitation, Cassano Murge, Bari, Italy. dscrutinio@fsm.it
Insights
In survivors of acute myocardial infarction (AMI), aspirin and ticlopidine showed similar efficacy in preventing major adverse cardiovascular events over six months. Both drugs were equally effective in reducing the combined endpoint of death, recurrent AMI, stroke, and angina.
Area of Science:
- Cardiology
- Pharmacology
- Clinical Trials
Background:
- Secondary prevention after acute myocardial infarction (AMI) is crucial.
- The efficacy of ticlopidine in this context has not been previously explored.
- Thrombolysis is a standard treatment for AMI.
Purpose of the Study:
- To compare the efficacy of aspirin versus ticlopidine in patients who survived AMI and received thrombolysis.
- To evaluate the effectiveness of these antiplatelet agents in secondary prevention.
Main Methods:
- A randomized, double-blind, multicenter trial involving 1,470 patients post-thrombolysis for AMI.
- Patients were allocated to receive either aspirin (160 mg/day) or ticlopidine (500 mg/day).
- The primary endpoint was a composite of fatal/nonfatal AMI, fatal/nonfatal stroke, angina, or death within six months.
Main Results:
- The primary endpoint occurred in 8.0% of patients in both the aspirin and ticlopidine groups (p=0.966).
- Nonfatal myocardial infarction was significantly lower in the ticlopidine group (1.1% vs 2.4%, p=0.049).
- No significant differences were observed in vascular death, nonfatal stroke, angina, or adverse reactions between the groups.
Conclusions:
- Ticlopidine and aspirin demonstrated comparable efficacy in preventing major adverse cardiovascular events in AMI survivors treated with thrombolysis.
- Neither drug showed superiority in reducing the combined endpoint of death, recurrent AMI, stroke, or angina.
- The study suggests similar roles for both agents in secondary prevention post-AMI.
Objectives:
We sought to compare the efficacy of aspirin and ticlopidine in survivors of acute myocardial infarction (AMI) treated with thrombolysis.
Background:
The role of ticlopidine in secondary prevention after AMI has not yet been explored.
Methods:
Of 4,696 patients with AMI treated with thrombolysis who were screened, 261 died in the hospital (5.6%) and 1,470 were enrolled in this randomized, double-blind, multicenter trial and allocated to treatment with either aspirin (160 mg/day) or ticlopidine (500 mg/day). The most frequent reasons for exclusion were refusal to give informed consent, planned myocardial revascularization, risk of noncompliance with study procedures, need for anticoagulant therapy and contraindications to the study treatments. The primary end point was the first occurrence of any of the following events during the six-month follow-up: fatal and nonfatal AMI, fatal and nonfatal stroke, angina with objective evidence of myocardial ischemia, vascular death or death due to any other cause.
Results:
The primary end point was recorded in 59 (8.0%) of the 736 aspirin-treated and 59 (8.0%) of the 734 ticlopidine-treated patients (p = 0.966). Vascular death was the first event in five patients taking aspirin and in six patients taking ticlopidine (0.7% vs. 0.8%; p = NS); nonfatal AMI in 18 and 8 (2.4% vs. 1.1%; p = 0.049); nonfatal stroke in 3 and 4 (0.4% vs. 0.5%; p = NS); and angina in 33 and 40 (4.5% vs. 5.4%; p = NS), respectively. The frequency of adverse reactions was not significantly different between the two groups.
Conclusions:
No difference was found between the ticlopidine and aspirin groups in the rate of the primary combined end point of death, recurrent AMI, stroke and angina.