This registry allows the study of the risk factors, natural history, and clinical manifestations of stroke in different ethnic groups.

No abstract

Despite its low efficacy, aspirin is the most widely used drug for secondary stroke prevention. The reasons why stroke recurs while patients are on aspirin are unknown. We have analyzed a series of patients who had recurrent strokes while on aspirin. Out of 2231 consecutive patients who were admitted to the Tel Aviv Medical Center from May 1988 through December 1992 with the diagnosis of ischemic stroke, 129 admissions were due to recurrent ischemic strokes while the patients were already on aspirin, and these were defined as aspirin failures. The clinical characteristics of those patients in whom aspirin treatment failed were compared with three control groups, each comprising 129 patients who had had only a single ischemic stroke and were then taking aspirin. One control group was matched for aspirin dose and date of first stroke; another control group was matched for age, sex, and date of first stroke; and a third control group was matched for age, sex, date of first stroke, and aspirin dose. Statistical analysis was carried out by two-tailed Student's t test and chi 2 test. The average period until stroke was longer for patients on higher aspirin doses. Patients matched for aspirin dose and date of first stroke did not differ significantly in age (72.4 years in aspirin failures versus 74.2 years in the first control group) and sex (89 versus 94 men, respectively). Matching for age, sex, and date of first stroke but not for aspirin dose demonstrated a trend toward high frequency of aspirin failure in patients taking lower doses of aspirin (chi 2 test for trend = 3.5; P = .06). Comparison of aspirin-failure patients with a control group matched for age, sex, date of first ischemic stroke, and aspirin dose demonstrated that these patients more commonly had statistically significant hyperlipidemia (odds ratio, 2.6; 95% confidence interval, 1.0 to 6.8; P = .04) and ischemic heart disease (odds ratio, 2.3; 95% confidence interval, 1.3 to 3.9; P = .002). We conclude that age and sex do not influence the efficacy of aspirin. Lower aspirin dose in patients with stroke recurrence suggests that aspirin doses of 500 mg daily or more should be used in secondary stroke prevention. Hyperlipidemia and ischemic heart disease are risk factors for stroke recurrence despite aspirin treatment, which requires further clinical and laboratory evaluation.

Background: Although aspirin (ASA) remains the most popular and accepted agent for secondary stroke prevention, its efficacy does not exceed 25%. Platelet function monitoring in ASA users suggests that some individuals exhibit a reduced or even absent antiplatelet response after ASA. This phenomenon, also known as ‘resistance’, is prevalent in stroke survivors. We sought to evaluate the blood lipid profile in poststroke ASA users dependent on their antiplatelet response to ASA. Methods: Ninety-six consecutive ASA users after first-ever ischemic stroke confirmed by imaging were prospectively enrolled. The platelet function analyzer (PFA-100, Dade Behring, USA) was utilized to assess the response after ASA. The lipid profile (total cholesterol, high-density lipoprotein, low-density lipoprotein and triglycerides) was measured using the Cardiochek instrument (Polymer Technology, USA) from the autologuos blood samples. Results: The poststroke duration was 3–26 months, and all patients were treated with ASA for at least 3 months. The allowed daily ASA doses were from 75 up to 325 mg, with a mean of 158 mg. The mean age of the patients was 71 years, almost 60% were women, and over 85% of the patients were treated with statins. Thirty-seven patients were identified as low ASA responders, while 59 patients exhibited an adequate response. There were no differences between ASA responders and nonresponders with regard to demographics, clinical characteristics, risk factors and concomitant medications. The lipid profile biomarkers were similar between groups with the exception of triglycerides, which were significantly increased in the patients with ASA resistance, compared with ASA responders. Conclusion: The fact that hypertriglyceridemia affects platelet response to ASA has potential practical implications in light of growing evidence that ASA may exert antiplatelet properties beyond the cyclooxygenase pathway. The mechanism of such an association is unclear but may be related to the diminished platelet membrane fluidity and inability of ASA to downregulate such ‘strong’ protected platelets.