Characterization of Paroxysmal Atrial Fibrillation in Atrial Septal Defects

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. OBJECTIVES: The purpose of this study was to explore differences in the prevalence of potential fractionation and low-voltage areas between uncorrected adult ASD patients with PAF and control patients, to elucidate predilection sites underlying PAF in ASD patients. METHODS: Epicardial sinus rhythm mapping of the right atrium and left atrium (LA) and Bachmann's bundle 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 congenital heart disease 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 (LVAs). RESULTS: A total of 48 patients (age: 57 ± 11 years, 64.6% men) were included. FPs were more frequently observed in the ASD-PAF group than in the ASD-No-AF group or control group, either in the entire atrium (4.6% [Q1-Q3: 3.3%-5.1%] vs 1.9% [Q1-Q3: 1.4%-3.1%] and 2.3% [Q1-Q3: 1.1%-3.3%]; P < 0.05 for all) or in the LA (4.3% [Q1-Q3: 2.5%-10.6%] vs 2.0% [Q1-Q3: 1.1%-2.6%]; P = 0.017 and 1.7% [Q1-Q3: 0.6%-3.6%]; P = 0.066). Furthermore, not at the right atrium, but only at the LA was the amount of LVA greater in ASD-PAF group (11.2% [Q1-Q3: 8.6%-19.4%] vs 4.1% [Q1-Q3: 2.6%-6.3%] and 3.9% [Q1-Q3: 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 with 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 congenital heart disease.