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Stroke. 2006;37:134-138
Published online before print November 23, 2005, doi: 10.1161/01.STR.0000195045.40409.85
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(Stroke. 2006;37:134.)
© 2006 American Heart Association, Inc.


Original Contributions

Antiplatelet Drugs In the Secondary Prevention After Stroke

Differential Efficacy in Large Versus Small Vessel Disease? A Subgroup Analysis From ESPS-2

Marie-José Ariesen, PhD; Ale Algra, MD, FAHA L. Jaap Kappelle, MD

From the Julius Center for Health Sciences and Primary Care (M.J.A., A.A.), University Medical Center, Utrecht, The Netherlands; and the Department of Neurology (A.A., L.J.K.), Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, The Netherlands.

Correspondence to Ale Algra, MD, FAHA, Department of Neurology and Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Str.06.131, PO Box 85500, 3508 GA Utrecht, The Netherlands. E-mail A.Algra{at}umcutrecht.nl

Background and Purpose— Arterial disease resulting in cerebral ischemia can be classified into large vessel disease (LVD) and small vessel disease (SVD). We assessed whether antiplatelet drugs were more efficacious in large than in small vessel cerebrovascular disease.

Methods— Individual patient data of the second European Stroke Prevention Study (n=6602), in which patients with a previous transient ischemic attack or ischemic stroke were randomized to aspirin, dipyridamole, their combination, or placebo, were reanalyzed. Type of vessel disease was classified according to clinical symptoms or physical examination. Presence of a lacunar syndrome was considered typical for SVD and evidence of cortical dysfunction for LVD. Vascular events (nonfatal stroke, nonfatal myocardial infarction, nonfatal other vascular event, or vascular death) were taken as outcome. Cox regression analyses were performed.

Results— A total of 419 first vascular events occurred in 2600 patients with SVD and 367 in 1816 patients with LVD (mean follow-up 1.7 years). For aspirin versus placebo, the hazard ratio (HR) was 0.86 (95% CI, 0.66 to 1.11) in patients with SVD and 0.80 (95% CI, 0.61 to 1.06) in those with LVD (Pinteraction=0.74). For dipyridamole versus placebo, the HR was 0.86 (95% CI, 0.67 to 1.12) in patients with SVD and 0.90 (95% CI, 0.68 to 1.19) in patients with LVD (Pinteraction=0.84). Similar observations were made for the outcome stroke only.

Conclusions— Our findings do not concur with the hypothesis that aspirin, dipyridamole, or the combination may be especially effective in preventing vascular events in patients with previous cerebral ischemia that was caused by LVD compared with SVD.


Key Words: aspirin • dipyridamole • vascular disease




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