Cheema A N, Ahmed M W, Kadish A H, Goldberger J J
Department of Medicine, Northwestern University, Chicago, Illinois, USA.
J Am Coll Cardiol. 1995 Aug;26(2):497-502. doi: 10.1016/0735-1097(95)80028-f.
This study sought to evaluate the effects of autonomic stimulation and blockade on the signal-averaged P wave duration.
Signal-averaged P wave duration has been shown to have prognostic implications for patients prone to develop atrial fibrillation, but autonomic influences on the signal-averaged P wave duration have not been studied.
In 14 healthy volunteers (8 men, 6 women; mean [ +/- SD] age 28.5 +/- 4.8 years, range 22 to 38), signal-averaged P wave duration was measured on day 1 at baseline, during sympathetic stimulation with infusions of epinephrine (50 ng/kg body weight per min) and isoproterenol (50 ng/kg per min), beta-blockade with propranolol (0.2 mg/kg) and autonomic blockade with propranolol followed by atropine (0.04 mg/kg). On a second day, 10 of the 14 subjects returned for repeat baseline recordings and recordings during parasympathetic blockade with atropine (0.04 mg/kg). Signal averaging was performed using a P wave template. Both unfiltered and filtered (least-squares fit filter with 100-ms window) P wave durations were measured. Day to day and interobserver variability were assessed by calculation of intraclass correlation coefficients.
The mean ( +/- SD) baseline filtered P wave duration on day 1 was 141 +/- 10 ms. Isoproterenol infusion significantly shortened the P wave duration to 110 +/- 16 ms (p < 0.001), and epinephrine resulted in significant prolongation to 150 +/- 10 ms (p < 0.05). Beta-adrenergic blockade increased the P wave duration to 153 +/- 10 ms (p < 0.005). Autonomic blockade shortened the P wave duration to 143 +/- 16 ms (p < 0.05 vs. beta-blockade). On the second day, the mean baseline P wave duration was slightly longer (144 +/- 10 ms, p < 0.02). Parasympathetic blockade with atropine resulted in mild shortening of the P wave duration to 136 +/- 15 ms (p < 0.1). Interobserver reproducibility was excellent (intraclass correlation coefficient 0.99). Day to day reproducibility was good (intraclass correlation coefficient 0.56).
The signal-averaged P wave duration is not a fixed variable because it may change significantly under different autonomic conditions. This has important implications for the application of this test to the heterogeneous population susceptible to atrial fibrillation.
本研究旨在评估自主神经刺激和阻断对信号平均P波时限的影响。
信号平均P波时限已被证明对易发生心房颤动的患者具有预后意义,但自主神经对信号平均P波时限的影响尚未得到研究。
在14名健康志愿者(8名男性,6名女性;平均[±标准差]年龄28.5±4.8岁,范围22至38岁)中,于第1天在基线状态下、静脉输注肾上腺素(50 ng/kg体重每分钟)和异丙肾上腺素(50 ng/kg每分钟)进行交感神经刺激期间、静脉注射普萘洛尔(0.2 mg/kg)进行β受体阻滞剂阻滞以及静脉注射普萘洛尔后再注射阿托品(0.04 mg/kg)进行自主神经阻滞后测量信号平均P波时限。在第二天,14名受试者中的10名返回进行重复基线记录以及在静脉注射阿托品(0.04 mg/kg)进行副交感神经阻滞后的记录。使用P波模板进行信号平均。测量未滤波和滤波(100毫秒窗口的最小二乘拟合滤波器)后的P波时限。通过计算组内相关系数评估每日和观察者间的变异性。
第1天平均(±标准差)基线滤波后的P波时限为141±10毫秒。静脉输注异丙肾上腺素使P波时限显著缩短至110±16毫秒(p<0.001),而肾上腺素使P波时限显著延长至150±10毫秒(p<0.05)。β肾上腺素能阻滞剂使P波时限增加至153±10毫秒(p<0.005)。自主神经阻滞使P波时限缩短至143±16毫秒(与β受体阻滞剂阻滞相比,p<0.05)。在第二天,平均基线P波时限略长(144±10毫秒,p<0.02)。静脉注射阿托品进行副交感神经阻滞使P波时限轻度缩短至136±15毫秒(p<0.1)。观察者间的可重复性极佳(组内相关系数0.99)。每日可重复性良好(组内相关系数0.56)。
信号平均P波时限不是一个固定变量,因为它在不同的自主神经状态下可能会发生显著变化。这对于将该测试应用于易患心房颤动的异质性人群具有重要意义。