4.1 Article

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

Journal

CORONARY ARTERY DISEASE
Volume 25, Issue 8, Pages 678-684

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCA.0000000000000143

Keywords

acute heart failure; atorvastatin reload; major adverse cardiac events; noncardiac emergency surgery

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ObjectivesThis 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 methodsIn 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 72h postoperative changes in high-sensitivity C-reactive protein and interleukin-6 levels were compared between the two groups.ResultsAHF 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).ConclusionAtorvastatin 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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