Bourn David W, Gray Richard A, Trayanova Natalia A
Department of Biomedical Engineering, Tulane University, New Orleans, Louisiana 70118, USA.
Heart Rhythm. 2006 May;3(5):583-95. doi: 10.1016/j.hrthm.2006.01.024. Epub 2006 Feb 28.
Studies have demonstrated that failed defibrillation shocks often are followed by an electrically quiescent period (isoelectric window); however, the underlying mechanisms remain incompletely understood. We recently suggested a new mechanism termed "virtual electrode polarization-induced propagated graded responses" (VEPiPGRs) that might play a role in the origin of the global postshock activation following the isoelectric window.
The purpose of this study to elucidate the circumstances under which VEPiPGR activations originate for shocks given to paced right ventricular preparations. Specifically, we examined the dependence of VEPiPGRs on coupling interval (CI) and shock polarity and whether VEPiPGRs emerge preferentially on the epicardium or the endocardium.
Simultaneous endocardial and epicardial activity in isolated right ventricular preparations (n = 4) was imaged optically following shocks of strength +/-5A. All VEPiPGRs were analyzed, and the time T from shock end to activation onset was recorded (isoelectric window is the smallest T among activations that propagated globally).
VEPiPGR activations occurred for CIs in the range from 80 to 150 ms. Average duration of T was 64.5 +/- 18.15 ms, with T decreasing as CI increased (Tmax = 82 ms, Tmin = 46 ms, linear-fit slope = -0.675). The average earliest CI at which cathodal (+5A) shocks resulted in VEPiPGRs was 87 ms compared with 116 ms for anodal (-5A) shocks. All VEPiPGR activations emerged first on the epicardium in a focal pattern, and all induced ventricular fibrillation.
The global activation that terminates the isoelectric window could result from VEPiPGRs that find an exit pathway. VEPiPGRs originate at the sites of maximum action potential abbreviation by the shock, always on the epicardium for the preparation used here.
研究表明,除颤电击失败后通常会出现电静止期(等电窗);然而,其潜在机制仍未完全明确。我们最近提出了一种新机制,称为“虚拟电极极化诱导的传播性分级反应”(VEPiPGRs),该机制可能在等电窗后的整体电击后激活的起源中起作用。
本研究的目的是阐明在对起搏右心室标本进行电击时,VEPiPGR激活产生的情况。具体而言,我们研究了VEPiPGRs对耦合间期(CI)和电击极性的依赖性,以及VEPiPGRs是否优先出现在心外膜或心内膜上。
在强度为±5A的电击后,对离体右心室标本(n = 4)的心内膜和心外膜活动进行同步光学成像。分析所有VEPiPGRs,并记录从电击结束到激活开始的时间T(等电窗是在整体传播的激活中最小的T)。
VEPiPGR激活发生在80至150 ms的CI范围内。T的平均持续时间为64.5±18.15 ms,T随CI增加而减小(Tmax = 82 ms,Tmin = 46 ms,线性拟合斜率 = -0.675)。阴极(+5A)电击导致VEPiPGRs的平均最早CI为87 ms,而阳极(-5A)电击为116 ms。所有VEPiPGR激活均首先以局灶性模式出现在心外膜上,并且均诱发心室颤动。
终止等电窗的整体激活可能源于找到出口途径的VEPiPGRs。VEPiPGRs起源于电击引起的最大动作电位缩短部位,在此处使用的标本中总是在心外膜上。