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Resumen de Rosuvastatin treatment in stable chronic obstructive pulmonary disease (RODEO): a randomized controlled trial

A. Neukamm, A.D. Høiseth, G. Einvik, Sarah Lehmann, T.A. Hagve, V. Søyseth, Torbjørn Omland

  • Objectives The objective of this study was to examine whether statin therapy is associated with enhanced endothelium-dependent vascular function, improved pulmonary function and reduced systemic inflammation in patients with chronic obstructive pulmonary disease (COPD).

    Design and setting This randomized, placebo-controlled, double-blind, parallel trial including patients with COPD was performed at two University hospitals in Norway.

    Subjects, intervention and measurements Patients with stable COPD (n = 99) were assigned randomly to receive rosuvastatin 10 mg (n = 49) or matching placebo (n = 50) once daily for 12 weeks. The primary outcome measure was change in endothelium-dependent vascular function measured using peripheral arterial tonometry and expressed as the reactive hyperaemia index. Secondary end-points were change in pulmonary function, as assessed by forced expiratory volume in 1 s (FEV1) and FEV1/forced vital capacity (FVC), and change in the circulating levels of the inflammatory markers interleukin-6 (IL6) and high-sensitivity C-reactive protein (hsCRP).

    Results In the overall study population, no significant between-group difference in change in endothelium-dependent vascular or pulmonary function was observed. Rosuvastatin therapy was associated with a reduction in hsCRP (−20% vs. 11%, P = 0.017) and an attenuation of the rise in IL6 concentration (8% vs. 30%, P = 0.028) compared with placebo. In a prespecified subgroup analysis of patients with a supra-median circulating hsCRP concentration (>1.7 mg L−1), rosuvastatin was associated with improved endothelium-dependent vascular function (13% vs. 2%, P = 0.026).

    Conclusions In stable COPD patients without the standard indications for statin therapy, rosuvastatin treatment is associated with a significant attenuation of systemic inflammation and improvement in endothelial-dependent vascular function in patients with evidence of systemic inflammation.


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