The Danish National Research Foundation Centre for Cardiac Arrhythmia, Department of Biomedical Sciences, The Panum Institute, University of Copenhagen, Copenhagen N, Denmark.
Acta Physiol (Oxf). 2012 Aug;205(4):494-506. doi: 10.1111/j.1748-1716.2012.02428.x. Epub 2012 Mar 14.
Endocardial pacing instituted to treat symptomatic bradycardia may nevertheless promote tachyarrhythmia in some pacemaker-implanted patients. We sought to determine the contributing electrophysiological mechanisms.
Left ventricular (LV) monophasic action potential duration (APD(90)) and effective refractory periods were determined in perfused guinea-pig hearts along with volume-conducted ECG recordings during epicardial and endocardial stimulations.
Consistent with electrotonic modulation of repolarization, APD(90) at a given (either epicardial or endocardial) recording site tended to be longer while pacing from the ipsilateral LV site as compared to stimulations applied at the opposite side of ventricular wall. As a result, the intrinsic transmural repolarization gradient was amplified during endocardial pacing while being significantly reduced upon epicardial stimulations. The maximum slope of APD(90) restitution was greater upon endocardial than epicardial pacing. The excitability was found to recur at earlier repolarization time point at endocardium than epicardium, thereby contributing to increased endocardial critical intervals for re-excitation. Premature extrasystolic beats could have been elicited at shorter coupling stimulation intervals and propagated with greater transmural conduction delay upon endocardial than epicardial stimulations. Endocardial site exhibited lower ventricular fibrillation thresholds and greater inducibility of tachyarrhythmia upon extrasystolic stimulations as compared to epicardium.
Arrhythmic susceptibility in guinea-pig heart is greater during endocardial than epicardial pacing because of greater transmural APD(90) dispersion, steeper electrical restitution slopes, greater critical intervals for LV re-excitation and slower transmural conduction of the earliest premature ectopic beats. Further studies are warranted to determine whether these effects may contribute to proarrhythmia in paced human patients.
为治疗症状性心动过缓而植入的心脏内心脏起搏可能会在某些植入起搏器的患者中引发心动过速性心律失常。我们试图确定促成这种心律失常的电生理机制。
在灌注的豚鼠心脏中，同时进行心外膜和心内膜刺激时，记录单相动作电位时程（APD90）和有效不应期，并记录容积传导心电图。
与复极化的电紧张调制一致，与刺激心室壁的对侧相比，在同侧 LV 部位起搏时，给定（心外膜或心内膜）记录部位的 APD90 往往更长。结果，心内膜起搏时，内在的跨壁复极梯度被放大，而心外膜刺激时则显著降低。与心外膜起搏相比，APD90 restitution 的最大斜率更大。发现兴奋在心脏内膜比心外膜更早的复极时间点再次出现，从而导致心脏内膜的再兴奋临界间隔增加。与心外膜刺激相比，在较短的偶联刺激间隔下，可以诱发更早的期前收缩，并在心内膜上传播更大的跨壁传导延迟。与心外膜相比，心脏内膜部位的心室颤动阈值较低，在期前刺激下诱发心动过速性心律失常的可能性更大。
与心外膜起搏相比，豚鼠心脏在心脏内膜起搏时更易发生心律失常，原因是跨壁 APD90 离散度更大、电复律斜率更陡、LV 再兴奋的临界间隔更大以及最早的异位搏动的跨壁传导速度更慢。需要进一步研究以确定这些效应是否会导致起搏患者的心律失常。
