Heart rate changes preceding ventricular ectopy in patients with ventricular tachycardia caused by reentry, triggered activity, and automaticity.
Heart rate changes preceding ventricular ectopy in patients with ventricular tachycardia caused by reentry, triggered activity, and automaticity.
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DOI：
10.1016/s0002-8703(98)70216-9
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发表时间：
1998-09
影响因子：
4.8
通讯作者：
K. Stein;L. Karagounis;S. Markowitz;J. Anderson;B. Lerman
中科院分区：
文献类型：
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作者：
K. Stein;L. Karagounis;S. Markowitz;J. Anderson;B. Lerman
目的虽然交感神经张力增强被认为是诱发心律失常的因素，阻断β可降低心肌梗塞存活者心源性猝死的风险，但自主神经系统在引发自发性室性异位和室性心动过速(VT)中的作用尚未完全阐明。本研究的目的是比较和对比折返型、触发型和自动型室性心动过速患者发生自发性室性心律失常前的自主神经张力。背景：折返性室速的流行模型是基于触发节拍与固定底物相互作用的。在这个模型中，自主神经张力的周期性波动构成了“第三因素”，它可能启动触发的早搏，并改变底物，促进心动过速的持续。与这一模型一致，肾上腺素能刺激可以促进折返性心律失常的诱发，以及由增强的自律性引起的心律失常，以及由环磷酸腺苷依赖的延迟后除极引起的触发活动引起的心律失常。方法与结果根据电生理检查结果，确诊冠心病患者26例为折返性室速，11例为触发活动所致特发性室速，4例为自律性增强所致特发性室速。每例患者均进行24小时心电监测，计算每次窦性心动过速前的平均窦性R-R间期以及窦性早搏、室性早搏(VPC)和复杂室性早搏(对联/非持续性室性心动过速)前15次的窦性R-R间期。此外，还测定了高频心率变异性。在自发性室性异位发作之前，所有三种心律失常机制的心率都加快。在触发性室性心动过速患者和折返性室速患者中，复杂室性异位发作前的R-R间期明显短于单发VPC前的相应间期[分别为P=0.006和0.01，R-R(-1)和R-R(-15)](P=0.007和P=0.05)。在高频心率变异性方面没有相应的差异。自动室性心动过速患者单个室上性心动过速前的R-R间期明显短于相应的窦性早搏前间期(p=0.0004和0.0001)，并伴有高频心率变异性的轻微降低(p=0.04)。结论室性心动过速患者自发性室性早搏前心率加快。这种加速与副交感神经收缩不成比例，提示内源性交感神经张力增加在由三种电生理机制：折返、触发活动和自律性引起的自发性室性心律失常的发生中起作用。(《心脏杂志》1998；136：425-34。)
Objectives Although enhanced sympathetic tone is thought to be proarrhythmic and β-blockade reduces the risk of sudden cardiac death in survivors of myocardial infarction, the role of the autonomic nervous system in triggering spontaneous ventricular ectopy and ventricular tachycardia (VT) has not been fully elucidated. The purpose of this study was to compare and contrast autonomic tone preceding spontaneous ventricular arrhythmias in patients with reentrant, triggered, and automatic forms of VT. Background The prevailing model of reentrant VT is based on a triggering beat interacting with a fixed substrate. Within this model, cyclic fluctuations in autonomic tone comprise a “third factor” that may initiate the triggering extrasystoles as well as alter the substrate, facilitating perpetuation of tachycardia. Consistent with this model, adrenergic stimulation can facilitate the induction of reentrant arrhythmias as well as arrhythmias resulting from enhanced automaticity and those caused by triggered activity resulting from cyclic adenosine monophosphate–dependent delayed afterdepolarizations. Methods and Results On the basis of the results at electrophysiologic study, 26 patients with coronary artery disease were identified as having reentrant VT, 11 were identified as having idiopathic VT caused by triggered activity, and 4 were identified as having idiopathic VT caused by enhanced automaticity. Each patient underwent 24-hour electrocardiographic monitoring, and the mean sinus R-R intervals immediately preceding each sinus beat as well as the 15 beats preceding sinus beats, premature ventricular contractions (VPCs), and complex ventricular ectopy (couplet/nonsustained VT) were computed. In addition, high-frequency heart rate variability was determined. Heart rate accelerated before spontaneous ventricular ectopy for all three arrhythmia mechanisms. R-R intervals preceding episodes of complex ventricular ectopy were significantly shorter than the corresponding intervals preceding single VPCs in patients with triggered VT [p = 0.006 and 0.01, R-R(-1) and R-R(-15), respectively] and in those with reentrant VT (p = 0.007 and p = 0.05). There were no corresponding differences in high-frequency heart rate variability. R-R intervals preceding single VPCs were significantly shorter than the corresponding intervals preceding sinus beats in patients with automatic VT (p = 0.0004 and 0.0001, respectively), which was accompanied by a small reduction in high-frequency heart rate variability (p = 0.04). Conclusions Heart rate accelerates before spontaneous ventricular ectopy in patients with VT. The acceleration is disproportionate to parasympathetic withdrawal, implicating increased endogenous sympathetic tone in the genesis of spontaneous ventricular arrhythmias caused by all three electrophysiologic mechanisms: reentry, triggered activity, and automaticity. (Am Heart J 1998;136:425-34.)