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Antiplatelets, ACE inhibitors, and statins combination reduces stroke severity and tissue at risk

From the Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.

Address correspondence and reprint requests to Dr. M. Selim, Department of Neurology–Stroke Division, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Palmer 127, Boston, MA 02215; e-mail: mselim{at}bidmc.harvard.edu

Background: Antiplatelets (APL), angiotensin-converting enzyme (ACE) inhibitors (ACEI), and statins (STAT) are commonly used for stroke prevention. The authors examined whether combination therapy with these agents has additive protective effects in reducing ischemic stroke severity.

Methods: The authors retrospectively analyzed data from 210 consecutive patients presenting within 24 hours of stroke onset. Baseline NIH Stroke Scale (NIHSS) score and diffusion-weighted imaging (DWI), perfusion-weighted imaging (PWI), and PWI–DWI mismatch lesion volumes as clinical and radiologic measures of stroke severity were measured among patients who were not taking APL, ACEI, or STAT before stroke onset vs those who were taking APL alone or in combination with either ACEI, STAT, or both.

Results: Sixty-nine patients were not on APL, ACEI, or STAT at stroke onset; 47 were on APL alone, 43 on dual (14 APL + STAT, 29 APL + ACEI), and 20 on triple combination therapy. Patients on triple therapy had lower NIHSS score (p = 0.001) and smaller mean PWI–DWI mismatch lesion volumes (p = 0.03) than those on two agents, APL alone, or no prestroke therapy. Higher percentages of patients on triple therapy had shorter length of hospitalization and better functional status upon discharge. Age, risk factor profile, blood pressure, glucose levels, onset to evaluation time, stroke subtypes, and DWI lesion volumes were comparable among all groups.

Conclusions: Prestroke use of available drugs for stroke prevention, in combination, may result in additive reduction in stroke severity, as measured by NIH Stroke Scale, and the volume of ischemic tissue at risk, as assessed by perfusion-weighted imaging–diffusion-weighted imaging mismatch. These findings require further validation in larger-scale, randomized, prospective studies.

Commentary, see page 1135

Supported in part by grants from the Harvard Center for Neurodegeneration and Repair (Dr. Selim) and the Doris Duke Charitable Foundation and the NINDS (1R01NS045049-01A1) (Dr. Schlaug).

Disclosure: The authors report no conflicts of interest.

Received September 12, 2005. Accepted in final form January 13, 2006.

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Neurology 2006 66: 1135. [Full Text]  

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