Effect of slow pathway ablation on ventricular rate during atrial fibrillation. Dependence on electrophysiological properties of the fast pathway.

Abstract

Catheter ablation of the posteroseptal right atrium has been proposed for control of ventricular rate in patients with tachycardic atrial fibrillation (AF). However, the exact mechanism of rate control is unclear. Because the ablation site corresponds to the location of the slow pathway in patients with AV nodal reentry tachycardia (AVNRT), we investigated whether selective ablation of this posterior AV nodal input can provide a sufficient reduction in heart rate during AF. In 30 patients with AVNRT, conduction properties of the AV nodal pathways were determined before and after slow pathway ablation. AF was induced by burst pacing at baseline and after ablation, and the mean ventricular cycle length was determined. After slow pathway ablation, the mean ventricular cycle length during AF increased (449 +/- 98 versus 515 +/- 129 milliseconds, P < .01). At baseline, the mean ventricular cycle length correlated with the Wenckebach cycle length of both the slow (r = .90) and fast (r = .86) pathways. After ablation, the mean ventricular cycle length was extremely well determined by the Wenckebach cycle length of the fast pathway (r = .94). However, the slope of the regression line was significantly steeper compared with baseline (1.50 versus 0.77, P < .0001), illustrating that the reduction in ventricular rate was not as evident if the fast pathway had a short Wenckebach cycle length. Selective elimination of the slow pathway reduces ventricular rate during AF. However, in patients with a short Wenckebach cycle length of the anterior AV nodal input that causes tachycardic AF, this effect may be insufficient to provide adequate control of ventricular rate.