What does this research mean for the field?

During chronic rapid atrial pacing, the progression of electrical remodeling is spatially inhomogeneous across the atria, leading to temporal increases in refractory period dispersion that correlate with heightened atrial fibrillation inducibility, particularly in the left atrium. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

January 1, 2001Open Access

Inhomogeneity in the Appearance of Electrical Remodeling During Chronic Rapid Atrial Pacing

Structured PICO

Does continuous rapid atrial pacing cause inhomogeneous electrical remodeling across different atrial sites in a canine model?

Population

5 adult beagle dogs weighing 11-14.5 kg

Intervention

Continuous rapid atrial pacing (400 beats/min) delivered at the right atrial appendage for 14 days

Comparator

Baseline (day 0) and recovery phase (7 days post-pacing)

Outcome

Changes in atrial effective refractory period (AERP), AERP dispersion (AERPd), atrial conduction time (CT), and inducibility of atrial fibrillation (AF)surrogate

Chronic rapid atrial pacing induces inhomogeneous electrical remodeling across the atria, with the left atrium showing greater vulnerability to AF induction, highlighting regional differences in arrhythmogenesis.

Abstract

In the present study, the long-term process of progression of electrical remodeling at various atrial sites, which is not well understood, was compared while monitoring continuously the electrophysiologic parameters at multirecording sites in canine atria during continuous atrial burst pacing. A rapid pacing device was implanted in 5 dogs, and continuous atrial burst pacing (400 beats/min) was delivered at the right atrial appendage (RAA). Four pairs of epicardial wire electrodes were sutured on (1) the RAA, (2) Bachmann's bundle (BB), (3) the right atrium close to the inferior vena cava (IVC), and (4) the left atrium (LA). The distal ends of those wires were exteriorized posteriorly and used for pacing and recording. The atrial effective refractory period (AERP), AERP dispersion (AERPd), atrial conduction time (CT) and inducibility of atrial fibrillation (AF) were evaluated during burst pacing for 14 days and during the subsequent 7 days' recovery. The AERP at the LA pacing site was shorter than that at the other sites on day 0. The AERP shortening was greater in the RAA and LA sites than in the BB and IVC sites. The AERPd increased during pacing and reached the maximum level on day 3, and then decreased during the recovery phase. Prolongation of CT tended to be longer between the RAAand IVC sites than that between the other sites. The incidence of AF induction became higher in accordance with the time course of the rapid pacing phase. There was another peak of AF induction on days 7-10. In a canine chronic rapid atrial stimulation model, the progression of electrical remodeling (ie, the shortening of the AERP and the prolongation of the CT) was not homogeneous in both atria, the AERPd showed a temporal increase between days 3 and 7 and matched the increase in AF inducibility at the LA pacing site, the increase in the AERPd was mainly caused by more rapid AERP shortening at the RAA or LA sites, and the LA site always showed a shorter AERP than the other atrial sites in the control state and during the rapid pacing phase, whereas AF inducibility was higher at the LA site than the other sites.

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