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European Heart Journal Advance Access originally published online on September 29, 2006
European Heart Journal 2006 27(24):2945-2955; doi:10.1093/eurheartj/ehl277
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Rapid immunomodulation by rosuvastatin in patients with acute coronary syndrome

Andreas Link1,*, Tarek Ayadhi1, Michael Böhm1 and Georg Nickenig2

1 Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, D-66421Homburg/Saar, Germany
2 Medizinische Klinik und Poliklinik II, Universitätsklinikum Bonn, D-53105 Bonn, Germany

Received 18 May 2006; revised 18 August 2006; accepted 11 September 2006; online publish-ahead-of-print 29 September 2006.

* Corresponding author. Tel: +49 6841 16 23372; fax: +49 6841 16 23369. E-mail address: link{at}med-in.uni-saarland.de

See page 2916 for the editorial comment on this article (doi:10.1093/eurheartj/ehl376)

Aims HMG-CoA reductase inhibitors (statins) reduce cardiovascular mortality and morbidity in patients with stable coronary artery disease as well as acute coronary syndrome (ACS). It is unclear how rapidly the beneficial effects of statins occur in patients with ACS and whether these drug properties are related to lipid lowering.

Methods and results Patients with troponin-positive ACS (n=35) were randomized to 20 mg/day rosuvastatin therapy or to placebo treatment. Anti-inflammatory effects of rosuvastatin measured by lymphocyte intracellular cytokine production were taken before initiation of treatment and on days 1, 3, and 42. Compared with placebo, rosuvastatin treatment significantly reduced plasma concentrations of pro-inflammatory cytokines TNF-{alpha} and IFN-{gamma} at 72 h. Rosuvastatin also induced a rapid and significant reduction of TNF-{alpha} and IFN-{gamma} production in stimulated T-lymphocytes at 72 h. When compared with placebo, rosuvastatin inhibited the Th-1-immune response measured at 72 h.

Conclusion Rosuvastatin exerts rapid immunomodulatory effects on the level of T-cell activation in patients with ACS.

Key Words: Acute coronary syndromes • Inflammation • Th-1-immune response • Statins


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