Noncapturing stimuli during the basic drive shorten ventricular refractoriness

Abstract

Studies of ventricular programmed stimulation in animals1 and a recent study in humans1 showed that increasing the stimulation intensity of the basic drive train (S1) shortened the effective refractory period (ERP). This effect was independent of the intensity of the extrastimulus (S2). The mechanism of this shortening of refractoriness by high-current intensity is unknown. The effect disappears when the sites of pacing and extrastimulation are separated by >2 cm,1 suggesting that high-current stimulation shortens refractoriness through changes in the sequence of local activation. Local sympathetic activation may also play a role, because autonomic blockade significantly attenuates the shortening in refractoriness that occurs with an increase in the strength of the current of the basic drive train.2 This study better defines the mechanism by which intense stimulation shortens refractoriness. High-current intensity stimuli were applied during the absolute refractory period of the basic drive train during measurement of ERP. This allowed evaluation of the effect of stimulation intensity on ventricular refractoriness independent of changes in local activation sequence.