Burgess M J, Pollard A E, Spitzer K W, Yang L
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City 84112, USA.
Circulation. 1995 Oct 1;92(7):1969-80. doi: 10.1161/01.cir.92.7.1969.
A short-long-short sequence of cycle lengths predisposes to reentrant tachyarrhythmias. There is limited information about the effects of premature ventricular contractions (PVCs) on repolarization of postextrasystolic depolarizations (PEDs). Such information would contribute to understanding the mechanism for facilitating reentry with short-long-short cycle lengths.
We introduced PVCs, over a range of coupling intervals and during a range of basic drive cycle lengths (BCLs), and determined PED repolarization. Our results from whole-animal experiments, isolated cell studies, and computer simulations are reported. In the whole-animal experiments, PED refractory periods (RPs) were longer than RPBCL. The greatest difference between RPPED and RPBCL (delta RPmax) occurred after short coupling interval PVCs and was 4.3 +/- 0.8, 4.2 +/- 0.8, and 2.1 +/- 0.5 ms (mean +/- SEM) during drives with short, intermediate, and long BCLs, respectively. The diastolic interval preceding the PED (DIPED) was inversely related to the coupling interval between the basic drive beat and the PVC and directly related to RPPED. PED action potential durations (APDs) of isolated canine myocytes were 9.8 +/- 4.9 ms (mean +/- SEM) longer than APD BCL (n = 19). The DiFrancesco-Noble membrane equations were used in simulations of action potential propagation in a one-dimensional cable, with stimulation protocols duplicating those in the animal experiments. PVCs prolonged APDPED, and APDPED was prolonged more during short than during long BCL drives. There was a direct relation between DIPED and APDPED. Analysis of the membrane currents over the time course of the PVCs and PEDs suggested that the ionic basis for PED repolarization prolongation was the interaction of Ito and Ik. Hyperpolarizing constant-current injections introduced immediately after the spike of isolated myocyte action potentials caused APD prolongation. This observation is consistent with the Ito and Ik interaction causing PED repolarization prolongation.
PED repolarization prolongation could provide sites for unidirectional block to propagation of PVCs after PEDs and could facilitate initiation of reentrant tachyarrhythmias after short-long-short sequences of cycle lengths.
长短短周期长度序列易引发折返性快速心律失常。关于室性早搏（PVC）对早搏后去极化（PED）复极化的影响，目前信息有限。此类信息将有助于理解长短短周期长度促进折返的机制。
我们在一系列联律间期以及一系列基础驱动周期长度（BCL）期间引入PVC，并测定PED复极化情况。报告了我们在全动物实验、分离细胞研究及计算机模拟方面的结果。在全动物实验中，PED不应期（RP）长于RPBCL。RPPED与RPBCL之间的最大差异（δRPmax）出现在短联律间期PVC之后，在短、中、长BCL驱动期间，分别为4.3±0.8、4.2±0.8和2.1±0.5毫秒（平均值±标准误）。PED之前的舒张间期（DIPED）与基础驱动搏动和PVC之间的联律间期呈负相关，与RPPED呈正相关。分离的犬心肌细胞的PED动作电位时程（APD）比APD BCL长9.8±4.9毫秒（平均值±标准误）（n = 19）。使用迪弗朗西斯科 - 诺布尔膜方程对一维电缆中的动作电位传播进行模拟，刺激方案与动物实验中的方案相同。PVC使APDPED延长，并且在短BCL驱动期间APDPED的延长幅度大于长BCL驱动期间。DIPED与APDPED之间存在直接关系。对PVC和PED时间过程中的膜电流分析表明，PED复极化延长的离子基础是Ito和Ik的相互作用。在分离的心肌细胞动作电位的锋电位之后立即进行超极化恒流注入会导致APD延长。这一观察结果与Ito和Ik相互作用导致PED复极化延长一致。
PED复极化延长可为PED后PVC传播的单向阻滞提供位点，并可能促进长短短周期长度序列后折返性快速心律失常的起始。
