Paroxysmal atrial fibrillation is associated with increased intra-atrial conduction delay

Abstract

Aims: A novel electrophysiological technique, paced electrogram fractionation analysis (PEFA), which measures activation delay of stimulated beats through the myocardium, has shown that long delays in activation are strongly associated with sudden cardiac death due to ventricular fibrillation. The aim of our study was to determine whether there are differences in intra-atrial conduction in patients with and without paroxysmal atrial fibrillation (PAF) using PEFA. Twenty patients (15 women) in the mean age 54.7 +/- 16.6 years, scheduled for transcatheter ablation of their arrhythmias, were divided into two groups: 10 controls without PAF and 10 patients with PAF.

Methods and results: During PEFA, pacing and recording catheters were placed in the coronary sinus (three sites: distal, mid, and proximal) and at four right atrium sites: crista terminalis (one site), RA isthmus (one site), and interatrial septum (two sites). The PEFA protocol involves pacing from one site and recording electrograms from other six sites. A decremental sequence, delivered at one site, had a cycle length of 490 ms (S1S1) with an extrastimulus inserted every third beat whose coupling interval (S1S2) is reduced by 1 ms on each occasion. This process is repeated from each atrial site. The S1S2 at which electrogram duration starts to prolong, and the increase in electrogram duration is determined at all sites. In three patients from the PAF group, atrial fibrillation was induced during PEFA and it was terminated by electrical cardioversion. No other complications were noted. The patients with PAF, compared with the control group, have abrupt increases in the electrogram duration, which occur, at significantly longer S1S2 (P < 0.0001). There were also significantly longer intra-atrial delays in the intrinsic deflection of the electrogram in PAF patient vs. control group (P < 0.0001).

Conclusions: Comparison of PAF and non-AF patient groups showed that intra-atrial conduction delay start in the PAF group earlier (with longer S1S2 intervals) and they are significantly longer in the PAF group. This suggests that atria in patients with PAF are diffusely diseased and that the measured activation delays form one component of an arrhythmogenic substrate.