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目的以正常犬左心室楔形心肌块为模型,观察不同部位起搏对3层心肌跨室壁复极离散的影响并探讨其可能的机制。方法按文献方法制备带冠状动脉分支的犬左心室楔形心肌块模型,将3根玻璃微电极插入心肌块的不同位置记录心内膜下心肌、中层心肌和心外膜下心肌的跨膜动作电位;同时记录心肌块的整体电活动(容积心电图)。从心肌块的心外膜面、心内膜面分别、同时或多部位发放刺激,记录并分析不同部位起搏时的QRS时限、QT间期、Tp-Te间期及心律失常的诱发率。结果反映心肌跨室壁复极离散的心电图指标如Tp-Te间期在心外膜刺激(Epi)时最大:(83.63±19.30)ms,其次为内外膜同时刺激(Bi):(75.63±16.47)ms,最小为心内膜刺激(Endo):(54.75±13.18)ms(两两比较,均P<0.01);Tp-Te指数(Tp-Te/QT)也有相似变化,上述部位刺激时分别为(0.28±0.05),(0.27±0.04)和(0.20±0.04)(两两比较,均P<0.01)。但是当从心内膜面或者心外膜面双部位发放刺激时,Tp-Te间期或Tp-Te/QT较单部位刺激时均明显缩短或减小(P<0.01)。此外,心外膜刺激、内外膜同时刺激及心内膜刺激时分别有6例(75%)、5例(60%)和1例(13%)诱发了室性心律失常(χ2=7.0,P=0.03)。结论心内、外膜面同时刺激使心室肌跨室壁复极离散度增大,发生恶性心律失常的危险性增加;而从心内膜面或者外膜面同一面双部位发放刺激并不延长心肌复极时间,与单部位刺激相比跨室壁复极离散度反而减小。这一发现或许能为改进心力衰竭时心脏再同步治疗的起搏方式提供借鉴。
Objective To investigate the effects of pacing in different parts on the transmural dispersion of 3-layer myocardium in normal dogs and to explore its possible mechanism. Methods The left ventricular wedge-shaped myocardial block model with coronary artery branches was prepared according to the literature method. Three glass microelectrodes were inserted into the myocardial block at different positions to record the transmembrane action potentials of the subendocardial, midmyocardial and epicardial myocardium ; While recording the overall electrical activity of myocardial block (volume electrocardiogram). From the epicardial surface and the endocardial surface of cardiac muscle block, stimuli were given at the same time or at multiple sites. The QRS duration, QT interval, Tp-Te interval and arrhythmia induction rate were recorded and analyzed. The results showed that the electrocardiogram indexes such as Tp-Te interval in epicardial stimulation (Epi) were the largest (83.63 ± 19.30) ms, followed by the biocompatibility (Bi) of 75.63 ± 16.47 ms, the minimum was Endo: (54.75 ± 13.18) ms (every two comparisons, both P <0.01); Tp-Te / QT also had similar changes. (0.28 ± 0.05), (0.27 ± 0.04) and (0.20 ± 0.04) respectively (all P <0.01). However, Tp-Te interval or Tp-Te / QT significantly shortened or decreased (P <0.01) compared with single-site stimulation when stimulation was given from the endocardial or epicardial planes. In addition, ventricular arrhythmia was induced in 6 (75%), 5 (60%) and 1 (13%) cases of epicardial and endo- and endocardial stimulation, respectively P = 0.03). Conclusions Simultaneous stimulation of cardiac and adventitial surfaces increases the transmural dispersion of ventricular muscle and increases the risk of malignant arrhythmia. However, stimulation from the same side of the endocardium or the adventitial surface does not extend Myocardial repolarization time, compared with single-site stimulation of transmural repolarization dispersion instead decreased. This finding may provide a reference for improving the pacing mode of cardiac resynchronization therapy in heart failure.