Short-Term Effect of Atrial Fibrillation on Atrial Contractile Function in Humans

Abstract

Background —Conversion of chronic atrial fibrillation (AF) is associated with atrial stunning, but the short-term effect of a brief episode of AF on left atrial appendage (LAA) emptying velocity is unknown. The purpose of this study was to determine whether a short episode of AF affects left atrial function and whether verapamil modifies this effect. Methods and Results —The subjects of this study were 19 patients without structural heart disease undergoing an electrophysiology procedure. In 13 patients, LAA emptying velocity was measured by transesophageal echocardiography in the setting of pharmacological autonomic blockade before, during, and after a short episode of AF. During sinus rhythm, the baseline LAA emptying velocity was measured 5 times and averaged. AF was then induced by rapid right atrial pacing. After either spontaneous or electrical conversion, LAA emptying velocity was measured immediately on resumption of sinus rhythm and every minute thereafter. The mean duration of AF was 15.3±3.8 minutes. The mean baseline emptying velocity was 70±20 cm/s. The first post-AF emptying velocity was 63±20 cm/s ( P =0.02 versus baseline emptying velocity). The post-AF emptying velocity returned to the baseline emptying velocity value after 3.0 minutes. The mean percent reduction in post-AF emptying velocity was 9.7±21% (range, 15% increase to 56% decrease). A second group of 6 patients were pretreated with verapamil (0.1-mg/kg IV bolus followed by an infusion of 0.005 mg · kg −1 · min −1 ). In these patients, the first post-AF emptying velocity, 58±14 cm/s, was not significantly different from the pre-AF emptying velocity, 60±13 cm/s ( P =0.08). Conclusions —In humans, several minutes of AF may be sufficient to induce atrial contractile dysfunction after cardioversion. When atrial contractile dysfunction occurs, there is recovery of AF within several minutes. AF-induced contractile dysfunction is attenuated by verapamil and may be at least partially mediated by cellular calcium overload.