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目的:探讨急性心肌缺血过程中肥厚左心室跨壁复极离散度变化及与室性心律失常关系。方法:分别记录肥厚及正常对照心室肌标本在模拟缺血过程中、不同刺激周长下内外膜动作电位及跨壁复极离散度变化;对比室性心律失常发生率、分析机制。结果:①和对照组相比,肥厚组在缺血各个时段跨壁复极离散度均显著升高,且随缺血时间、刺激周长的延长逐步递增。②肥厚组在缺血过程中早后除极、延迟后除极发生率显著高于对照组,且多次形成跨壁折返性心律失常。对照组虽有延迟后除极,但未能形成跨壁折返。结论:肥厚心室跨壁复极离散度存在缺血时间、刺激周长的双重依赖;在此基础上早后除极、延迟后除极诱发跨壁折返是缺血肥厚心室心律失常的主要机制之一。
Objective: To investigate the changes of left ventricular transmural repolarization dispersion and its relationship with ventricular arrhythmia in acute myocardial ischemia. Methods: The changes of action potentials and transmural repolarization changes in hypertrophic and normal control ventricular myocytes during simulated ischemia and at different stimulus weeks were compared. The incidence and the mechanism of ventricular arrhythmia were compared. Results: ① Compared with the control group, the transmural repolarization dispersion in hypertrophic group increased significantly at different time points and gradually increased with the prolongation of ischemia and stimulation. ② In the hypertrophic group, the depolarization and anterior depolarization rates were significantly higher than those in the control group during ischemia, and transmural reentry arrhythmia was formed many times. Although the control group after delaying depolarization, but failed to form a transmural reentry. CONCLUSION: There is a dual dependence of ischemic time and perimeter stimulation on transmural repolarization dispersion in hypertrophic ventricular. On the basis of this, depolarization and depolarization-induced transmural reentry are the main mechanisms of ischemic hypertrophy and ventricular arrhythmias one.