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既往前壁心肌梗死患者运动诱发ST段抬高的临床意义

The clinical significance of exercise-induced ST-segment elevation in previous anterior myocardial infarction.

作者信息

Yamaki M, Kubota I, Ikeda K, Tonooka I, Tsuiki K, Yasui S

出版信息

Jpn Circ J. 1985 Sep;49(9):949-59. doi: 10.1253/jcj.49.949.

Abstract

To investigate the mechanism of exercise-induced ST elevation in previous anterior myocardial infarction, exercise body surface mapping was performed on 22 patients with anterior myocardial infarction. ST elevation was compared with the findings of exercise radionuclide ventriculography and exercise thallium-201 myocardial perfusion imaging. ST-segment was quantified by the integral of ST-segment voltage. The maximal value of ST segment integral out of the 87 leads on the body surface was defined as ST max. The percent of change in ST max after exercise was closely correlated to the decrease in ejection fraction (r = 0.76). Furthermore, 9 of the 12 patients with increased ST max after exercise had exercise-induced regional wall motion abnormalities mainly in the apical and anterolateral segments, while other 10 patients without increased ST max did not (p less than 0.01). There was no difference in % change of ST max a) between anterior reversible defect (+) group and the (-) group; b) between inferior reversible defect (+) group and the (-) group; c) between single vessel (isolated left anterior descending artery stenosis) group and the multivessel group. This fact indicated that exercise-induced ST elevation did not result from the exercise-induced myocardial ischemia of the infarctional segment or the remote non-infarctional segment. We concluded that exercise-induced ST elevation in previous anterior myocardial infarction is mainly due to the aggravation of anterior wall motion abnormalities induced by exercise.

摘要

为研究既往前壁心肌梗死患者运动诱发ST段抬高的机制,对22例前壁心肌梗死患者进行了运动体表心电图描记。将ST段抬高与运动放射性核素心室造影及运动铊-201心肌灌注显像结果进行比较。ST段通过ST段电压积分进行量化。体表87个导联中ST段积分的最大值定义为ST max。运动后ST max的变化百分比与射血分数的降低密切相关(r = 0.76)。此外,运动后ST max升高的12例患者中有9例出现运动诱发的局部室壁运动异常,主要位于心尖和前侧壁段,而其他10例ST max未升高的患者则未出现(p<0.01)。ST max的变化百分比在以下几组之间无差异:a)前壁可逆性缺损(+)组与(-)组之间;b)下壁可逆性缺损(+)组与(-)组之间;c)单支血管病变(孤立性左前降支狭窄)组与多支血管病变组之间。这一事实表明,运动诱发的ST段抬高并非由梗死节段或远隔非梗死节段的运动诱发心肌缺血所致。我们得出结论,既往前壁心肌梗死患者运动诱发的ST段抬高主要是由于运动诱发的前壁运动异常加重所致。

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