心力衰竭犬心肌动作电位时程及跨室壁复极离散度变化

Action potential duration and transmural dispersion of repolarization changes in heart failure canines

目的研究心力衰竭犬心肌动作电位时程(APD)和跨室壁复极离散度(TDR)的变化,探讨心力衰竭发生恶性室性心律失常的可能机制。方法应用心室快速起搏方法建立心力衰竭犬模型(n=8),制作动脉灌注犬左室楔形心肌组织块模型,同时记录跨室壁心电图及跨膜动作电位,观察心衰犬和正常犬(n=8)心内膜、M层、心外膜的APD和TDR。结果 (1)组织学检查:对照组心肌组织无显著改变,心衰组心肌细胞扭曲、水肿,病理改变明显。(2)心脏超声检查:对照组手术前后各项指标均无显著改变(P>0.05);心衰组术后5周舒张末期室间隔厚度(IVSd)、收缩末期室间隔厚度(IVSs)、舒张末期左室后壁厚度(LVPWd)、左室后壁收缩末期厚度(LVPWs)、左室射血分数(LVEF)均降低,左室舒张末期容积(LVEDV)、左室收缩末期容积(LVESV)均升高,差异有统计学意义(P<0.05),而每搏输出量(SV)无显著改变(P>0.05)。(3)心电生理改变:术后5周对照组心内膜、M层、外膜的APD_(90)(ms)分别为275.1±13.8、307.8±12.3和259.9±9.6;心衰组心内膜、M层、外膜APD_(90)(ms)分别为302.4±11.3、369.1±12.1、287.9±9.3,2组间比较差异有统计学意义(P<0.05)。对照组TDR、Tp-e分别为(47.8±6.8)ms和(46.8±6.0)ms,心衰组分别为(81.3±6.7)ms和(79.9±4.5)ms,2组间比较差异有统计学意义(P<0.05)。结论犬心力衰竭时,心肌各层细胞APD不均一延长,TDR增大,发生恶性室性心律失常的风险增加。

Objective To investigate heart failure myocardial action potential duration （APD） and transmural disper- sion of repolarization （TDR） , and to explore the possible mechanisms of malignant ventricular arrhythmias in heart failure oc- curred. Methods By using ventricular pacing fast method to establish a canine model of heart failure （ n = 8）, making arte- rial perfusion canine left ventricular wedge block model of the cardiac tissue, simultaneous recording of the cross wall electro- cardiogram and trans-membrane action potential, observation of heart failure in dogs and normal dogs （ n = 8 ） the endocar- dial, M layer, epicardial APD and TDR. Results （ 1 ） Histological examination： compared with the myocardial tissue of the control group, no significant changes in myocardial cells of the heart failure group distorted edema, pathological changes. （2） Cardiac ultrasound ： the control group before and after surgery, the indicators had no significant change （ P 〉 0.05 ） ; heart failure group, five weeks after the end-diastolic inter-ventrieular septum thickness （ IVSd ）, end-systolic ventricular septal thickness （IVSs） decreased left ventricular end-diastolic wall thickness （LVPWd） , end-systolic left ventricular posterior wall thickness （LVPWs） , left ventricular ejection fraction （LVEF） and left ventricular end-diastolic volume （LVEDV） , left ven- tricular end-systolic volume （LVESV） were increased, the difference was statistically significant （ P 〈 O. 05 ）, and stroke volume （SV） no significant change （ P 〉0.05）. （3） ECG physiological change： the control group after five weeks endocar- dial, M layer, the outer membrane of APDg0 （ms） were 275.1 ± 13.8,307.8 ± 12.3 and 259.9 ± 9.6 ; heart intima, M la- yer, adventitia APD90 （ms） were 302.4 ± 11.3,369.1 ± 12.1,287.9 ± 9.3, respectively in heart failure group, the diffe- rence in this 2 group was statistically significant （ P 〈 0.05 ）. TDR and Tp-e in control group were （47.8 ± 6.8 ） ms and （ 46.8 ± 6.0 ） ms, respectively, and （ 81.3 ± 6.7 ） ms and （79.9 ± 4.5 ） ms in heart failure group, the difference between this two groups was statistically significance （ P 〈 0.05 ）. Conclusion In canine heart failure mode, myocardial layers cells APD heterogeneity extend, TDR increases, and risk of malignant ventricular arrhythmias was increased.