Sayer J W, Gutteridge C, Syndercombe-Court D, Wilkinson P, Timmis A D
Department of Cardiology, Royal Hospitals Trust, London School of Hygiene and Tropical Medicine, United Kingdom.
J Am Coll Cardiol. 1998 Dec;32(7):1962-8. doi: 10.1016/s0735-1097(98)00481-1.
To examine circadian changes in the sympathovagal balance, the activity of the renin-angiotensin system and hemostatic variables in patients with stable coronary artery disease, and the effects of beta-adrenoceptor blockade and angiotensin-converting enzyme inhibition.
Sympathovagal balance and key components of the fibrinolytic system show circadian variability. The effects of beta-adrenergic blocking agents and angiotensin-converting enzyme inhibitors on these autonomic and hemostatic rhythms are not well defined.
Twenty patients with coronary artery disease underwent 24-h Holter monitoring for heart rate variability and blood sampling (6 hourly for 24 hours) after three consecutive treatment phases, (firstly with placebo, then bisoprolol, and finally quinapril). The effects on sympathovagal balance, hemostatic variables and the renin-angiotensin system activity were measured.
The fibrinolytic capacity showed marked circadian variation at the end of the placebo phase (p = 0.002), plasminogen activator inhibitor-1 (PAI-1) activity peaking at 06.00 AM when tissue plasminogen activator (tPA) activity was at its nadir. Sympathovagal balance showed a sharp increase at approximately the same time but plasma renin activity did not rise until later in the day. Inspection of the 24-h profiles suggested that bisoprolol reduced sympathovagal balance and the morning peak of PAI-1 activity and antigen, with a small increase in tPA activity, although these changes were not significant. Quinapril produced a substantial rise in renin (p = 0.01) but did not significantly affect either PAI-1 or tPA. Sympathovagal balance was unaffected by quinapril.
In patients with stable coronary artery disease, angiotensin-converting enzyme inhibition with quinapril does not affect either sympathovagal balance or the endogenous fibrinolytic system. Our data suggest that the sympathoadrenal system may modify fibrinolytic activity, judged by the response to beta-adrenoreceptor blockade with bisoprolol.
研究稳定性冠心病患者交感迷走神经平衡、肾素 - 血管紧张素系统活性及止血变量的昼夜变化，以及β - 肾上腺素能受体阻滞剂和血管紧张素转换酶抑制剂的作用。
交感迷走神经平衡和纤维蛋白溶解系统的关键成分呈现昼夜变化。β - 肾上腺素能阻滞剂和血管紧张素转换酶抑制剂对这些自主神经和止血节律的影响尚不明确。
20例冠心病患者在连续三个治疗阶段（首先使用安慰剂，然后使用比索洛尔，最后使用喹那普利）后，进行24小时动态心电图监测以评估心率变异性，并进行血液采样（每6小时一次，共24小时）。测量对交感迷走神经平衡、止血变量和肾素 - 血管紧张素系统活性的影响。
在安慰剂阶段结束时，纤维蛋白溶解能力呈现明显的昼夜变化（p = 0.002），纤溶酶原激活物抑制剂 -1（PAI -1）活性在上午06:00达到峰值，此时组织纤溶酶原激活物（tPA）活性处于最低点。交感迷走神经平衡在大致相同时间急剧增加，但血浆肾素活性直到当天晚些时候才升高。对24小时曲线的检查表明，比索洛尔降低了交感迷走神经平衡以及PAI -1活性和抗原的早晨峰值，tPA活性略有增加，尽管这些变化不显著。喹那普利使肾素大幅升高（p = 0.01），但对PAI -1或tPA均无显著影响。交感迷走神经平衡不受喹那普利影响。
在稳定性冠心病患者中，使用喹那普利抑制血管紧张素转换酶既不影响交感迷走神经平衡，也不影响内源性纤维蛋白溶解系统。我们的数据表明，根据对比索洛尔β - 肾上腺素能受体阻滞的反应判断，交感肾上腺系统可能会改变纤维蛋白溶解活性。
