Abstract
Atrial fibrillation (AF) is frequently observed under conditions that are associated with atrial dilatation. The aim of this study was to investigate the effects of atrial dilatation on the substrate of AF. In 15 Langendorff-perfused rabbit hearts, the interatrial septum was perforated, and after occlusion of the caval and pulmonary veins, biatrial pressure was increased by raising the level of an outflow cannula in the pulmonary artery. Right and left atrial effective refractory periods (AERPs), monophasic action potentials (MAPs), and inducibility of AF by single premature stimuli were measured as a function of atrial pressure. Increasing the atrial pressure from 0.5+/-0.7 to 16.2+/-2.2 cm H2O resulted in a progressive shortening of the right AERP from 82.2+/-9.8 to 48.0+/-5.1 ms. In the left atrium, an increase in pressure up to 7.4+/-0.3 cm H2O had no effect on the AERP. At higher pressures, however, the left AERP also shortened, from 67.5+/-7.5 to 49.3+/-2.0 ms. The duration of MAPs also decreased by an increase in atrial pressure, showing a high correlation with the shortening in AERP (r=.94, P<.01). All these changes were completely reversible within 3 minutes after release of the atrial stretch. Dilatation of the atria was a major determinant for the vulnerability to AF. The inducibility of AF increased from 0% at low pressures to 100% when the atrial pressure was >10 cm H2O. Release of the atrial wall stress resulted in prompt cardioversion of AF. The increased vulnerability for AF was highly correlated with the shortening in AERP (logistic regression r=.97). No correlation was found with the spatial dispersion between right and left AERPs. Increased atrial pressure in the isolated rabbit heart resulted in a significant increase in vulnerability to AF that was closely correlated to shortening of the AERP. These changes were completely reversible within 3 minutes after release of the atrial stretch, resulting in prompt termination of AF.
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