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无症状心肌缺血中的β-肾上腺素能阻滞剂

Beta-adrenergic blockers in silent myocardial ischemia.

作者信息

Pepine C J, Hill J A, Imperi G A, Norvell N

机构信息

Department of Medicine, University of Florida, Gainesville 32610.

出版信息

Am J Cardiol. 1988 Jan 29;61(3):18B-21B. doi: 10.1016/0002-9149(88)91350-1.

Abstract

Factors contributing to the development of exercise-induced painful ischemia, such as actions of the central nervous system and catecholamines, have been well identified, but the mechanisms by which nonexercise-related silent episodes of ischemia are provoked are unknown. Possible mechanisms receiving much study in recent years are those having the potential to influence the myocardial oxygen supply-demand relation. Beta-adrenergic receptor stimulations, by increasing myocardial oxygen demand through augmentation of heart rate and contractility (beta 1), may mediate responses that cause ischemia or perpetuate ischemic episodes induced by other means. Other receptors (beta 2) may mediate coronary and peripheral vascular constriction, limiting myocardial oxygen supply and further increasing myocardial oxygen demand. Studies have investigated the effect of beta blockade on ischemic episodes in patients with a variety of clinical forms of coronary heart disease. Beta blockade has been shown to reduce the frequency and duration of silent and painful ischemic episodes in patients with effort angina and rest angina. The data suggest that heart rate and perhaps other changes observed with use of beta blockade play an important role in silent ischemia; heart rate at specific times throughout the day, particularly in the late A.M., and the increase in heart rate seen in conjunction with silent ischemic episodes are all decreased with administration of beta blockade. Results of a recent study focusing only on silent ischemia showed that beta-blocker treatment with metoprolol, compared with placebo, significantly reduced total silent ischemic time (frequency and duration of episodes) in all periods examined.

摘要

促成运动诱发疼痛性缺血发展的因素,如中枢神经系统和儿茶酚胺的作用,已得到充分确认,但引发与运动无关的无症状性缺血发作的机制尚不清楚。近年来受到大量研究的可能机制是那些有可能影响心肌氧供需关系的机制。β-肾上腺素能受体刺激通过增加心率和心肌收缩力(β1)来增加心肌需氧量,可能介导导致缺血的反应或使其他方式诱发的缺血发作持续存在。其他受体(β2)可能介导冠状动脉和外周血管收缩,限制心肌氧供应并进一步增加心肌需氧量。研究已经调查了β受体阻滞剂对患有各种临床形式冠心病患者缺血发作的影响。β受体阻滞剂已被证明可减少劳力性心绞痛和静息性心绞痛患者无症状和疼痛性缺血发作的频率和持续时间。数据表明,心率以及使用β受体阻滞剂时观察到的其他变化可能在无症状性缺血中起重要作用;全天特定时间的心率,尤其是上午晚些时候的心率,以及与无症状性缺血发作同时出现的心率增加,在使用β受体阻滞剂后均会降低。最近一项仅关注无症状性缺血的研究结果表明,与安慰剂相比,美托洛尔β受体阻滞剂治疗在所有检查时间段均显著减少了总的无症状性缺血时间(发作频率和持续时间)。

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