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Effect of HMGcoA Reductase Inhibitors on Stroke: A Meta-Analysis of Randomized, Controlled Trials

Heiner C. Bucher, MD, MPH; Lauren E. Griffith, MS; and Gordon H. Guyatt, MD, MSc
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From Kantonsspital Basel, Basel, Switzerland; and McMaster University, Hamilton, Ontario, Canada. Grant Support: In part by grant 32-38793.930 from the Swiss National Research Foundation. Requests for Reprints: Heiner C. Bucher, MD, Medizinische Universitats-Poliklinik, Kantonsspital Basel, CH-4031 Basel, Switzerland. Current Author Addresses: Dr. Bucher: Medizinische Universitats-Poliklinik, Kantonsspital Basel, CH-4031 Basel, Switzerland.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1998;128(2):89-95. doi:10.7326/0003-4819-128-2-199801150-00002
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Background: Stroke is a leading cause of death in the industrialized world, and hypercholesterolemia may be a risk factor for stroke.

Objective: To determine whether reducing cholesterol levels with HMGcoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors or other antilipidemic interventions reduces risk for nonfatal and fatal stroke.

Data Sources: A systematic search in the MEDLINE and EMBASE databases of the English-language and non-English-language literature published from 1966 through October 1996.

Study Selection: All randomized, controlled trials of any cholesterol-lowering intervention that reported data on nonfatal and fatal strokes, on death from coronary heart disease, and on overall mortality were included. Whether treatment effects differed according to the type of cholesterol-lowering intervention used was investigated.

Data Extraction: Trials were reviewed for methods, inclusion and exclusion criteria, and outcomes.

Data Synthesis: 28 trials (for a total of 49 477 study participants in the intervention group and 56 636 participants in the control group) were included. The risk ratio for nonfatal and fatal stroke with HMGcoA reductase inhibitors was 0.76 (95% CI, 0.62 to 0.92; test of heterogeneity, P > 0.2). The risk ratios for nonfatal and fatal stroke with fibrates, resins, and dietary interventions were all close to 1.0, and the difference between the HMGcoA reductase inhibitor effect and the pooled estimate for all other interventions would, under the null hypothesis, be unlikely to occur by chance (P = 0.01). Trials with HMGcoA reductase inhibitors also showed reductions in rates of death from coronary heart disease and overall mortality.

Conclusion: This meta-analysis of randomized, controlled trials suggests that in hyperlipidemic patients who have not previously had stroke, HMGcoA reductase inhibitors reduce the incidence of stroke.

Figures

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Figure 1.
Risk ratio and summary estimates with 95% CIs for nonfatal and fatal stroke in randomized, controlled trials comparing HMGcoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors with placebo.P

> 0.2 (Breslow-Day test for heterogeneity). 4S = Scandinavian Simvastatin Survival Study; CARE = Cholesterol and Recurrent Events Trial; KAPS = Kuopio Atherosclerosis Prevention Study; PMG = Pravastatin Multinational Study Group for Cardiac Risk Patients; REGRESS = Regression Growth Evaluation Statin Study; WOSCOPS = West of Scotland Coronary Prevention Study Group.

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