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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。
OBJECTIVE: To observe the effect of pacing in different parts on the transmural repolarization and refractory period dispersion of three-layer myocardium in dogs with heart failure and its possible mechanism of arrhythmia from repolarization and refractory periods. Methods: Eight normal dogs and five dogs with heart failure model were used to simulate the cardiac resynchronization therapy in patients with congestive heart failure. They were stimulated by right ventricular endocardium, left ventricular epicardium and biventricular respectively. Body recording and comparison of single-phase action potential duration, refractory period and cross-wall dispersion in three-layer canine myocardium. In heart failure dogs, verapamil was given interventions and the above experiment was repeated. Results: The duration of action potential and refractory period were prolonged in the three layers of heart of dogs with heart failure, and the prolongation of the action potential of middle myocardium was the most obvious (279.30 ± 54.81 ms vs 270.03 ± 57.58 ms, P <0.01) (29.80 ± 25.67) ms vs (20.60 ± 12.65) ms, P <0.01], and the discrepancy of refractory period was reduced [(29.21 ± 15.83) ms vs (31.25 ± 20.83) ms, P> 0.05]. Left ventricular epicardium and biventricular stimulation increased the transmural repolarization dispersion, but had no significant effect on the non-ventricular septal dispersion. Verapamil could extend the middle layer to a certain extent And epicardial myocardial action potential duration and refractory period, reducing cross-wall repolarization and refractory period dispersion [Heart failure dogs given verapamil (24.50 ± 15.18 msvs normal dogs (31.25 ± 20.83 ) ms, P <0.05]. CONCLUSIONS: In dogs with heart failure, the transmural repolarization dispersion increases and the refractory period decreases discretely. Verapamil decreases the transmural repolarization and refractory period dispersion in dogs with heart failure. The left ventricular epicardium participates in pacing Mode of myocardial refractory period had no significant effect, but increased transmural repolarization dispersion, and this effect can not be corrected verapamil.