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Submitted on March 15, 2006
From the Klinik und Poliklinik für Neurologie (M.E.), Charité Universitätsmedizin Berlin, Campus Mitte, Berlin, Germany; and the Klinik für Innere Medizin III (U.L.), Universität des Saarlandes, Homburg, Germany. * To whom correspondence should be addressed. E-mail: matthias.endres{at}charite.de.
Background and Purpose--Statins reduce the risk for myocardial infarctions and stroke which may in part depend on cholesterol-independent (pleiotropic) vasoprotective effects. Here, we review evidence to suggest that the abrupt discontinuation of statin medication exerts negative vascular effects in patients with acute vascular events. Summary of Review--It is increasingly recognized that statins (HMG-CoA reductase inhibitors) exert rapid cholesterol-independent effects. Cessation of statin treatment confers overshoot activation of heterotrimeric G-proteins Rho and Rac causing production of reactive oxygen species and suppression of NO bioavailability. In humans, discontinuation of statin therapy leads to a proinflammatory, prothrombotic state with impaired endothelium function. In patients with acute coronary syndromes, abrupt discontinuation of statin therapy significantly increases morbidity and mortality, whereas in stable vascular patients discontinuation may be safe. Recent prospective data indicated that the cessation of statin medication in acute ischemic stroke patients confers a significantly higher likelihood of early neurological deterioration and poor outcome. Conclusions--We propose that in all acute ischemic stroke patients chronically treated with statins before the event, treatment should be continued and the patient should receive medication at the day of the stroke.
Revised on June 19, 2006
Accepted on July 31, 2006
Discontinuation of Statin Treatment in Stroke Patients
Matthias Endres MD* and Ulrich Laufs MD
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