Progression of paroxysmal atrial fibrillation to persistent atrial fibrillation in patients with bradyarrhythmias

Abstract

Introduction: The experimental concept that "atrial fibrillation (AF) begets AF" implies that atrial tachyarrhythmia (AT)/AF burden uniformly increases over time. However, the temporal patterns of paroxysmal AT/AF burden progression, its conversion to persistent AF, and the relationship to underlying disease in humans are unknown. We analyzed the average daily AT/AF burden in patients with concomitant bradycardia and paroxysmal AF to examine these issues.

Methods: Three hundred thirty patients with a history of paroxysmal AF (mean age 70 +/- 10 years; 61% male) were implanted with a pacemaker that automatically recorded the cumulative daily AT/AF burden. Persistent AT/AF was defined as 7 consecutive days with >23 hours of AT on the device data logs. Antiarrhythmic drug therapy was required to be stable for at least 7 months.

Results: Average follow-up was 401 +/- 123 days. Seventy-eight patients (24%) progressed to persistent AT/AF during the follow-up period with a mean interval of 147 +/- 149 days. Mean AT/AF burden increased progressively (slope 14 s/d, P < .001) over 500 days after implant, and median AT/AF burden also increased (P < .01) in this subgroup of patients. This increase was highly correlated with the presence of structural heart disease (P < .001). There was a concomitant decrease in atrial premature beat (APB) frequency. Most patients transitioning to persistent AF were in sinus rhythm with minimal AT/AF burden in the days immediately before persistent AF. Neither mean nor median AT/AF burden increased over time in patients remaining in paroxysmal AF (slope 0 s/d, P = .7) despite a higher APB frequency than in patients with heart disease (P =.003) and a higher likelihood of daily AT/AF events (P < .001).

Conclusions: Temporal patterns of AT/AF burden in patients developing persistent AF show a progressive increase with a sudden transition to persistent AF. This is more consistent with substrate changes, rather than increased density of triggering APBs or paroxysmal AT/AF events. Thus, progression to persistent AF is probably related to an AF substrate, which is undergoing progressive structural remodeling owing to heart disease and other factors and is now suddenly capable of sustaining prolonged or multiple ATs. Therapies directed at the atrial substrate may be needed to prevent persistent AF.