Introduction: Acute inflammation is associated with a deterioration of endothelial function. Statins reduce cardiovascular risk by lipid lowering and non-lipid pleiotropic effects. It has not been defined whether atorvastatin modifies the effects of acute inflammation on endothelial function in dyslipidemic patients.

Methods: We generated a transient systemic inflammation by Salmonella Typhi vaccination in 30 volunteers with mild dyslipidemia. They were studied 4 days after randomly taking atorvastatin 40 mg or placebo once daily at bedtime. Conduit artery endothelial performance was assessed before and 8 hours after vaccination. Flow-mediated dilation (FMD) of the brachial artery, an index of endothelial function, and the endothelium-independent nitrate-induced dilation (NID) were measured by using high resolution ultrasonography.

Results: There were no differences in all baseline characteristics among the two groups. In the placebo group, vaccination caused a significant decrease of FMD at 8 hours (by 2.65±1.08%, P < 0.05, left figure), indicating an unfavourable effect of inflammation on endothelial function. In contrast, in the pretreated with atorvastatin group, the decrease of FMD after vaccination (by 0.22±0.53%) was significantly smaller compared with placebo (P < 0.05 by 2-way repeated-measures ANOVA, left figure), denoting that the adverse effect of inflammation on endothelial function is abrogated by atorvastatin. We did not observe any significant change of NID after vaccination in any group (P=NS, right figure).

Conclusion: In dyslipidemic patients, atorvastatin abrogates the deterioration of endothelial function caused by an acute inflammatory stimulus. This finding provides valuable insights into the protective effect of atorvastatin on arterial function and on the cardiovascular system overall.