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European Heart Journal Advance Access originally published online on June 27, 2007
European Heart Journal 2007 28(17):2102-2109; doi:10.1093/eurheartj/ehm247
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Protective effect of atorvastatin on acute systemic inflammation-induced endothelial dysfunction in hypercholesterolaemic subjects

Charalambos Vlachopoulos*, Konstantinos Aznaouridis, Anna Dagre, Carmen Vasiliadou, Constantina Masoura, Elli Stefanadi, John Skoumas, Christos Pitsavos and Christodoulos Stefanadis

Peripheral Vessels and Hypertension Units, First Department of Cardiology, Athens Medical School, Hippokration Hospital, Vas. Sofias avenue 114, Athens 11528, Greece

Received 26 February 2007; revised 15 April 2007; accepted 18 May 2007; online publish-ahead-of-print 27 June 2007.

* Corresponding author. Tel: +30 697 2272727; fax: +30 210 7485039. E-mail address: cvlachop{at}otenet.gr

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 µmol/L, P = 0.007) and antioxidant capacity (by 20.6 µmol/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.

Key Words: Statin • Endothelium • Hypercholesterolaemia • Inflammation • Nitric oxide


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