陈昕,任卫东,唐力,马春燕,王立建,富维强.心肌声学造影评价梗死前心绞痛对心肌微循环损伤的保护作用[J].中国医学影像技术,2006,22(9):1354~1356
心肌声学造影评价梗死前心绞痛对心肌微循环损伤的保护作用
Assessment of protective effect of preinfarction angina on myocardial and microvascular damage by myocardial contrast echocardiography
投稿时间:2006-04-06  修订日期:2006-08-02
DOI:
中文关键词:  超声心动描记术  心肌声学造影  梗死前心绞痛
英文关键词:Echocardiography  Myocardial contrast echocardiography  Preinfarction angina
基金项目:
作者单位E-mail
陈昕 中国医科大学附属第一医院心血管检查科,辽宁 沈阳 110001 chen_heart@hotmail.com 
任卫东 中国医科大学附属第一医院心血管检查科,辽宁 沈阳 110001  
唐力 中国医科大学附属第一医院心血管检查科,辽宁 沈阳 110001  
马春燕 中国医科大学附属第一医院心血管检查科,辽宁 沈阳 110001  
王立建 中国医科大学附属第一医院心血管检查科,辽宁 沈阳 110001  
富维强 中国医科大学附属第一医院心血管检查科,辽宁 沈阳 110001  
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中文摘要:
      目的 利用经静脉心肌声学造影(MCE)技术探讨梗死前心绞痛(PA)对急性心肌梗死心肌微血管损伤的影响。方法 根据有无PA将首次急性心肌梗死(AMI)的37例患者分为两组,无PA组19例,有PA组18例。患者入院当天行心脏超声检查记录室壁运动和左室容积(EDV和ESV)。住院期间行MCE评价心肌危险区域中无再流范围。AMI后3个月再次行心脏超声检查评价左室重构。结果 MCE显示无PA组心肌危险区域节段中无再流范围高于有PA组(P<0.05);EDV和ESV初诊时两组间无显著性差异。然而无PA组在3个月随访时超声结果显示左室容积较初诊时增加(P<0.0001),PA组左室容积较初诊时并无显著性改变。结论 心肌梗死前心绞痛可以减少无再流,保护心肌微循环,有利于再血管化后左室功能的恢复,并防止左室重构的发生。
英文摘要:
      Objective To evaluate the relationship between preinfarction angina (PA), microvascular reflow, and myocardial function using myocardial contrast echocardiography (MCE). Methods In 37 patients with a first acute myocardial infarction, we noninvasively assessed the microvascular perfusion with intravenous myocardial contrast echocardiography and 3-month follow-up echocardiography. The percentage extent of contrast defect after MCE within the risk area and left ventricular volume were evaluated. Results Typical angina was present in 19 patients and absent in 18 patients during the 7 days preceding the myocardial infarction. Compared with those patients without PA, patients with PA showed a greater microvascular reflow extent (P<0.05). The patients with PA had a better regional myocardial function expressed with significantly less pronounced left ventricular dilation at follow-up despite being similar in the first echocardiogram. Conclusion Presence of preinfarction angina, because of the preconditioning effect, reduces myocardial damage and favors myocardial viability, limiting left ventricular remodeling.
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