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[【学科前沿】] 心房利钠肽减少急性心肌梗死面积

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发表于 2007-10-31 14:06:30 | 显示全部楼层 |阅读模式
Atrial Natriuretic Peptide Reduces Infarct Size in Acute MI

OSAKA, Japan, Oct. 26 -- Acute myocardial infarction patients treated with atrial natriuretic peptide had smaller infarcts, fewer reperfusion injuries, and better outcomes compared with a control group, investigators reported.

Atrial natriuretic peptide treatment reduced infarct size by almost 15%, and patients treated with the peptide had a significantly higher ejection fraction at six months, Masafumi Kitakaze, M.D., of the National Cardiovascular Center here, and colleagues, stated in the Oct. 27 issue of The Lancet.

\"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,\" the authors concluded.

A separate placebo-controlled comparison showed that the nicorandil, a combined potassium-channel opener and nitrate compound, revealed no acute impact of intravenous treatment, but chronic oral therapy did improve left ventricular ejection fraction (LVEF).

Reperfusion of ischemic myocardium reduces infarct size and improves left ventricular function after acute MI. However, reperfusion also can cause tissue damage. Only a few medications have demonstrated the ability to decrease ischemia or reperfusion injury, Dr. Kitakaze and colleagues wrote.

Atrial natriuretic peptide suppresses the renin-angiotensin-aldosterone system and endothelin-1, which influence infarct size and cardiac remodeling, they continued. As a result, atrial natriuretic peptide might have potential to improve outcomes in acute MI.

Investigators randomized 569 acute MI patients who were undergoing reperfusion therapy to intravenous atrial natriuretic peptide (0.025 礸/kg/min for three days) or placebo. The primary endpoints were infarct size, estimated by creatine kinase values, and LVEF six to 12 months post-MI.

Total creatine kinase averaged 66,459.9 IU/mL/h in patients who received atrial natriuretic peptide versus 77,878.9 IU/mL/h in the placebo group.

The difference translated into 14.7% reduction in infarct size in favor of the peptide group (P=0.016). LVEF at six to 12 months was 44.7% in the atrial natriuretic peptide group and 42.5% in the placebo group (P=0.026).

The incidence of reperfusion injury was reduced by 26% in the treatment group (P=0.019). Those patients also had lower rates of cardiac death and hospital readmission for heart failure (P=0.0112).

The second study involved 545 acute MI patients who were randomized to intravenous nicorandil (0.067 mg/kg bolus, followed by 1.67 礸/kg/min as a 24-hour infusion) or placebo. Additionally, 61 patients assigned to nicorandil were given oral therapy during follow-up at the discretion of their physicians.

The total creatine kinase was 70,520.5 IU/mL/h in patients who received intravenous nicorandil and 70,852.7 IU/mL/h in the placebo group. Overall, ejection fraction at six to 12 months did not differ between groups. However, patients who received oral therapy had an improvement in LVEF between the acute and chronic phases of treatment (P=0.0338).
http://www.medpagetoday.com/Card ... lInfarction/tb/7130
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