Characterization of paroxysmal atrial fibrillation in atrial septal defects: contribution of a left atrial substrate
N L Ramdat Misier, C Zhang, Y J H Taverne, H N Nguyen, M S Van Schie, L Dai, M H C Linderhof, V Yildirim, W J Van Leeuwen, P C Van De Woestijne, A E Van Den Bosch, N M S De GrootAbstract
Background
Atrial septal defect (ASD) is associated with severe right atrial dilatation, which may contribute to the arrhythmogenic substrate underlying paroxysmal atrial fibrillation (PAF). However, detailed characterization of electrical properties has not been systemically performed in these patients with PAF.
Purpose
to explore differences in the prevalence of potential fractionation and low-voltage areas between ASD patients with PAF and control patients, in order to elucidate predilection sites underlying PAF in ASD patients.
Methods
Epicardial sinus rhythm mapping of the right and left atrium (RA, LA) and Bachmann's bundle (BB) was performed during cardiac surgery. Sixteen adult ASD patients with PAF (ASD-PAF group) were matched with 16 ASD patients without AF (ASD-No-AF group) and 16 patients without CHD but with PAF (control group). Unipolar potentials were classified as single potentials, short double potentials, long double potentials, or fractionated potentials (FPs). Potentials with amplitudes < 1.0 mV were labeled as low voltage areas (LVA).
Results
A total of 48 patients (age: 57±11 years, 64.6% male) were included. FPs were more frequently observed in the ASD-PAF group than in the ASD-No-PAF group or control group, either in the entire atrium (4.6%[3.3-5.1] vs 1.9%[1.4-3.1] and 2.3%[1.1-3.3], P<0.05 for all) or in the LA (4.3%[2.5-10.6] vs 2.0%[1.1-2.6], P=0.017 and 1.7%[0.6-3.6], P=0.066). Furthermore, not at the RA, but only at the LA was the amount of LVA greater in ASD-PAF group (11.2%[8.6-19.4] vs 4.1%[2.6-6.3] and 3.9%[2.0-8.2], P<0.05 for all).
Conclusions
Electrical properties in uncorrected adult ASD patients with PAF are characterized by significantly more FP and LVA compared to control patients with PAF or ASD patients without PAF. Importantly, these differences in conduction abnormalities are restricted to the LA, supporting the role of the LA in the pathophysiology of PAF in right-sided heart CHD.