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阵发性室上性心动过速时ST段压低的意义

Significance of ST segment depression during paroxysmal supraventricular tachycardia.

作者信息

Nelson S D, Kou W H, Annesley T, de Buitleir M, Morady F

机构信息

Division of Cardiology, University of Michigan, Ann Arbor.

出版信息

J Am Coll Cardiol. 1988 Aug;12(2):383-7. doi: 10.1016/0735-1097(88)90410-x.

Abstract

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (+/- SD) of 38 +/- 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias. A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 +/- 12 beats/min increased to 180 +/- 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 +/- 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 +/- 26 beats/min in five patients resulted in greater than or equal to 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 +/- 13% to -27 +/- 20% (p less than 0.05) indicating net myocardial lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在阵发性室上性心动过速期间,患者常出现胸痛及明显的ST段压低,提示急性心肌缺血。本研究的目的是评估室上性心动过速期间的ST段压低是否由心肌乳酸净生成所反映的心肌缺血所致。25例(14例男性,11例女性)有阵发性室上性心动过速病史且平均年龄(±标准差)为38±14岁的患者接受了电生理检查。其中24例患者无冠心病证据,1例患者曾接受冠状动脉搭桥手术。19例患者为顺向型房室折返性心动过速,6例患者为房室结折返性心动过速。在基线、室上性心动过速发作5分钟和10分钟时,记录12导联心电图,并同时采集股动脉和冠状窦血样测定乳酸。室上性心动过速期间,平均基线心率83±12次/分钟增至180±25次/分钟。所有患者12导联中有1至9个导联出现1至8毫米的ST段压低。64%的患者在室上性心动过速期间出现胸痛。基线心肌乳酸摄取率为28±13%,心动过速发作5分钟或10分钟时无显著变化。相比之下,在7例已知冠心病的对照患者组中,5例患者以168±26次/分钟的频率进行心房起搏,导致12导联中有2至7个导联ST段压低≥1毫米,乳酸摄取率从基线的29±13%变为-27±20%(p<0.05),表明有心肌乳酸净生成。(摘要截短于250字)

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