GW24-e2265 Bi-atrial repolarisation alternans heterogeneity and paroxysmal atrial fibrillation

Objectives Repolarisation alternans, a beat-to-beat alternationin monophasic action potential (MAP), has been shown to initiatere entry in the ventricle and predicting ventricular arrhythmias. Recently, repolarisation alternans reveals vulnerability to atrial fibrillation. This study aimed to investigate the biatriums repolarisation properties to explore the substrates of the initiation and perpetuation of paroxysmal atrial fibrillation (PAF). Methods Biatrial monophasic action potentials (MAP) were recorded with an Ag-AgCl catheter in 14 anaesthetised dogs. Action potential duration (APD) alternans and paroxysmal atrial fibrillation (PAF) were induced by atrial burst pacing and programmed stimulation. Duration from the onset of upstroke to 90% repolarisation of the APD (APD90) was measured. Results APD90 originated from LA was shorter than those recorded from RA in all dogs (157.4 ± 43.5, 170.9 ± 37.9, P < 0.05). APD alternans was observed in 10 of 14 dogs at mean cycle length (CL) of 158.5 ± 23.2 ms (LA 8/14 vs RA 5/14). Paroxysmal atrial fibrillation (AF) was induced in 11 of 14 dogs at a mean CL of 137.4 ± 21.3 ms (LA 9/14 vs RA 7/14). Of 16 biatrial pacing that developed AF, 10 progressive pacing first caused alternans of APD at mean CL of 162.9 ± 25.4 ms, followed by AF at mean CL of 137.2 ± 21.6 ms. Induction of AF was always preceded by APD alternans (10/16). In 12 biatrial pacing that did not develop AF, APD alternans was less common (3 /12, P < 0.05), and occurred only at faster pacing (CL = 110.4 ± 26.3ms, P < 0.05). In 11 dogs induced AF, the incidence of APD alternans preceding AF was significantly higher in LA than in RA (7/11 vs 3/11, P < 0.05). In addition, CL induced APD alternans was also significantly longer in LAthan in RA (165.1 ± 21.7 vs 143.6 ± 23.8 ms, P < 0.05). Conclusions Rapid atrial pacing induced APD alternans and was associated with initiation of AF. The APD alternans between LA and RA was not uniform, which creates critical gradients or dispersion of repolarisation. These findings suggested that the repolarisation heterogeneity of APD alternans between LA andRA may serve as critical substrate for re-entrant arrhythmias and vulnerability to AF and may be one of the important mechanisms responsible for the initiation of AF.