Mechanism of propensity to atrial fibrillation in patients undergoing isthmus ablation for typical atrial flutter.

Mechanism of propensity to atrial fibrillation. Patients undergoing isthmus ablation for atrial flutter (AFL) may reveal postablation atrial fibrillation (AF). The electrophysiological mechanism is unclear. In patients with idiopathic AF, enhanced spatial dispersion of right atrial refractoriness was the substrate for the initiation of AF. We hypothesize that dispersion of right atrial refractoriness in patients undergoing AFL ablation is the major cause of postablation AF. Consecutive patients (n=42) undergoing isthmus ablation for typical AFL were included. Twelve right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol, starting with one extrastimulus, followed by more aggressive pacing until AF was induced. Mean fibrillatory intervals were used to assess local refractoriness of each recording site. Spatial dispersion of right atrial refractoriness was calculated as the coefficient of dispersion (CD-value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). A CD-value of 3.0 or less was defined as normal, whereas CD-value greater than 3.0 was considered enhanced dispersion. PES and refractoriness analysis were followed by isthmus ablation. Of the 42 patients, 29 had CD-value of 3.0 or less. In these 29 patients, AF was induced with 1 extrastimulus in only 1 patient, with 2 extrastimuli in 4 patients and burst pacing was required to induce AF in 24 of these 29 patients. Prior to the procedure, 5 of 29 patients had AF episodes, after ablation 6 of 29 patients. Of the 42 patients, 13 had CD-value greater than 3.0, AF was induced with a single extrastimulus in 11 patients, with 2 extrastimuli in the remaining 2 patients. Of the 13 patients, 11 had AF episodes both before and after ablation (P<0.001). Enhanced spatial dispersion of right atrial refractoriness may be the substrate for propensity to AF in patients with AFL. The substrate was associated with enhanced inducibility of atrial fibrillation.