Key result
Atorvastatin 40 mg daily preserved endothelium-dependent flow-mediated dilation following acute inflammation compared to placebo (decrease of 0.15% vs 2.55%; P=0.005).
Why the study?
Does atorvastatin 40 mg once daily prevent acute systemic inflammation-induced endothelial dysfunction in volunteers with mild hypercholesterolaemia?
RCT (n=50)
double-blind
randomized
Does atorvastatin 40 mg once daily prevent acute systemic inflammation-induced endothelial dysfunction in volunteers with mild hypercholesterolaemia?
Absolute Event Rate: 0.15% vs 2.55%
p-value: p=0.005
Short-term pretreatment with high-dose atorvastatin effectively prevents acute inflammation-induced endothelial dysfunction in patients with mild hypercholesterolemia.
Supports short-term high-dose atorvastatin pretreatment to protect endothelial function in acute inflammation; extends pleiotropic statin benefits in mild hypercholesterolemia.
AIMS: Recent studies suggest an association between acute inflammation and deterioration of arterial function. The effect of acute inflammation on endothelial function and the role of treatment with statins have not been investigated in subjects with dyslipidaemia. METHODS AND RESULTS: In this randomized, placebo-controlled, double-blind study, we generated a transient systemic inflammation by Salmonella typhi vaccination in 50 volunteers with mild hypercholesterolaemia after 4 days of treatment with atorvastatin 40 mg or placebo once daily. Endothelium-dependent flow-mediated dilation (FMD) of the brachial artery and circulating levels of endothelial and inflammatory markers were measured before and 8 h after the vaccine. Vaccination produced a decline on FMD at 8 h (absolute decrease of 2.55%, P = 0.001), indicating an unfavourable effect on endothelial function. In contrast, in atorvastatin-treated subjects, FMD was preserved after vaccination (decrease of 0.15%, P = 0.005 vs. placebo). The vaccination-induced decline in plasma level of nitric oxide metabolites (by 6.0 micromol/L, P = 0.007) and antioxidant capacity (by 20.6 micromol/L, P = 0.001) in the placebo group were completely abolished by atorvastatin (P = 0.038 and P = 0.005, respectively, vs. placebo). In contrast, atorvastatin had no significant effect on cytokine levels. CONCLUSION: Acute inflammation is aetiologically associated with the deterioration of vasomotor and systemic endothelial function in hypercholesterolaemic patients. Atorvastatin effectively abrogates these deleterious effects.
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Vlachopoulos et al. (2007) conducted an RCT in mild hypercholesterolaemia (n=50). atorvastatin vs. placebo was evaluated on Endothelium-dependent flow-mediated dilation (FMD) of the brachial artery 8 h after vaccination (p=0.005). Atorvastatin 40 mg daily preserved endothelium-dependent flow-mediated dilation following acute inflammation compared to placebo (decrease of 0.15% vs 2.55%; P=0.005).
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