Acute effects of statin on reduction of angiopoietin-like 2 and glyceraldehyde-derived advanced glycation end-products levels in patients with acute myocardial infarction: a message from SAMIT (Statin for Acute Myocardial Infarction Trial)

Springer Science and Business Media LLC - Tập 31 - Trang 1583-1589 - 2015
Mitsuhiro Shimomura1, Jun-ichi Oyama1, Masayoshi Takeuchi2, Yoshisato Shibata3, Yusuke Yamamoto4, Tomohiro Kawasaki5, Hiroshi Komoda1, Kazuhisa Kodama1, Masashi Sakuma1, Shigeru Toyoda6, Yohei Inoue3, Daigo Mine1, Masahiro Natsuaki4, Aiko Komatsu1, Yutaka Hikichi1, Sho-ichi Yamagishi7, Teruo Inoue6, Koichi Node1
1Department of Cardiovascular Medicine, Saga University, Saga, Japan
2Department of Advanced Medicine, Medical Research Institute, Kanazawa Medical University, Ishikawa, Japan
3Department of Cardiology, Miyazaki Medical Association Hospital, Miyazaki, Japan
4Division of Cardiology, Cardiovascular and Aortic Center, Saiseikai Fukuoka General Hospital, Fukuoka, Japan
5Cardiovascular Center, Shin-Koga Hospital, Fukuoka, Japan
6Department of Cardiovascular Medicine, Dokkyo Medical University School of Medicine, Tochigi, Japan
7Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Fukuoka, Japan

Tóm tắt

Experimental ischemia–reperfusion models have shown that 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, statins, have cardioprotective effects. SAMIT (Statin Acute Myocardial Infarction Trial) is a multicenter prospective open randomized trial, designed to evaluate the effects of statin treatment from the earliest stage on cardioprotection in patients with acute myocardial infarction (AMI). Patients were randomly assigned to receive atorvastatin (initial dose of 40 mg at admission followed by the maintenance dose of 10 mg/day for 30 days) or not (control), and then immediately underwent percutaneous coronary intervention (PCI) for the culprit lesion. The primary endpoints were infarct size and left ventricular function. The secondary endpoints were major adverse cardiac and cerebrovascular events (MACCE) and various biomarkers. There were no significant differences in baseline characteristics between 2 groups of the statin treatment group and the control group. The left ventricular ejection fraction increased at 6 months after the onset of AMI, compared with the baseline level in the atorvastatin group (P < 0.05), while it did not change in the control group. Although there were no significant differences in the MACCE, the changes in the levels of angiopoietin-like protein 2 (ANGPTL2) (P < 0.05), and glyceraldehyde-derived advanced glycation end-products, (TAGE) (P < 0.01) were suppressed at 2 weeks in the atorvastatin group, compared with the control group. Statin therapy started early after the onset reduced the levels of ANGPTL2 and TAGE, and thus, might have cardioprotective effects in patients with AMI.

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