Electrophysiological effect of varied rate and extent of acute in vivo left ventricular load increase

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Abstract
Study objective — The aim was to determine whether the rate, the magnitude, or both, of increased left ventricular wall stress in vivo has consistent and prominent effects on repolarisation, afterdepolarisations, or arrhythmogenicity. Design — Ten anaesthetised dogs underwent transient proximal aortic occlusion. Wall stress was estimated from pressure-volume data obtained by volume catheter, normalised to preocclusion values, and correlated with simultaneously determined changes in monophasic action potential duration (MAPd). Data were obtained during both fast (>50% rise in wall stress within two beats) and slow occlusions, as well as during innervated and denervated conditions. Experimental material — Adult mongrel dogs (20-25 kg) were used. Measurements and main results — Two- to threefold increases in wall stress resulted in less than 5 ms shortening in MAPd and there was little correlation between wall stress and MAPd shortening. The strongest relation between normalised wall stress (EWSnorm) and MAPd was observed under denervated conditions during rapid aortic occlusion (∆MAPd = −2.5×EWSnorm +2.1, r2 = 0.44, pv 56%, p = 0.01), but was unrelated to the level of wall stress increase or the presence of afterdepolarisations. Conclusions — Marked acute increases in left ventricular loading in vivo minimally alter repolarisation, and rarely lead to afterdepolarisations. The speed rather than magnitude of load change appears more important in the development of ventricular ectopy. These findings suggest that load induced ventricular ectopy is due to stretch induced automaticity rather than triggered activity or re-entry.

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