| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2707973 | Journal of Stroke and Cerebrovascular Diseases | 2008 | 7 Pages |
BackgroundStatins, 3-hydroxy-3-methylglutaryl-coenzymeA reductase inhibitors, have pleiotropic effects that are independent of their cholesterol-lowering activities. For example, they improve vascular endothelial function and exert anti-inflammatory effects. In large clinical trials they reduced the incidence of stroke and myocardial infarction; however, little is currently known regarding the mechanism or mechanisms underlying their clinically confirmed stroke protection.Patients and MethodsWe assessed 10 patients who had experienced a stroke at least 6 months earlier; they received low-dose (5 mg) simvastatin. Using our triple-injection technetium 99m-ethylcysteinate dimer method, we determined their cerebral blood flow and cerebrovascular reactivity. A second assessment of at-rest cerebral blood flow and cerebrovascular reactivity was performed 4 or more months (mean 6 months) after the start of statin administration. We used acetazolamide (1 g) as the vasodilator. The region of interest was the middle cerebral artery territory on a 3-dimensional stereotaxic region of interest template.ResultsStatin administration did not significantly affect the regional cerebral blood flow at rest. Before statin treatment, the patients' vasoreactivity, determined by the triple-injection technetium 99m-ethylcysteinate dimer method, demonstrated delayed, poor, or near-normal response patterns. Statin treatment improved vasoreactivity in all patients. Their mean serum total cholesterol level before statin administration was 200 mg/dL (range 187-256 mg/dL). Statin treatment significantly reduced their mean serum total cholesterol to 180 mg/dL (range 128-220 mg/dL) (P < .01).ConclusionsThe clinically confirmed stroke protection activity exerted by statins may be attributable to improved cerebrovascular reactivity.
