EFFECT OF SUSTAINED LOAD ON DISPERSION OF VENTRICULAR REPOLARIZATION AND CONDUCTION TIME IN THE ISOLATED INTACT RABBIT HEART

Introduction: It is well known that myocardial stretch can elicit vent ricular 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. Methods and Results: To examine th e influence of sustained load on several electrophysiologic parameters , a latex balloon was placed into the left ventricle of ten isolated L angendorff-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 (APD(90)) from 5 to 6 epicardial electrodes located on both ventricles and one right ventricular endocardial contact electrode; dispersion of APD(90) (rang e of MAP durations from all electrodes); effective refractory period ( ERP) and longest activation time (pacing stimulus to MAP upstroke). Af ter baseline recordings, the balloon inside the left ventricle was fil led with a volume of 1.0 mt of fluid by means of a servo-controlled pu mp. The ERP was significantly shortened from 198 +/- 9 msec at baselin e to 183 +/- 8 msec during sustained load (P < 0.03). Similarly, the a verage APD(90) was shortened from 180 +/- 5 msec at baseline to 175 +/ - 6 msec during sustained load (P < 0.006) with steady-state pacing an d from 178 +/- 6 msec to 170 +/- 8 msec during premature extrastimulat ion (P < 0.03). At the same time, dispersion of APD(90) was increased from 27 +/- 5 msec to 38 +/- 6 msec (P < 0.002) during steady-state pa cing and from 28 +/- 4 msec to 38 +/- 6 msec (P = 0.013) during premat ure extrastimulation. The longest activation time among all MAP record ings was increased from 39 +/- 2 msec to 43 +/- 3 msec (P = 0.003) dur ing steady-state pacing and from 56 +/- 6 msec to 69 +/- 6 msec during premature extrastimulation (P < 0.003). Conclusions: Sustained load s hortens the ERP and the mean APD(90), and at the same time increases d ispersion of APD(90) and prolongs activation times, These findings pro vide additional insight into the arrhythmogenic mechanisms of sustaine d mechanical load.