Stretch Effects on Atrial Conduction: A Potential Contributor to Arrhythmogenesis

Abstract

The role of atrial stretch in the development and maintenance of atrial fibrillation (AF) is well-recognized, nevertheless the mechanisms underlying the phenomenon are not fully understood. Atrial dilatation may contribute to the occurrence of atrial arrhythmias through the modulation of several electrophysiological parameters, promoting focal arrhythmias or maintaining irregular activation through substrate modification. An important factor, leading to the formation of an arrhythmic substrate, has been identified in the stretch-induced modulation of atrial conduction. Experimental and clinical studies evaluating the effect of stretch on conduction are reviewed and the potential contribution of this factor to arrhythmogenesis is discussed. In both animal and human atria, acute stretch has been demonstrated to depress and increase the heterogeneity of conduction velocity, with effects dependent on the underlying atrial architecture. Stretch-induced alterations of conduction properties have been shown to be paralleled by an increased vulnerability of the atria to the occurrence of AF episodes. Slowed propagation may indeed favor the formation of reentries by wavelength shortening, while conduction heterogeneities may contribute to wavefront breakup. Conduction changes observed during acute stretch may even worsen during prolonged stretch conditions, where structural alterations, such as fibrosis and cell hyperthrophy, may lead to an electrical dissociation between muscle bundles and between atrial wall layers. All these findings provide evidence for the crucial role of stretch-induced conduction disturbances in the formation of the complex, multidimensional, arrhythmic substrate leading to the perpetuation of AF.