Intensive statin therapy stabilizes C-reactive protein, but not chemokine in stable coronary artery disease treated with an everolimus-eluting stent. Issue 5 (August 2016)

• Record Type: Journal Article
• Authors: Sukegawa, Hiroaki; Maekawa, Yuichiro; Yuasa, Shinsuke; Anzai, Atsushi; Kodaira, Masaki; Takei, Makoto; Sano, Fumiya; Ueda, Ikuko; Kawakami, Takashi; Hayashida, Kentaro; Kohno, Takashi; Kohsaka, Shun; Abe, Takayuki; Fukuda, Keiichi
• Is Part Of: Coronary artery disease. Volume 27:Issue 5(2016:Aug.)
• Publication Date: 2016-08
• Subjects: coronary artery disease -- everolimus-eluting stent -- inflammatory marker -- statin; Coronary heart disease -- Periodicals; Coronary Disease -- Indexes; Coronary Disease -- Periodicals; 616.123005
• DOI: 10.1097/MCA.0000000000000375
• Languages: English
• ISSNs: 0954-6928

Abstract

Abstract : Background: Besides its potent plasma cholesterol-lowering activity, statin treatment has several other important effects, including lowering high-sensitive C-reactive protein (hs-CRP), levels, and stabilizing risk factors of atherosclerosis, thereby reducing the risk of cardiovascular events. Our aim in this study was to identify how intensive statin therapy can affect plasma levels of inflammatory markers over the long term. Methods and results: We used a prospective, randomized, open blinded-endpoint design. A total of 30 patients with stable coronary artery disease treated with everolimus-eluting stent implantation were randomized to receive rosuvastatin 2.5 (standard therapy group) or 10 mg (intensive therapy group) for 12 months. Plasma levels of hs-CRP, pentraxin-3, monocyte chemoattractant protein-1, and CXC chemokine ligand 4 were measured after a percutaneous coronary intervention, at 1, 3, 6, 9, and 12 months. Levels of LDL cholesterol (LDL-C) and HDL cholesterol were also measured. We investigated short-term and long-term clinical outcomes. After 12 months of therapy, the intensive therapy group had lower levels of LDL-C than the standard therapy group. Plasma levels of hs-CRP largely fluctuated in the standard therapy group, whereas they were stable in the intensive therapy group during the follow-up period. There were no significant differences in serum pentraxin-3, monocyte chemoattractant protein-1, and CXC chemokine ligand 4 levels, or in the incidence of any clinical adverse events, between the standard and the intensive therapy groups. Conclusion: Intensive rosuvastatin therapy stabilizes hs-CRP levels, but not chemokine levels, besides lowering LDL-C levels. Thus, this therapy may inhibit the progression of atherosclerosis by stably inhibiting the inflammatory cascade.