慢性心力衰竭致心室颤动诱颤阈值变化的电生理机制研究

The electrophysiological mechanism for the altered inducibility of ventricular fibrillation in a canine heart failure model

目的研究慢性心力衰竭(简称心衰)易于促发心室颤动(简称室颤)可能的电生理机制。方法 12只比格犬随机分为对照组(n=6)和心衰组(n=6)。通过右室心尖部快速起搏4周制作犬充血性心衰模型。经左侧颈内动脉将64极伞状电极置于左室进行整体心内膜电生理标测。采用S1S2刺激方案测定心室有效不应期(ERP);通过连续S1S1刺激法诱发室颤;测定不同起搏周期最后一次起搏心律时每个电极的激动恢复间期并计算64个电极之间的变异系数。同时,比较两组心脏在300 ms起搏时的整体左室心内膜激动传导时间和分布。结果与对照组相比,心衰组左室ERP显著延长(180±6.7 ms vs 158±6.9 ms,P<0.01);在300,250,200和150 ms周期起搏时的左室激动恢复间期显著延长。两组不应期离散度在300 ms和250 ms起搏时无显著差异,但在200 ms和150 ms起搏时,心衰组不应期离散度显著增大。心衰组左室心内膜传导较对照组延迟达17.9%(41.2±0.7 ms vs 34.9±1.6 ms,P<0.01)。与对照组相比,心衰组更易诱发室颤(127±17 ms vs 103±8 ms,P<0.01)。结论心室复极延长、传导速度减慢以及不应期离散度增大可能是慢性心衰者易于促发室颤的原因。

Objective To investigate the potential mechanism in which the inducibility of ventricular fibrillation （VF） was altered by globally endocardial mapping for left ventricle （LV） in a canine heart failure （HF） model. Methods Twelve dogs were randomly divided into two groups （ control group, n = 6 ; HF group, n = 6）. HF was induced by rapid pa- cing at the RV apex for 4 weeks. A 64-unipolar basket catheter was placed into LV through left internal carotid for globally endocardial mapping of the LV. Ventricular effective refractory period （VERP） was measured by S1S2 program, and VF was induced by continuous S1S1 pacing protocol. Activation recovery intervals （ARIs） for 64 unipolars of the basket cathe- ter were determined at the last pacing cycle length （PCL）. The coefficient of variation among the 64 ARIs was calculated to represent the dispersion of endocardial refractoriness. Globally endocardial conduction duration and distribution of activation propagation were analyzed at the PCL of 300 ms in both control and failing hearts. Results Compared with control, VERP in failing hearts were prolonged obviously （ 180±6.7 ms vs 158±6.9 ms ,P〈0.01 ）. Also, ARIs in HF group were sig- nificantly increased at the PCL of 300, 250, 200 and 150 ms, respectively. Dispersion of refractoriness in HF group was not obviously changed at the PCL of 300 ms and 250 ms. However, compared with control, the dispersion was significantly in- creased at the PCL of 200 and 150 ms. Conduction duration was delayed by 17.9% in HF group （41.2±0.7 ms vs 34.9±1.6 ms,P〈0.01）. VF was earlier to be induced in fail- ing hearts during S1S1 continuous pacing （127± 17 ms vs 103＋8 ms, P〈0.01）. Conclusion This study docu- mented that prolongation of repolarization, decrease of ac- tivation propagation, and rate dependency of repolarization heterogeneity indicate the increased inducibility of VF.