Niemelä M J, Airaksinen K E, Huikuri H V
Department of Medicine, University of Oulu, Finland.
J Am Coll Cardiol. 1994 May;23(6):1370-7. doi: 10.1016/0735-1097(94)90379-4.
This study assessed the effects of beta-blockade on heart rate variability in patients with coronary artery disease and determined whether the effects of metoprolol in a controlled-release formulation and atenolol differ with regard to electrocardiographic measures of cardiac autonomic control.
Low heart rate variability is common in coronary artery disease and is associated with increased mortality. Beta-adrenergic blocking drugs may increase heart rate variability in healthy subjects, but there is limited knowledge of whether they are able to modify heart rate variability in patients with uncomplicated coronary artery disease.
In a randomly allocated, double-blind crossover study with three 2-week treatment periods, 200 mg of controlled-release metoprolol once a day, 100 mg of atenolol once a day or placebo once a day were administered in 18 male patients with stable coronary artery disease. The 24-h heart rate variability was measured in both the time and frequency domains.
Beta-blockade induced a significant increase in heart rate variability, but no significant differences were found between atenolol and metoprolol. The average 24-h high frequency power increased by 64% after atenolol and by 62% after metoprolol. The root-mean-square successive difference of normal RR intervals increased by 70% after atenolol and by 62% after metoprolol, and the standard deviations of RR intervals increased by 20% and 16%, respectively. Beta-blockade had no significant effects on the amplitude of the circadian rhythm of heart rate variability, although both metoprolol and atenolol blunted the abrupt decrease of high frequency power after arousal.
Beta-blockade by metoprolol and atenolol enhance the heart rate variability in patients with coronary artery disease. This may contribute to the protective effects of beta-blockade in ischemic heart disease.
本研究评估β受体阻滞剂对冠心病患者心率变异性的影响，并确定控释美托洛尔和阿替洛尔在心脏自主神经控制的心电图测量方面的效果是否存在差异。
低心率变异性在冠心病中很常见，且与死亡率增加相关。β肾上腺素能阻断药物可能会增加健康受试者的心率变异性，但对于它们是否能够改变无并发症冠心病患者的心率变异性，了解有限。
在一项随机分配的双盲交叉研究中，有三个为期2周的治疗期，对18名稳定型冠心病男性患者每日给予一次200mg控释美托洛尔、一次100mg阿替洛尔或一次安慰剂。在时域和频域中测量24小时心率变异性。
β受体阻滞剂使心率变异性显著增加，但阿替洛尔和美托洛尔之间未发现显著差异。阿替洛尔治疗后平均24小时高频功率增加64%，美托洛尔治疗后增加62%。阿替洛尔治疗后正常RR间期的均方根连续差值增加70%，美托洛尔治疗后增加62%，RR间期标准差分别增加20%和16%。β受体阻滞剂对心率变异性昼夜节律的幅度没有显著影响，尽管美托洛尔和阿替洛尔都减弱了觉醒后高频功率的突然下降。
美托洛尔和阿替洛尔进行β受体阻滞可增强冠心病患者的心率变异性。这可能有助于β受体阻滞剂在缺血性心脏病中的保护作用。
