急性心肌梗死后存活心肌对梗死相关血管晚期血运重建术后左室功能的影响

Influence of viable myocardium on left ventricular function after late revascularization of infarct-related artery in acute myocardial infarction

目的 探讨存活心肌对急性心肌梗死(AMI)后梗死相关血管(IRA)晚期血运重建术后远期左室功能以及左室重构的影响。方法 69例AMI未接受早期再灌注治疗者，于发病10～21 d行IRA经皮冠状动脉血运重建(PCI)术，术前于AMI发病后5～10 d应用小剂量多巴酚丁胺(5和10μg·min^(-1)·Kg^(-1))超声心动图负荷试验检测存活心肌，并分别测定和计算给药前后左室腔大小、左室射血分数(LVEF)以及室壁运动积分(WMS)。按有无存活心肌分为存活心肌组和无存活心肌组，超声心动图随访术后6个月时两组左室腔大小、LVEF和WMS的变化。结果157个运动异常节段中89个节段(57％)有存活心肌，有存活心肌组26例(占38％)，无存活心肌组43例(占62％)。存活心肌组术后6个月LVEF较术前明显提高(P＜0．05)，收缩末期容积指数(LVESVI)和WMS明显降低(P＜0．05和P＜0．01)；而无存活心肌组LVEF较术前明显降低(P＜0．01)，LVESVI和左室舒张末期容积指数(LVEDVI)较术前明显增加(P＜0．05)，WMS无明显变化。存活心肌组多巴酚丁胺负荷时的LVEF和WMS明显改善，且与6个月时的测定值相近；而无存活心肌组PCI前应用多巴酚丁胺LVEF和WMS均无明显变化。结论 AMI后有存活心肌者晚期血运重建有利于改善远期左室功能和减少左室重构。心肌梗死后早期小剂量多巴酚丁胺负荷状态下左室收缩功能的提高预示晚期血运重建术后心功能改善。

Objective To assess whether the presence of viable myocardium can change the long-term left ventricular remodeling and improve left ventricular function after late revascularization of infarct-related artery in patients with acute myocardial infarction （AMI）. Methods Sixty-nine patients with first acute myocardial infarction who had not received early reperfusion therapy were studied by low dose dobutamine stress echocardiography （LDSE） 5 to 10 days after AMI. Wall motion abnormality and left ventricular size were measured at the same time. Successful percutaneous coronary intervention（PCI） was done in all patients 10 to 21 days after AMI onset. The patients were divided into two groups based on the presence or absence of viable myocardium. Echocardiography was repeated six months later. Results There were 157 segments with motion abnormality, of which, 89（57% ） were viable during LDSE. Twenty-six patients had viable myocardium and 43 did not have. In patients with viable myocardium group, left ventricular ejection fraction （LVEF） was increased （ P 〈 0.05）, and left ventricular end systolic volume index （LVESVI） and wall motion score （WMS） were decreased （ P 〈 0.05 and P 〈 0.01 ） significantly at 6 months compared with baseline. However, in patients without viable myocardium, LVEF was decreased （ P 〈 0.01）, LVESVI and left ventricular end diastolic volume index （LVEDVI） were increased （ P 〈0.05） significantly after 6 months, and the WMS did not change （ P 〉 0.05）. LVEF increased （P 〈 0.05） and WMS decreased （P 〈 0.05） on LDSE during acute phase in patients with viable myoeardium, but they did not change in the group without viable myocardium. Conclusions Late revascularization of infarct-related artery in patients with viable myocardium after AMI is associated with long-term preservation of left ventricular function and less ventricular remodeling. Improvement of left ventricular systolic function on LDSE indicates late phase recovery of left ventricular function after late revascularization.