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目的探讨心肌动作电位动态变化在室颤机制中的作用。方法37只健康雄性3月龄大约克猪随机分为两组:22只猪结扎冠状动脉左前降支第一分支制备心肌梗死模型,15只同家系同月龄大约克猪入选对照组。4周后右室程序刺激猪的在体心肌,三层心肌针式复合电极记录刺激过程中陈旧性梗死心脏和正常结构心脏左室前壁心肌跨壁复极离散度(TDR),动作电位时程(APD)与舒张间期(DI)的动态变化等电生理参数。采用方差分析及q检验。结果心肌梗死4周后,陈旧性心梗组存活18只,其中12只诱发室颤,刺激周期为(190±5)ms;对照组全部存活,其中5只诱发室颤,刺激周期为(175±5)ms。两组间的差异有统计学意义[(190±5)ms vs(175±5)ms,P=0.001]。与正常心脏相比,陈旧性心梗组TDR显著增大[(15.66±4.45)ms vs(25.72±6.70)ms,P=0.001]。但是诱发室颤组与未诱发室颤组比较,两组TDR的差异无统计学意义[(20.43±7.01)ms vs(22.32±7.53)ms,P=0.45]。心肌APD恢复斜率最大值以及斜率大于1所占的比例从高到低依次为:陈旧性心梗诱发室颤组[MI+VF(+)组],假手术诱发颤动组[SO+ VF(+)组],假手术未能诱发颤动组[SO+VF(-)组],陈旧性心梗未能诱发颤动组[MI+VF (-)组]。结论APD恢复性质在室颤的维持机制中占有重要地位。APD恢复曲线越陡峭越容易发生室颤。TDR是心脏固有异质性的表现之一,对室颤的发生不具有明确的预测性。
Objective To investigate the role of dynamic changes of myocardial action potential in ventricular fibrillation. Methods Thirty-seven healthy male Yorkshire piglets at 3 months of age were randomly divided into two groups: 22 pigs were ligated with the first branch of the left anterior descending coronary artery to prepare a myocardial infarction model, and 15 of the same family with the same age were selected as the control group. After 4 weeks, right ventricular program stimulated porcine myocardium in the myocardium, and the three-layer cardiac needle-type composite electrode recorded the myocardial infarction heart and the left ventricular anterior wall of the normal structure in the process of stimulating the cardiac transmural repolarization dispersion (TDR) and the action potential (APD) and diastolic interval (DI) dynamic changes and other electrophysiological parameters. Analysis of variance and q test. Results After 4 weeks of myocardial infarction, 18 patients in the old myocardial infarction group survived, of which 12 induced ventricular fibrillation and the stimulation period was (190 ± 5) ms. The control group all survived, 5 of them induced ventricular fibrillation and the stimulation period was (175 ± 5) ms. The difference between the two groups was statistically significant [(190 ± 5) ms vs (175 ± 5) ms, P = 0.001]. Compared with normal heart, TDR in old myocardial infarction group increased significantly ([(15.66 ± 4.45) ms vs (25.72 ± 6.70) ms, P = 0.001]. However, there was no significant difference in TDR between the two groups ([20.43 ± 7.01] vs (22.32 ± 7.53) ms, P = 0.45]. The maximal recovery slope of myocardial APD and the ratio of slope greater than 1 were descending order: MI + VF (+) group in old myocardial infarction, SO + VF (+) group in sham group, Group], sham group [SO + VF (-) group) and sham group [MI + VF (-) group) caused by sham operation. Conclusion The nature of APD recovery plays an important role in the maintenance of ventricular fibrillation. The steeper APD recovery curve is more prone to ventricular fibrillation. TDR is one of the manifestations of inherent cardiac heterogeneity and is not predictive of the occurrence of ventricular fibrillation.