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Randomized Controlled Trial
. 2014 Dec;25(8):678-84.
doi: 10.1097/MCA.0000000000000143.

Inhibition of inflammation mediates the protective effect of atorvastatin reload in patients with coronary artery disease undergoing noncardiac emergency surgery

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Randomized Controlled Trial

Inhibition of inflammation mediates the protective effect of atorvastatin reload in patients with coronary artery disease undergoing noncardiac emergency surgery

Yang Qu et al. Coron Artery Dis. 2014 Dec.

Abstract

Objectives: This study aimed to (a) investigate whether atorvastatin reload protects against acute heart failure (AHF) in patients with stable coronary artery disease (CAD) undergoing noncardiac emergency surgery and decreases the incidence of major adverse cardiac events (MACE) during hospitalization and (b) elucidate its possible mechanism of action.

Materials and methods: In total, 500 patients with stable CAD before noncardiac emergency surgery were randomized either to the atorvastatin reload or to the placebo group. All patients received atorvastatin treatment postoperatively. The primary end point was the incidence of AHF during hospitalization, and the secondary end point was the incidence of MACE during hospitalization. Preoperative and 72 h postoperative changes in high-sensitivity C-reactive protein and interleukin-6 levels were compared between the two groups.

Results: AHF during hospitalization occurred in 5.2% of patients in the atorvastatin reload group and 11.2% in the placebo group (P=0.0225). MACE during hospitalization occurred in 2.4% of patients in the atorvastatin reload group and 8.0% in the placebo group (P=0.0088). According to multivariable analysis, atorvastatin reload conferred a 50% reduction in the risk of AHF during hospitalization (odds ratio, 0.50; 95% confidence interval, 0.2-0.8; P=0.005). The median decrease in the high-sensitivity C-reactive protein and interleukin-6 levels was significantly greater in the atorvastatin reload group (P<0.001).

Conclusion: Atorvastatin reload may improve the clinical outcome of patients with stable CAD undergoing noncardiac emergency surgery by decreasing the incidence of AHF and MACE during hospitalization. The mechanism of this protective effect may involve inhibition of inflammation.

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