Steingart R M, Matthews R, Gambino A, Kantrowitz N, Katz S
Health Sciences Center, State University of New York at Stony Brook.
Am J Cardiol. 1989 Apr 1;63(12):767-71. doi: 10.1016/0002-9149(89)90039-8.
Coronary reperfusion in myocardial infarction improves infarct zone motion, but its effect on the global ejection fraction has been less consistent. The directional movement of the ejection fraction is determined by the opposing influences of improved infarct zone motion and diminishing hyperkinesia in the noninfarct zone. Noninfarct zone hyperkinesia has been attributed to catecholamine stimulation, the Frank-Starling mechanism or intraventricular interactions that unload noninfarcted segments. To investigate the influence of catecholamine stimulation, 9 men presenting with a first myocardial infarction (mean age 53 +/- 13 years) were studied. Coronary reperfusion was accomplished less than 4 hours after the onset of myocardial infarction. Radionuclide ventriculography was then performed before and immediately after the intravenous administration of 15 mg of metoprolol. End-diastolic volume did not change, but end-systolic volume increased 28% after metoprolol (p = 0.041). The ejection fraction decreased from 55 +/- 13% before metoprolol to 45 +/- 14% after its administration (p = 0.002). There was no effect of intravenous metoprolol on infarct zone motion, whereas motion in the noninfarcted segment decreased (p = 0.002). The patients underwent repeat ventriculography after receiving metoprolol, 100 mg orally twice a day for 9 days. Infarct zone motion improved (p less than 0.002) and the ejection fraction increased to 55 +/- 12% (p less than 0.02). Normal zone motion did not change. Thus, compensatory hyperkinesia is at least in part caused by catecholamine stimulation. Conclusions regarding the effects of reperfusion on global ventricular performance can be influenced by the timing of ejection fraction determinations relative to metoprolol therapy.
心肌梗死时的冠状动脉再灌注可改善梗死区运动，但其对整体射血分数的影响则不太一致。射血分数的方向性变化取决于梗死区运动改善与非梗死区运动亢进减弱这两种相反作用的影响。非梗死区运动亢进被认为与儿茶酚胺刺激、Frank-Starling机制或使非梗死节段负荷减轻的室内相互作用有关。为研究儿茶酚胺刺激的影响，对9例首次发生心肌梗死的男性患者（平均年龄53±13岁）进行了研究。在心肌梗死发病后4小时内实现冠状动脉再灌注。然后在静脉注射15mg美托洛尔之前及之后立即进行放射性核素心室造影。舒张末期容积未改变，但美托洛尔注射后收缩末期容积增加了28%（p=0.041）。射血分数从美托洛尔注射前的55±13%降至注射后的45±14%（p=0.002）。静脉注射美托洛尔对梗死区运动无影响，而非梗死节段的运动减弱（p=0.002）。患者在接受美托洛尔治疗后进行了重复心室造影，美托洛尔口服剂量为100mg，每日2次，共9天。梗死区运动改善（p<0.002），射血分数增加至55±12%（p<0.02）。正常区运动未改变。因此，代偿性运动亢进至少部分是由儿茶酚胺刺激引起的。关于再灌注对整体心室功能影响的结论可能会受到相对于美托洛尔治疗而言射血分数测定时间的影响。
