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

心室性损害时心律失常的倾向被认为是由于心肌牵拉或其他因素引起的心脏电状态改变所致。这一机制尚不清楚，然而，电和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着重要作用。本研究对野百合碱(MCT)诱导的大鼠肺动脉高压模型进行了体内电生理研究，以了解其心脏电特性和心律失常的发生情况。[方法与材料]6周龄雄性SD大鼠给予MCT 0.060 mg/g(MCT)或生理盐水作为对照组(CTR)。注射后4周进行体表心电图和体内EPS检查。戊巴比妥钠(0.033 mg/g)腹腔注射麻醉。记录6导联肢体心电图后，用切割法将8个电极的2Fr导管插入心脏。远端4个电极放置在右室，其余电极放置在右心房进行刺激和记录。常规方法检测窦房结、房室结、房室结的电特性及心律失常情况。[结果]MCT大鼠(n=12)和CTR大鼠(n=25)的数据如下。心电图：SCL162±7ms，157±3ms，PR 45±1ms，46±1ms，QRS 24±1ms，35±0ms(p&lt；0.05)，校正QT 75±6ms，57±1ms(p&lt；0.05)。EPS：SNRT 179±4ms，190±4ms，AVERP 78±2ms，81±2ms，AERP 46±3ms，22±2ms(p&lt；0.05)，文克巴赫型房室传导阻滞率98±2ms，98±1ms，2：1率83±2ms，85±1ms，文克巴赫型VA阻滞率131±2ms，149±5ms，RVERP 63±5ms，42±2ms(p&lt；0.05)。房性心动过速的诱发率分别为0/12和7/25，室性心动过速的诱发率分别为1/12和3/25。

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.