Interaction Between Electrical and Pathological Myocardial Remodeling Induced by Right and Left Ventricular Pressure Overload

心室损伤下的心律失常倾向被认为是由心室心肌拉伸或其他因素引起的心脏电状态的改变引起的。其机制尚不清楚，但电性心肌重构与病理性心肌重构之间的相互作用可能在这种心律失常中起重要作用。本研究通过对MCT诱导的肺动脉高压模型大鼠进行体内电生理研究，探讨MCT诱导的肺动脉高压模型大鼠的心电特性及其对心律失常的影响。【方法与材料】6周龄雄性SD大鼠给予0.06Omg/g MCT （MCT）或生理盐水作为对照组（CTR）。注射后4周，观察体表心电图和体内EPS。腹腔注射戊巴比妥（0.033mg/g）麻醉。记录6导联肢体心电图后，采用切切法将2导联8极电极导管插入心脏。远端4个电极置于右心室，其余电极置于右心房进行刺激和记录。采用常规方法评价窦房结、心房、房室结和心室的电特性和心律失常的前兆。【结果】MCT大鼠（n=12）和CTR大鼠（n=25）的数据如下：sECG: SCL 162±7ms、157±3ms, PR 45±1ms、46±1ms, QRS 24±1ms、35±0ms (p<0.05)，校正QT 75±6ms、57±1ms （p<0.05）。EPS: SNRT 179±4ms、190±4ms, AVERP 78±2ms、81±2ms, AERP 46±3ms、22±2ms (p<0.05)， Wenckebach型房颤阻断率快速心房起搏98±2ms、98±1ms， 2:1率83±2ms、85±1ms， Wenckebach型房颤阻断率快速心室起搏131±2ms、149±5ms， RVERP 63±5ms、42±2ms （p<0.05）。在0/12和7/25动物中诱发心房心动过速，而在1/12和3/25动物中诱发室性心动过速。

Propensity for proarrhythmia under the cardiac ventricular damages are considered to result from the changes of the electrical status in the heart by ventricular myocardial stretch or by other factors. This mechanism is still unknown, however, the interaction between the electrical and the pathological myocardial remodeling may play an important role in this proarrhythmia. In this study, in vivo electrophysiological studies (EPS) were performed to the monocrotaline (MCT) induced pulmonary artery hypertension model rats in order to elucidate their cardiac electrical properties and proarrhythmia. [Methods and Materials] 6weeks old male SD rats were administered MCT 0.06Omg/g (MCT) or normal saline as a control group (CTR). 4 weeks after the injection, surface ECG recordings and in vivo EPS were performed. Pentobarbital (0.033mg/g) were given into peritoneal space for the anesthesia. After 6leads-limb-ECG was recorded, 2Fr catheter with 8 polar electrodes was inserted into the heart by cut down method. The distal 4 electrodes were placed in the right ventricle while the others in the right atrium for stimulation and recording. The conventional method were used for the evaluation of electrical properties and proarrhythmia in sinus node, atrium, atrioventricular (AV) node and ventricle. [Results] The data in MCT rats (n=12) and CTR rats (n=25) were described below. sECG : SCL 162±7ms, 157±3ms, PR 45±1ms, 46±1ms, QRS 24±1ms, 35±0ms (p<0.05), corrected QT 75±6ms, 57±1ms (p<0.05). EPS : SNRT 179±4ms, 190±4ms, AVERP 78±2ms, 81±2ms, AERP 46±3ms, 22±2ms (p<0.05), Wenckebach type AV block rate by rapid atrial pacing 98±2ms, 98±1ms, 2 : 1 rate 83±2ms, 85±1ms, Wenckebach type VA block rate by rapid ventricular pacing 131±2ms, 149±5ms, RVERP 63±5ms, 42±2ms (p<0.05). Atrial tachycardia were induced in 0/12 versus 7/25 animals, whereas ventricular tachycardia in 1/12 versus 3/25.