Division of Cardiology, Matsuyama Red Cross Hospital, Matsuyama, Japan.
Circ J. 2011;75(6):1400-8. doi: 10.1253/circj.cj-10-0751. Epub 2011 Apr 26.
Muscle sympathetic nerve firing rate increases as chronic heart failure (CHF) progresses, yet its oscillation, particularly within the frequency range encompassing 0.13 Hz, diminishes. The current study tested the hypothesis that chronic therapy with lipophilic β-adrenoceptor antagonists augments the modulation of muscle sympathetic nerve activity variability (MSNAV) at this frequency range.
In 21 CHF angiotensin converting enzyme (ACE) inhibitor-treated patients (age: 53 ± 2, ejection fraction: 20 ± 2%), MSNA was recorded before and after 4 months of β-blockade with either metoprolol (up to 50mg b.i.d.) or carvedilol (up to 25mg b.i.d.). Harmonic MSNAV was assessed by coarse graining spectral analysis. Both drugs lowered heart rate similarly (-13 ± 2 beats/min; P < 0.001) but neither affected MSNA burst frequency (-7 ± 4 bursts/min, not significant). Before β-blockade, harmonic MSNA power in the region encompassing 0.13 Hz was essentially absent. Beta-blockade increased the mean values for total power (from 0.00 to 0.50 Hz; 5.2 ± 0.8 to 6.8 ± 1.2U(2); P < 0.001) and for harmonic MSNA spectral power across the 0.1-0.22 Hz frequency range (from 0.48 ± 0.10 to 1.50 ± 0.32 U(2), F = 12.2; P < 0.001). Both carvedilol and metoprolol had a similar effect.
In patients with CHF receiving ACE inhibitors, adding a β-adrenoceptor antagonist restores low and high frequency harmonic oscillations in MSNA. Beta-1 antagonism is sufficient to achieve this response. Augmented modulation of sympathetic outflow could contribute to the beneficial effects of β-blockade in CHF on sudden death and disease progression.
随着慢性心力衰竭（CHF）的进展，肌肉交感神经放电率增加，但它的振荡，特别是在包含 0.13 Hz 的频率范围内，减弱。本研究检验了这样一个假设，即亲脂性β-肾上腺素能受体拮抗剂的慢性治疗增强了肌肉交感神经活动变异性（MSNAV）在该频率范围内的调制。
在 21 例接受血管紧张素转换酶（ACE）抑制剂治疗的 CHF 患者（年龄：53 ± 2，射血分数：20 ± 2%）中，在接受美托洛尔（最高 50mg b.i.d.）或卡维地洛（最高 25mg b.i.d.）β-阻断治疗 4 个月前后记录 MSNA。通过粗粒化谱分析评估谐波 MSNAV。两种药物均使心率相似地降低（-13 ± 2 次/分；P < 0.001），但均不影响 MSNA 爆发频率（-7 ± 4 次/分，无显著性差异）。在β-阻断之前，包含在 0.13 Hz 范围内的谐波 MSNA 功率基本上不存在。β-阻断增加了总功率的平均值（从 0.00 到 0.50 Hz；5.2 ± 0.8 到 6.8 ± 1.2U(2)；P < 0.001）和 0.1-0.22 Hz 频率范围内的谐波 MSNA 谱功率（从 0.48 ± 0.10 到 1.50 ± 0.32 U(2)，F = 12.2；P < 0.001）。卡维地洛和美托洛尔均有类似的作用。
在接受 ACE 抑制剂治疗的 CHF 患者中，添加β-肾上腺素能受体拮抗剂可恢复 MSNA 的低频和高频谐波振荡。β-1 拮抗足以实现这种反应。交感神经输出的增强调节可能有助于β-阻断在 CHF 中的有益作用，即降低猝死和疾病进展的风险。
