Ramzy Ihab S, Daly Caroline A, O'Sullivan Christine A, Lam Yat-Yin, Kemp Michael, Hooper James, Dancy Mark, Henein Michael Y
Central Middlesex Hospital, Cardiology Department, London, UK.
Int J Cardiol. 2007 Apr 12;117(1):51-8. doi: 10.1016/j.ijcard.2006.04.052. Epub 2006 Dec 8.
The objective of this study was to assess natriuretic peptide release following acute myocardial infarction, and its relationship with ventricular function.
A total of 44 patients with acute myocardial infarction were studied; 13 anterior, age (57+/-12 years) and 31 inferior, age (58+/-12 years). Peptide levels and left ventricular function by echocardiography were assessed at admission and on days 7 and 30 after thrombolysis. Healthy volunteers (n=21) served as controls.
Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) levels rose from admission to day 7 (p=0.002). While ANP remained elevated at day 30 in both groups, BNP levels fell in patients with anterior myocardial infarction (p=0.03). Left ventricular fractional shortening was reduced at admission in the two groups (p=0.01) but returned towards normal in 7 days (p=0.001) in inferior myocardial infarction and in 30 days in anterior myocardial infarction (p=0.02). Left ventricular long axis amplitude was universally reduced at admission (p=0.01) and remained abnormal at day 30 (p=0.01) in both groups. At day 7, BNP and ANP levels inversely correlated with long axis amplitude of lateral wall in anterior myocardial infarction; (r=-0.7, p=0.01). BNP correlated inversely with fractional shortening in anterior myocardial infarction (r=-0.7, p=0.01) at day 30.
The elevated peptide levels at 7 days post-myocardial infarction correlate with reduced mechanical activity of the adjacent noninfarcted segment. Natriuretic peptides release seem to be related to failure of compensatory hyperdynamic activity of the noninfarcted area rather than directly from the injured myocardial segments.
本研究旨在评估急性心肌梗死后利钠肽的释放情况及其与心室功能的关系。
共研究了44例急性心肌梗死患者；其中13例为前壁心肌梗死，年龄（57±12岁），31例为下壁心肌梗死，年龄（58±12岁）。在入院时以及溶栓后第7天和第30天，通过超声心动图评估肽水平和左心室功能。健康志愿者（n = 21）作为对照。
心房利钠肽（ANP）和B型利钠肽（BNP）水平从入院到第7天升高（p = 0.002）。虽然两组在第30天时ANP仍保持升高，但前壁心肌梗死患者的BNP水平下降（p = 0.03）。两组入院时左心室缩短分数均降低（p = 0.01），但下壁心肌梗死患者在7天内恢复正常（p = 0.001），前壁心肌梗死患者在30天内恢复正常（p = 0.02）。两组入院时左心室长轴振幅均普遍降低（p = 0.01），且在第30天时仍异常（p = 0.01）。在第7天时，前壁心肌梗死患者中BNP和ANP水平与侧壁长轴振幅呈负相关；（r = -0.7，p = 0.01）。在第30天时，前壁心肌梗死患者中BNP与缩短分数呈负相关（r = -0.7，p = 0.01）。
心肌梗死后7天肽水平升高与相邻非梗死节段机械活动降低相关。利钠肽释放似乎与非梗死区域代偿性高动力活动衰竭有关，而非直接源于受损心肌节段。
