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Human atrial natriuretic peptide and nicorandil as adjuncts to reperfusion treatment for acute myocardial infarction (J-WIND): two randomised trials

Authors :
Yasunori Shintani
Masafumi Myoishi
Shigeru Fukuzawa
Masaharu Ishihara
Natsuki Nakamura
Toshimitsu Hamasaki
Masafumi Kitakaze
Kouki Watanabe
Osamu Seguchi
Yoshiyuki Nagai
Kazuo Kimura
Tetsuo Minamino
Soichiro Kitamura
Atsushi Hirayama
Takahiro Ohara
Yoshihiko Saito
Kenshi Fujii
Shinsuke Nanto
Jiyoong Kim
Hitonobu Tomoike
Masanori Asakura
Hiroshi Asanuma
Source :
The Lancet. 370:1483-1493
Publication Year :
2007
Publisher :
Elsevier BV, 2007.

Abstract

Summary Background Patients who have acute myocardial infarction remain at major risk of cardiovascular events. We aimed to assess the effects of either human atrial natriuretic peptide or nicorandil on infarct size and cardiovascular outcome. Methods We enrolled 1216 patients who had acute myocardial infarction and were undergoing reperfusion treatment in two prospective, single-blind trials at 65 hospitals in Japan. We randomly assigned 277 patients to receive intravenous atrial natriuretic peptide (0·025 μg/kg per min for 3 days) and 292 the same dose of placebo. 276 patients were assigned to receive intravenous nicorandil (0·067 mg/kg as a bolus, followed by 1·67 μg/kg per min as a 24-h continuous infusion), and 269 the same dose of placebo. Median follow-up was 2·7 (IQR 1·5–3·6) years for patients in the atrial natriuretic peptide trial and 2·5 (1·5–3·7) years for those in the nicorandil trial. Primary endpoints were infarct size (estimated from creatine kinase) and left ventricular ejection fraction (gauged by angiography of the left ventricle). Findings 43 patients withdrew consent after randomisation, and 59 did not have acute myocardial infarction. We did not assess infarct size in 50 patients for whom we had fewer than six samples of blood. We did not have angiographs of left ventricles in 383 patients. Total creatine kinase was 66 459·9 IU/mL per h in patients given atrial natriuretic peptide, compared with 77 878·9 IU/mL per h in controls, with a ratio of 0·85 between these groups (95% CI 0·75–0·97, p=0·016), which indicated a reduction of 14·7% in infarct size (95% CI 3·0–24·9%). The left ventricular ejection fraction at 6–12 months increased in the atrial natriuretic peptide group (ratio 1·05, 95% CI 1·01–1·10, p=0·024). Total activity of creatine kinase did not differ between patients given nicorandil (70 520·5 IU/mL per h) and controls (70 852·7 IU/mL per h) (ratio 0·995, 95% CI 0·878–1·138, p=0·94). Intravenous nicorandil did not affect the size of the left ventricular ejection fraction, although oral administration of nicorandil during follow-up increased the left ventricular ejection fraction between the chronic and acute phases. 29 patients in the atrial natriuretic peptide group had severe hypotension, compared with one in the corresponding placebo group. Interpretation Patients with acute myocardial infarction who were given atrial natriuretic peptide had lower infarct size, fewer reperfusion injuries, and better outcomes than controls. We believe that atrial natriuretic peptide could be a safe and effective adjunctive treatment in patients with acute myocardial infarction who receive percutaneous coronary intervention.

Details

ISSN :
01406736
Volume :
370
Database :
OpenAIRE
Journal :
The Lancet
Accession number :
edsair.doi.dedup.....deed7224fe7f5ee9ebdff0f02a9435b6
Full Text :
https://doi.org/10.1016/s0140-6736(07)61634-1