心力衰竭犬跨室壁心肌复极时间和不应期离散度的致心律失常机制研究

Role of transmural dispersion of myocardial repolarization time and effective refractory period in development of arrhythmias in heart failure canine

目的:从复极和不应期两个角度,观察不同部位起搏对心力衰竭犬三层心肌跨室壁复极和不应期离散度的影响及其可能的致心律失常机制。方法:正常犬8只和心力衰竭模型犬5只,模拟临床上充血性心力衰竭患者接受心脏再同步治疗的情况,分别从右心室心内膜、左心室心外膜和双心室发放刺激,在体记录和比较犬三层心肌的单相动作电位时程、不应期及其跨室壁离散度。在心力衰竭犬组,给予维拉帕米进行干预并重复上述实验。结果:心力衰竭犬三层心肌的动作电位时程与不应期均有延长,中层心肌动作电位时程延长最明显[(279.30±54.81)ms vs(270.03±57.58)ms,P<0.01],跨室壁复极离散显著增大[(29.80±25.67)ms vs(20.60±12.65)ms,P<0.01],不应期离散有所减小[(29.21±15.83)ms vs(31.25±20.83)ms,P>0.05];左心室心外膜和双心室刺激增加跨室壁复极离散度,但对跨室壁不应期离散度无明显影响;维拉帕米能在一定程度上延长中层和心外膜下心肌的动作电位时程与不应期,减小跨室壁复极和不应期离散[心力衰竭犬给予维拉帕米后(24.50±15.18)msvs正常犬(31.25±20.83)ms,P<0.05]。结论:心力衰竭犬跨室壁复极离散增大、不应期离散减小;维拉帕米减小心力衰竭犬跨室壁复极与不应期离散;左心室心外膜参与的起搏方式对心肌不应期无明显影响,但增大跨室壁复极离散,且这一效应不能被维拉帕米矫正。

AIM： To investigate the effects of different pacing sites on the transmural dispersion of myocardial repolarization time and refractory period,and its role in the development of arrhythmias in heart failure canine.METHODS： Eight normal and five heart failure canines were studied.To imitate cardiac resynchronization therapy which is used in heart failure patients,stimulation was delivered to the canines＇ heart from right ventricular endocardium,left ventricular epicardium and both of them.Monophasic action potential duration（MAPD）,effective refractory period（ERP） across the 3 layers of myocardium and their transmural dispersion were recorded in vivo and compared.Verapamil was applied with the heart failure canines and the above-mentioned tests were repeated.RESULTS： Compared with the normal animals,longer MAPD and ERP were detected in heart failure canines,and the more significant difference of mid-layer myocardium [（279.30±54.81）ms vs（270.03±57.58）ms,P〈0.01] was also observed.An increase in transmural dispersion of repolarization（TDR） was noticed [（29.80±25.67）ms vs（20.60±12.65）ms,P〈0.01],while the ERP slightly decreased [（29.21±15.83） ms vs（31.25±20.83）ms,P〉0.05] in heart failure canines.Left ventricular epicardial or biventricular pacing enlarged TDR but had no impact on the transmural dispersion of ERP.Verapamil prolonged MPAD and ERP of mid-layer myocardium and sub-epicardium,and also decreased the TDR and the transmural dispersion of ERP [（24.50±15.18）ms in heart failure canines with verapamil vs（31.25±20.83）ms in normal canines,P〈0.05].CONCLUSION： Heart failure canines have larger TDR but smaller transmural dispersion of ERP,which can be further decreased by verapamil.Biventricular or left ventricular epicardial pacing produces no effect on ERP but enlarges TDR,which can not be corrected by verapamil.