Mechanism of postsystolic contraction and of multiple myocardial contractions during each single cardiac cycle

Abstract

Postsystolic contraction and other forms of phenomenon of multiple myocardial contractions are characterised by secondary or even tertiary contraction that follow regular one during each single cardiac cycle, triggered by a single sinus node impulse. These additional contractions occur at circumscribed areas of different myocardial regions, in many cardiac patients and healthy subjects. The mechanism of onset and perpetuation of the phenomenon is unknown. Our hypothesis is based on idea of existence of accessory, dead-end, slow-conducting, low-voltage pathways, derived from atrioventricular node or the bundle of His. Secondary contraction could occur in the following way: sinus node impulse divides into two pathways, the main atrioventricular conduction axis that depolarises the entire myocardium and the accessory pathway that depolarises again target region of myocardium where it ends blindly. Slow conduction through such accessory pathway enables a delay of secondary depolarisation needed to overcome the absolute refractory period of the myocardium following the 'regular' contraction. Electrocardiographic signal of a postsystolic potential is not visible at body surface because the pathway is low-voltage. The purpose of multiple myocardial contractions could be, although rarely, completing of current ejection, but more often, in the case of postsystolic contraction it could be a postsystolic tightening of the myocardium which would influence the regular contraction of the next cardiac cycle with the aim to reverse or prevent ventricular remodelling. In those circumstances, regional pathological function of ventricles (deformation of remodelled ventricle during the contraction, maybe during the relaxation as well, and furthermore asynchronous, but otherwise suboptimal contraction as well) would be detected by hypothetical myocardial receptors for strain and stretch, which would activate and sustain the function of accessory dead-end pathways by a neuroendocrine feed-back mechanism. The hypothesis is supported by anatomical findings of dead-end tracts originating from atrioventricular node and disappearing in the muscular part of interventricular septum. Extensive differences in the velocity of impulse propagation, which exist along the conduction system, allow the possibility that the accessory pathways are of slow-conducting properties. Low-amplitude signal of such pathways was confirmed by our intracardiac electrophysiological recording. Feed-back mechanism based on myocardial receptors for strain and stretch is a relevant option, keeping in mind well-known receptor based regulatory mechanisms across the cardiovascular system. The phenomenon is easily detectible, but hard to explain, so even considering herein presented hypothesis implies a need for change of settled perception of myocardial kinetics, and of physiological and pathological function of conducting system.