心肌缺血时复极和传导交替是T波电交替的电生理机制

Repolarization and Conduction Alternans are the Mechanisms of T-Wave Alternans in Myocardial Ischemia

目的:探讨缺血性T波电交替(TWA)的电生理学机制。方法:在体实验组家兔10只,开胸后结扎左冠状动脉前降支(LAD),造成心肌缺血模型,在结扎LAD前、结扎后60min重复观测缺血区域心室壁内膜下层、中层和外膜下层的单相动作电位时程(MAPD)、有效不应期(ERP),快速心室刺激诱发TWA。离体实验组家兔10只,快速开胸取出心脏后作Langendorff灌流,先用正常Tyrode’s液灌流30 min再用模拟缺血液灌流。在Tyrode’s液灌流20min后、模拟缺血液灌流60min后重复观测模拟肢体导联心电图,以及左心室前壁、侧壁、右心室和心尖部心外膜的MAPD、ERP,快速心室刺激诱发TWA。结果:缺血后各位点MAPD的频率适应性降低,MAPD90和ERP缩短。与生理状态相比,心肌细胞复极梯度发生了明显重排。20个在体和离体心脏在缺血后全部可用快速心室刺激诱发TWA,诱发TWA的心动周期(CL)窗口在130-170ms之间,CL=140,150ms时可稳定地诱发TWA。TWA时伴有单相动作电位复极和传导的交替。离体心外膜增频刺激时,CL=170 ms开始出现TWA,随后的减频刺激至CL=200ms时TWA消失,即TWA的滞后现象。结论:心肌细胞复极不均一可能是引起心电图T波的原因之一。心肌缺血使心脏正常的复极梯度发生改变,在快速心室刺激时易于发生动作电位复极和传导的交替,在体表心电图上表现为TWA。

Objective： To investigate the electrophysiological basis of T-wave alternans（TWA） under myocardial ischemia conditions.Methods： Ten rabbits underwent thoracotomy and ligation of left anterior descending（LAD） coronary in vivo.Before and 30 minutes after the LAD ligation,monophasic action potential duration（MAPD） and effective refractory period（ERP） were determined in the endocardium,midmyocardium,and epicardium of the ischemia area,and rapid ventricular stimulation was conducted to induce the TWA.Another ten rabbits also underwent thoracotomy incisions and their hearts were excised rapidly for converse Langendorff-perfusion through aorta.Their hearts were reperfused with normal Tyrode＇s solution for 30 minutes and then with simulant ischemia solution.After 20 minutes of reperfusion with normal Tyrode＇s solution and 60 minutes of reperfusion with simulant ischemia solution,MAPD and ERP of four epicardium sites（frontal wall and lateral wall of left ventricle,right ventricle,and cardiac apex） were determined,and rapid ventricular stimulation was conducted at cardiac apex to induce the TWA.Results： After an hour of ischemia,the rate adaptation trait of MAPD was damaged,while MAPD90 and ERP were shortened.Comparing with those under normal conditions,the gradients of repolarization reset thoroughly.During ischemia,TWA could be induced using rapid ventricular stimulation in all 20 hearts,the CL window for TWA induction was located between 130 to 170 ms,and TWA could be induced steadily at the CL of 140 to 150 ms.TWA was accompanied with the alternans in MAP repolarization and conduction.In isolated rabbit＇s heart,as CL shortened,TWA developed firstly at the CL of 170 ms and the alternans augmented with the rate.When CL subsequently prolonged,TWA persisted and disappeared at the CL of 200 ms.Conclusion： The repolarization heterogeneity of cardiac myocyte may underlie the formation of T wave.Myocardial ischemia alters the normal gradients of repolarization,and the TWA in surface ECG induced by rapid ventricular stimulation is the manifestation of myocardial repolarization and conduction alternans.