Pretnar-Oblak J et al. (2006) Influence of atorvastatin treatment on L-arginine cerebrovascular reactivity and flow-mediated dilatation in patients with lacunar infarctions. Stroke 37: 2540–2545

Accumulating evidence indicates that statin therapy might protect against stroke. It is postulated that statins might exert this protective effect through the improvement of endothelial homoeostasis by increasing the bioavailability of nitric oxide. Using cerebrovascular reactivity to L-arginine as a reflection of cerebral endothelial function, and flow-mediated dilatation to evaluate systemic endothelial function, Pretnar-Oblak et al. carried out a small study to examine the effect of statin treatment on patients with lacunar infarctions (LI), who are thought to have a primary endothelial impairment.

The study comprised 18 patients with LI, 20 age-matched individuals showing similar cardiovascular risk factors (CRFs) to those exhibited by the LI group, and 19 age-matched healthy individuals. Cerebral and systemic endothelial function were measured in all participants at study start and 3 months later; between these time points, the patients with LI and those with CRF received daily atorvastatin treatment (40 mg).

At baseline, L-arginine reactivity was lower in patients with LI and in those with CRFs than in healthy controls (P ≤0.05 for both). Following atorvastatin treatment, L-arginine reactivity improved significantly over baseline in both the LI group and the CRF group (P ≤0.01 for both). Flow-mediated dilatation also improved in both of these groups following atorvastatin treatment; however, the improvement was more pronounced in those with LI, perhaps indicating a systemic predilection for endothelial damage. The authors conclude that a large double-blind study is warranted to further confirm the beneficial effect of statins on endothelial function.