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在电生理实验室中诱发心率和血压波动。

Induction of heart rate and blood pressure turbulence in the electrophysiologic laboratory.

作者信息

Roach Daniel, Koshman Mary-Lou, Duff Henry, Sheldon Robert

机构信息

Cardiovascular Research Group, Faculty of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada.

出版信息

Am J Cardiol. 2002 Nov 15;90(10):1098-102. doi: 10.1016/s0002-9149(02)02775-3.

DOI:10.1016/s0002-9149(02)02775-3
PMID:12423710
Abstract

Heart rate turbulence (HRT) is a transient tachycardia and/or bradycardia that follows ventricular premature complexes (VPCs). Absent or blunted HRT is associated with a poor prognosis in patients with heart disease, but its physiology is unknown. We hypothesized that HRT might be mediated by baroreflexes following early depolarizations. We sought to induce and characterize HRT in the electrophysiologic laboratory by introducing 1 ventricular extrastimulus every 60 seconds in 23 patients who underwent invasive electrophysiologic studies. On average, HRT was characterized by an initial RR interval decrease of 38 ms occurring 3.4 seconds after early depolarization. This was followed by a transient RR interval increase of 88 ms occurring 5.4 seconds later. HRT was preceded by similar hypotensive and/or hypertensive blood pressure turbulence. Baroreflex sensitivity estimates from post-VPCs and sinus sequences were similar (12.3 +/- 10.3 vs 10.2 +/- 8.9 ms/mm Hg, p = 0.51). The failure to induce HRT was associated with a limited initial hypotensive phase of blood pressure turbulence (-7.9 vs -12.1 mm Hg, p = 0.037). Patients with structural heart disease had reduced turbulence onset and reduced turbulence slope relative to those with structurally normal hearts, although blood pressure response was similar in both groups. HRT is an inducible, transient tachycardia and/or bradycardia that likely arises from a baroreflex response to transient hypotension following VPCs. Patients with structural heart disease have blunted HRT.

摘要

心率震荡(HRT)是指室性早搏(VPC)后出现的短暂性心动过速和/或心动过缓。HRT消失或减弱与心脏病患者的不良预后相关,但其生理机制尚不清楚。我们推测HRT可能由早期去极化后的压力反射介导。我们试图在电生理实验室中,通过对23例接受有创电生理研究的患者每60秒引入1次心室额外刺激来诱导并描述HRT。平均而言,HRT的特征为早期去极化后3.4秒RR间期初始下降38毫秒。随后在5.4秒后RR间期短暂增加88毫秒。HRT之前有类似的低血压和/或高血压性血压震荡。室性早搏后和窦性心律序列的压力反射敏感性估计相似(12.3±10.3对10.2±8.9毫秒/毫米汞柱,p = 0.51)。未能诱导出HRT与血压震荡的初始低血压期有限有关(-7.9对-12.1毫米汞柱,p = 0.037)。与结构正常心脏的患者相比,结构性心脏病患者的震荡起始和震荡斜率降低,尽管两组的血压反应相似。HRT是一种可诱导的短暂性心动过速和/或心动过缓,可能源于对室性早搏后短暂低血压的压力反射反应。结构性心脏病患者的HRT减弱。

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