Aronson D, Burger A J
Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Ann Noninvasive Electrocardiol. 2001 Apr;6(2):98-106. doi: 10.1111/j.1542-474x.2001.tb00093.x.
One of the putative mechanisms for the salutary effects of beta-blockers in patients with congestive heart failure (CHF) is their ability to improve autonomic dysfunction. However, patients with profound neurohumoral abnormalities derive little survival benefit from beta-blockers. The purpose of the current study was to evaluate the effect of beta-blockers on heart rate variability (HRV) in decompensated CHF.
Time and frequency domain HRV indices were obtained from 24-hour Holter recordings and compared to assess the role of beta-blockade in 199 patients (mean age 60 +/- 14 years) with decompensated CHF. Neurohormonal differences were assessed by measuring norepinephrine, endothelin-1, tumor necrosis factor-alpha, and interleukin-6 in a subset of 64 patients.
All HRV indices were markedly suppressed but were substantially higher in patients who were on beta-blockers. Time domain measures of parasympathetic cardiac activity, the percentage of R-R intervals with > 50 ms variation (4.9 +/- 0.6 vs 7.7 +/- 1.2%, P = 0.006) and the square root of mean squared differences of successive R-R intervals (22.7 +/- 2.0 vs 31.6 +/- 4.1 ms, P = 0.004), were higher in the beta-blocker group. Spectral analysis revealed that the total power and the ultra-low frequency power were significantly higher in patients on beta-blockers (82% and 59%, respectively). The high frequency power, a spectral index of parasympathetic modulation, was 41% higher in the beta-blocker group (121 +/- 25 vs 171 +/- 27 ms(2), P = 0.02). Norepinephrine and interleukin-6 levels were substantially lower in patients on beta-blockers (28% and 61%, respectively). However, these differences did not reach statistical significance.
Beta-blockers improve the impaired cardiac autonomic regulation during high sympathetic stress of decompensated CHF. This effect may play an important role in protecting the myocardium and preventing arrhythmias during transient increases in sympathetic activity.
β受体阻滞剂对充血性心力衰竭(CHF)患者产生有益作用的一种假定机制是其改善自主神经功能障碍的能力。然而,存在严重神经体液异常的患者从β受体阻滞剂中获得的生存益处甚微。本研究的目的是评估β受体阻滞剂对失代偿性CHF患者心率变异性(HRV)的影响。
从24小时动态心电图记录中获取时域和频域HRV指标,并对199例(平均年龄60±14岁)失代偿性CHF患者进行比较,以评估β受体阻滞剂的作用。通过测量64例患者亚组中的去甲肾上腺素、内皮素-1、肿瘤坏死因子-α和白细胞介素-6来评估神经体液差异。
所有HRV指标均明显受到抑制,但在服用β受体阻滞剂的患者中显著更高。β受体阻滞剂组中,副交感神经心脏活动的时域测量指标,即R-R间期变化>50 ms的百分比(4.9±0.6对7.7±1.2%,P = 0.006)和连续R-R间期均方差的平方根(22.7±2.0对31.6±4.1 ms,P = 0.004)更高。频谱分析显示,服用β受体阻滞剂的患者总功率和超低频功率显著更高(分别为82%和59%)。作为副交感神经调节频谱指标的高频功率,β受体阻滞剂组高41%(121±25对171±27 ms²,P = 0.02)。服用β受体阻滞剂的患者去甲肾上腺素和白细胞介素-6水平显著更低(分别为28%和61%)。然而,这些差异未达到统计学意义。
β受体阻滞剂可改善失代偿性CHF在高交感神经应激期间受损的心脏自主神经调节。这种作用可能在交感神经活动短暂增加期间保护心肌和预防心律失常方面发挥重要作用。