Zabel M, Portnoy S, Franz M R
Division of Clinical Pharmacology, Georgetown University Medical Center, Washington, DC, USA.
J Cardiovasc Electrophysiol. 1996 Jan;7(1):9-16. doi: 10.1111/j.1540-8167.1996.tb00455.x.
It is well known that myocardial stretch can elicit ventricular arrhythmias in experimental models. However, previous reports have predominantly documented stretch-induced arrhythmias during short, pulsatile stretch. The arrhythmogenic mechanism of sustained static stretch is incompletely understood.
To examine the influence of sustained load on several electrophysiologic parameters, a latex balloon was placed into the left ventricle of ten isolated Langendorff-perfused rabbit hearts and filled with a neutral volume of fluid. The heart was paced from a catheter inside the right ventricle (apicoseptal endocardial position), and the following parameters were studied during steady-state pacing with a cycle length of 500 msec (S1) and during extrastimulation (S2, base drive of 8 beats): monophasic action potential (MAP) durations at 90% repolarization (APD90) from 5 to 6 epicardial electrodes located on both ventricles and one right ventricular endocardial contact electrode; dispersion of APD90 (range of MAP durations from all electrodes); effective refractory period (ERP) and longest activation time (pacing stimulus to MAP upstroke). After baseline recordings, the balloon inside the left ventricle was filled with a volume of 1.0 mL of fluid by means of a servo-controlled pump. The ERP was significantly shortened from 198 +/- 9 msec at baseline to 183 +/- 8 msec during sustained load (P < 0.03). Similarly, the average APD90 was shortened from 180 +/- 5 msec at baseline to 175 +/- 6 msec during sustained load (P < 0.006) with steady-state pacing and from 178 +/- 6 msec to 170 +/- 8 msec during premature extrastimulation (P < 0.03). At the same time, dispersion of APD90 was increased from 27 +/- 5 msec to 38 +/- 6 msec (P < 0.002) during steady-state pacing and from 28 +/- 4 msec to 38 +/- 6 msec (P = 0.013) during premature extrastimulation. The longest activation time among all MAP recordings was increased from 39 +/- 2 msec to 43 +/- 3 msec (P = 0.003) during steady-state pacing and from 56 +/- 6 msec to 69 +/- 6 msec during premature extrastimulation (P < 0.003).
Sustained load shortens the ERP and the mean APD90, and at the same time increases dispersion of APD90 and prolongs activation times. These findings provide additional insight into the arrhythmogenic mechanisms of sustained mechanical load.
众所周知，在实验模型中，心肌拉伸可引发室性心律失常。然而，先前的报告主要记录了短时间搏动性拉伸期间的拉伸诱导性心律失常。持续静态拉伸的致心律失常机制尚未完全了解。
为了研究持续负荷对多个电生理参数的影响，将一个乳胶气球置于十颗离体Langendorff灌注兔心脏的左心室内，并注入适量的中性液体。通过右心室内的导管（心尖间隔内膜位置）对心脏进行起搏，在周期长度为500毫秒的稳态起搏期间（S1）以及额外刺激期间（S2，基础驱动为8次搏动），研究以下参数：来自位于两个心室的5至6个心外膜电极以及一个右心室内膜接触电极的90%复极化时的单相动作电位（MAP）持续时间（APD90）；APD90的离散度（所有电极的MAP持续时间范围）；有效不应期（ERP）和最长激活时间（起搏刺激至MAP上升支）。在基线记录后，通过伺服控制泵向左心室内的气球注入1.0毫升液体。持续负荷期间，ERP从基线时的198±9毫秒显著缩短至183±8毫秒（P<0.03）。同样，在稳态起搏期间，平均APD90从基线时的180±5毫秒缩短至175±6毫秒（P<0.006），在早搏额外刺激期间从178±6毫秒缩短至170±8毫秒（P<0.03）。同时，在稳态起搏期间，APD90的离散度从27±5毫秒增加至38±6毫秒（P<0.002），在早搏额外刺激期间从28±4毫秒增加至38±6毫秒（P = 0.013）。在所有MAP记录中，最长激活时间在稳态起搏期间从39±2毫秒增加至43±3毫秒（P = 0.003），在早搏额外刺激期间从56±6毫秒增加至69±6毫秒（P<0.003）。
持续负荷缩短ERP和平均APD90，同时增加APD 的离散度并延长激活时间。这些发现为持续机械负荷的致心律失常机制提供了更多见解。
