However, there is increasing evidence that statins have anti-inflammatory and anti-thrombotic effects aside from their cholesterol-lowering effect [12,13]. Statin therapy has selleck products been shown to reduce cardiovascular events, including myocardial infarction, stroke, and death [14-16]. Moreover, early statin treatment may reduce the severity and improve the outcome of myocardial infarction, ischemic stroke, and intra-cerebral hemorrhage [17-20].Although statin therapy is widely used in patients at high-risk for major vascular events, the benefits of pre-existing statin therapy in patients with acute ischemic stroke remain controversial. Multiple studies have demonstrated improved clinical outcomes in patients taking statins at stroke onset [18,19]; however, mechanisms conferring this protection have not been well studied.

Thus, this prospective cohort study aimed to test the difference in platelet activity between patients taking statins before and after acute ischemic stroke by assessing CD62P and CD63 expression. This study also analyzed if prior statin treatment could reduce the neurologic deterioration and improve the functional outcome of patients with ischemic stroke.Materials and methodsStudy participantsConsecutive patients with acute ischemic stroke admitted to the Department of Neurology of Chang Gung Memorial Hospital-Kaohsiung, Taiwan, from August 2009 to July 2010 were evaluated. Acute ischemic stroke was defined as acute-onset loss of focal cerebral function persisting for at least 24 hours.

The diagnosis of stroke was made based on clinical presentation, neurologic examination, and results of brain magnetic resonance imaging (MRI) with magnetic resonance angiography (MRA). Patients with cardio-embolic stroke were excluded, as well as those with underlying neoplasm, vasculitis, hematologic disorders that affect platelet count or function, end-stage renal disease, liver cirrhosis, and congestive heart failure. As pathogenesis and treatment could be different between patients with cardio-embolic and non-cardio-embolic ischemic stroke, those with cardio-embolism were excluded by clinical presentation, ECG, and cardiac ultrasound, while those who received intravenous thrombolytic therapy were also excluded.To avoid the confounding factor of anti-platelet therapies or dosage effects on measured platelet activity, all patients taking one or more anti-platelet medication (e.

g. aspirin, dipyradimole, or clopidogrel) prior to stroke onset were excluded from enrollment. All enrolled patients were treated with aspirin (100 mg/day) therapy post-stroke. The Institutional Review Committee on Human Research approved the study protocol and the participating subjects provided informed consent.Demographic data, history of risk factors (i.e., hypertension, diabetes mellitus, dyslipidemia, cigarette smoking, and cardiovascular Batimastat disease), and history of previous vascular events (i.e.