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(Stroke. 2004;35:2706.)
© 2004 American Heart Association, Inc.
Articles |
From the University of Washington School of Medicine (K.B.), Seattle Wash, and the Henry Ford Health Sciences Center (M.C.), Detroit Mich.
Correspondence to Dr Kyra Becker, Harborview Medical Center, Box 359775, 325 9th Avenue, Seattle, Washington 981042499. Email kjb@u.washington.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Epidemiological studies suggest that hyperlipidemia is not a major risk factor for stroke, yet 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) decrease the risk of stroke in patients with vascular disease or at high risk of vascular disease.16 Moreover, the benefit of statins appears to be independent of baseline cholesterol; persons with normal cholesterol experience a similar degree of risk reduction as patients with elevated cholesterol.3 Results of dedicated stroke trials to determine the benefit of statins in secondary stroke prevention are not yet available, although the Heart Protection Study did include a large population of patients with cerebrovascular disease and stroke.3 Interestingly, among patients with a history of stroke, statins did not decrease the risk of recurrent stroke, but did decrease the risk of myocardial infarction.7
While epidemiological studies fail to show a dramatic effect of hyperlipidemia on ischemic stroke risk, low cholesterol levels are associated with an increased risk of intracerebral hemorrhage (ICH).8,9 Importantly, statin therapy has not been associated with an increased risk of ICH in any of the studies done to date.4,5,7 Furthermore, statin use may be associated with lessened stroke severity in patients with ischemic stroke, and animal data points to a similar benefit in ICH.10,11 These observations, along with the disconnect between the epidemiologic data regarding the role of cholesterol in stroke risk and the benefit of statins in stroke prevention suggest that the benefits of statins may be related to nonlipid effects of the drugs. Indeed, statins affect multiple biological systems, including the
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