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Stroke complicating acute myocardial infarction. A meta-analysis of risk modification by anticoagulation and
P T Vaitkus1, J A Berlin, J S Schwartz
1Cardiovascular Section, School of Medicine, University of Pennsylvania, Philadelphia.
Insights
Systemic anticoagulation may reduce stroke incidence post-myocardial infarction, though trial heterogeneity complicates interpretation. Thrombolysis does not increase stroke risk overall, but tissue plasminogen activator shows higher stroke rates than streptokinase.
Area of Science:
- Cardiology
- Neurology
- Pharmacology
Background:
- Myocardial infarction (MI) survivors face stroke risk.
- Systemic anticoagulation and thrombolysis are used post-MI.
- Impact on stroke incidence requires clarification.
Purpose of the Study:
- To meta-analyze the effect of anticoagulation and thrombolysis on stroke incidence after MI.
- To compare stroke risk among different thrombolytic agents.
Main Methods:
- Computerized and manual literature search for controlled clinical trials.
- Inclusion of MI trials reporting total strokes in treated and control groups.
- Mantel-Haenszel odds ratio and 95% confidence interval (CI) for pooling.
Main Results:
- Anticoagulation trials showed a reduced stroke risk (OR=0.46, 95% CI: 0.30-0.64), but with significant heterogeneity.
- Thrombolytic trials (all, t-PA, streptokinase) did not show increased stroke risk (ORs: 1.08, 1.28, 1.02).
- Direct comparison of t-PA vs. streptokinase revealed excess strokes with t-PA (OR=0.73, 95% CI: 0.61-0.86).
Conclusions:
- Anticoagulants may reduce stroke post-MI, but heterogeneity limits definitive conclusions.
- Thrombolysis is not associated with increased stroke risk overall.
- Tissue plasminogen activator (t-PA) appears to carry a higher stroke risk compared to streptokinase.
Background:
The objective of this meta-analysis was to examine the impact of systemic anticoagulation and thrombolysis on the total incidence of stroke following myocardial infarction. Additionally, we sought to compare the relative risk of stroke with different thrombolytic agents.
Methods:
A computerized and manual literature search for controlled clinical trials of anticoagulants and thrombolytic agents in myocardial infarction reporting on total strokes in treated and control patients was used. Pooling was performed by calculating the Mantel-Haenszel odds ratio and 95% confidence interval (CI).
Results:
The Mantel-Haenszel pooled odds ratio for anticoagulation trials was 0.46 (95% CI, 0.30 to 0.64), suggesting a benefit of anticoagulant therapy. However, a statistically significant degree of variability (heterogeneity) was present among study results. The odds ratios for all thrombolytic trials, tissue plasminogen activator, and streptokinase trials, respectively, were 1.08 (95% CI, 0.87 to 1.35), 1.28 (95% CI, 0.76 to 2.17), and 1.02 (95% CI, 0.80 to 1.30), suggesting no overall excess of stroke with thrombolysis. The pooled odds ratio for three studies directly comparing streptokinase and tissue plasminogen activator was 0.73 (95% CI, 0.61 to 0.86), suggesting an excess of stroke for patients treated with tissue plasminogen activator in comparison with streptokinase-treated patients.
Conclusions:
The available data may support a role for anticoagulants in reducing the incidence of stroke after myocardial infarction, but the heterogeneity among the trials makes interpretation of this effect difficult. Although the available data do not indicate an increase in stroke with thrombolysis, a direct comparison of tissue plasminogen activator and streptokinase reveals an excess of strokes with tissue plasminogen activator.