【心肌梗死初期ST段抬高——急性冠状动脉闭塞引起的神经体液诱导代谢过程表达的后遗症?】

G Jentsch, B Kottwitz
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引用次数: 0

摘要

人工冠状动脉闭塞会立即引起st段抬高(ST-E),因此急性心肌梗死的ST-E被认为是急性冠状动脉闭塞的结果。但在心肌梗死早期,ST-E与冠状动脉闭塞之间不存在显著相关性。早期ST-E似乎主要是交感神经-肾上腺素能诱导的缺血心肌代谢过程的结果。在梗死发作后90分钟内β受体阻断使ST-E在1小时内降低73 +/- 6%。所有伴有ST-E的第一前壁梗死患者在急性期接受受体阻滞剂治疗可获得良好的预后。因此,早期ST-E可以被认为是交感神经肾上腺素能引起的心肌代谢变化的标志。因此,在急性期(前壁梗死)β受体阻断似乎是有治疗意义的。
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[ST elevation in the initial phase of myocardial infarct--a sequela of acute coronary occlusion of an expression of neurohumorally-induced metabolic processes?].

The artificial coronary artery occlusion results immediately in ST-segment elevation (ST-E), therefore the ST-E in acute myocardial infarction is considered to be the result of acute coronary occlusion. But in the early phase of myocardial infarction a significant correlation between ST-E and occlusion of the coronary artery does not exist. The early ST-E seems to be predominantly the consequence of sympathico-adrenergic induced metabolic processes in the ischemic myocardium. The beta receptor blockade during the first 90 minutes after the onset of infarction decreased the ST-E by 73 +/- 6% within one hour. Treatment with beta receptor blockers in the acute phase in all patients with first anterior wall infarcts accompanied with ST-E leads to a favorable prognosis. Early ST-E can therefore be considered as a sign of sympathico-adrenergic induced changes in myocardial metabolism. Thus the beta receptor blockade in the acute phase (of anterior wall infarctions) seems to be therapeutically indicated.

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