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(Stroke. 2004;35:175.)
© 2004 American Heart Association, Inc.

Original Contributions

Antiplatelet Effect of Aspirin in Patients With Cerebrovascular Disease

Mark J. Alberts, MD; Deborah L. Bergman, RN, NP; Elise Molner, RN; Borko D. Jovanovic, PhD; Issei Ushiwata, MD Jun Teruya, MD

From the Departments of Neurology (M.J.A.), and Preventative Medicine (B.D.J.), Feinberg School of Medicine, Northwestern University Medical School, Chicago, Ill; Northwestern Memorial Hospital (D.L.B.), Chicago, Ill; Emergency Department (E.M.), Barnes-Jewish Hospital, St. Louis, Mo; the Department of Neurosurgery (I.U.), San-ai Hospital, Saitama, Japan; Blood Bank and Coagulation and the Pheresis Service (J.T.), Texas Children’s Hospital, Houston; and the Departments of Pathology, Pediatrics, and Medicine (J.T.), Baylor College of Medicine, Houston, Texas.

Correspondence to Mark J. Alberts, MD, Professor of Neurology, Director, Stroke Program, Northwestern University, Feinberg School of Medicine, 710 N Lake Shore Dr, Chicago, IL 60611. E-mail m-alberts{at}northwestern.edu

Background and Purpose— Aspirin is used commonly to prevent ischemic strokes and other vascular events. Although aspirin is considered safe and effective, it has limited efficacy with a relative risk reduction of 20% to 25% for ischemic stroke. We sought to determine if aspirin as currently used is having its desired antiplatelet effects.

Methods— We ascertained patients with cerebrovascular disease who were taking only aspirin as an antiplatelet agent. Platelet function was evaluated using a platelet function analyzer (PFA-100). PFA test results were correlated with aspirin dose, formulation, and basic demographic factors.

Results— We ascertained 129 patients, of whom 32% were taking an enteric-coated aspirin preparation and 32% were taking low-dose (162 mg/d) aspirin. For the entire cohort, 37% of patients had normal PFA-100 results, indicating normal platelet function. For the patients taking low-dose aspirin, 56% had normal PFAs compared with 28% of those taking 325 mg/d of aspirin, while 65% of patients taking enteric-coated aspirin had normal PFAs compared with 25% taking an uncoated preparation (P<0.01 for both comparisons). Similar results were obtained if PFA results were analyzed using mean closure times (low-dose aspirin, 183 sec; high-dose aspirin, 233 sec; enteric-coated, 173 sec; uncoated, 235 sec; P<0.01 for comparisons). Older patients and women were less likely to have a therapeutic response to aspirin, independent of aspirin dose or formulation.

Conclusions— A significant proportion of patients taking low-dose aspirin or enteric-coated aspirin have normal platelet function as measured by the PFA-100 test. If these results correlate with clinical events, they have broad implications in determining how aspirin is used and monitored.

Key Words: antiplatelet therapy • aspirin • cerebrovascular disorders • stroke, ischemic

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