Andrews T C, Parker J D, Jacobs S, Friedman R, Cummings N, MacCallum G, Mannting F, Tofler G H, Carlson W, Muller J E, Stone P H
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, USA.
J Am Coll Cardiol. 1998 Nov 15;32(6):1680-6. doi: 10.1016/s0735-1097(98)00445-8.
We sought to determine the effect of nifedipine gastrointestinal therapeutic system (GITS) or atenolol on ischemic left ventricular dysfunction induced by mental stress.
The efficacy of conventional antianginal therapy in preventing myocardial ischemia induced by mental stress is unknown.
Nifedipine GITS, atenolol and placebo were administered to 15 subjects with stable angina in a double-blind crossover trial. Subjects underwent a series of mental stressors at the end of each treatment. Radionuclide ventriculography was performed at baseline and at peak mental stress. Other measured variables included time to ischemia on exercise treadmill testing, ischemia on 48-h ambulatory electrocardiogram (ECG) monitoring, and resting and mental stress-induced levels of plasma catecholamines, tissue plasminogen activator antigen, plasminogen activator inhibitor-1 and platelet aggregability.
Mental stress resulted in a significant increase in plasma epinephrine and norepinephrine levels during each treatment phase. Atenolol therapy was associated with lower baseline and postmental stress rate-pressure product compared with nifedipine or placebo. Therapy with either nifedipine GITS or atenolol prevented the development of wall-motion abnormalities and the decline in regional ejection fraction (EF) in the segment with the largest deterioration in wall motion during placebo therapy. Both medications prevented the decrease in global EF in subjects who demonstrated at least a 5% fall in global EF on placebo therapy. No therapy exerted a statistically significant benefit on exercise performance or frequency of ischemia during ambulatory ECG monitoring.
Both nifedipine GITS and atenolol are effective at preventing mental stress-induced wall-motion abnormalities, although the mechanisms may be different.
我们试图确定硝苯地平胃肠道治疗系统(GITS)或阿替洛尔对精神应激诱发的缺血性左心室功能障碍的影响。
传统抗心绞痛疗法在预防精神应激诱发的心肌缺血方面的疗效尚不清楚。
在一项双盲交叉试验中,对15例稳定型心绞痛患者给予硝苯地平GITS、阿替洛尔和安慰剂。在每种治疗结束时,受试者接受一系列精神应激源刺激。在基线和精神应激高峰时进行放射性核素心室造影。其他测量变量包括运动平板试验中出现缺血的时间、48小时动态心电图(ECG)监测中的缺血情况,以及静息和精神应激诱发的血浆儿茶酚胺、组织纤溶酶原激活物抗原、纤溶酶原激活物抑制剂-1水平和血小板聚集性。
在每个治疗阶段,精神应激导致血浆肾上腺素和去甲肾上腺素水平显著升高。与硝苯地平或安慰剂相比,阿替洛尔治疗的基线和精神应激后率压乘积较低。硝苯地平GITS或阿替洛尔治疗均可预防安慰剂治疗期间壁运动恶化最严重节段的壁运动异常发展和局部射血分数(EF)下降。两种药物均预防了在安慰剂治疗期间整体EF至少下降5%的受试者的整体EF下降。在动态心电图监测期间,没有一种治疗对运动表现或缺血频率有统计学上的显著益处。
硝苯地平GITS和阿替洛尔在预防精神应激诱发的壁运动异常方面均有效,尽管其机制可能不同。