Paroxysmal lone atrial fibrillation is associated with an abnormal atrial substrate

Abstract

<h4>Objectives</h4>The purpose of this study was to determine whether patients with paroxysmal "lone" atrial fibrillation (AF) have an abnormal atrial substrate.<h4>Background</h4>While "AF begets AF," prompt termination to prevent electrical remodeling does not prevent disease progression.<h4>Methods</h4>Twenty-five patients with paroxysmal lone AF, without arrhythmia in the week prior, and 25 reference patients with left-sided accessory pathways were studied. Multipolar catheters placed at the lateral right atrium (RA), crista terminalis, coronary sinus, septal RA, and sequentially within the left atrium (LA) determined the effective refractory period (ERP) at 10 sites, conduction time along linear catheters, and conduction characteristics at the crista terminalis. Bi-atrial electroanatomic maps were created to determine regional differences in conduction velocity and voltage.<h4>Results</h4>Patients with AF demonstrated the following compared with reference patients: larger atrial volumes (RA: 94 +/- 18 ml vs. 69 +/- 9 ml, p = 0.003; LA: 99 +/- 19 ml vs. 77 +/- 17 ml, p = 0.006); longer ERP (at 600 ms: 255 +/- 25 ms vs. 222 +/- 16 ms, p < 0.001; at 450 ms: 234 +/- 20 ms vs. 212 +/- 14 ms, p = 0.004); longer conduction time along linear catheters (57 +/- 18 ms vs. 47 +/- 10 ms, p = 0.01); longer bi-atrial activation time (128 +/- 17 ms vs. 89 +/- 10 ms, p < 0.001); slower conduction velocity (RA: 1.3 +/- 0.3 mm/ms vs. 2.1 +/- 0.5 mm/ms; LA: 1.2 +/- 0.2 mm/ms vs. 2.2 +/- 0.4 mm/ms, p < 0.001); greater proportion of fractionated electrograms (27 +/- 8% vs. 8 +/- 5%, p < 0.001); longer corrected sinus node recovery time (265 +/- 57 ms vs. 185 +/- 60 ms, p = 0.002); and lower voltage (RA: 1.7 +/- 0.4 mV vs. 2.9 +/- 0.4 mV; LA: 1.7 +/- 0.7 mV vs. 3.3 +/- 0.7 mV, p < 0.001).<h4>Conclusions</h4>Patients with paroxysmal lone AF, remote from arrhythmia, demonstrate bi-atrial abnormalities characterized by structural change, conduction abnormalities, and sinus node dysfunction. These factors are likely contributors to the "second factor" that predisposes to the development and progression of AF.