Characterization of atrial remodeling studied remote from episodes of typical atrial flutter

Abstract

Atrial electrical remodeling has been shown after termination of atrial flutter (AFL); however, whether abnormalities persist beyond an arrhythmic episode is not known. We aimed to characterize the atrial substrate, remote from arrhythmia, in patients with typical AFL. We compared 20 patients, studied remote from episodes of typical AFL and without a history of atrial fibrillation, to 20 reference patients. Multipolar catheters placed at the lateral right atrium (RA), coronary sinus, crista terminalis, and septal RA measured the effective refractory period at 5 sites; conduction characteristics at the crista terminalis; and the conduction time along the lateral RA and coronary sinus. Electroanatomic right atrial maps were created to determine regional differences in voltage and conduction. Patients with AFL demonstrated the following compared to the reference patients: a larger right atrial volume (121 ± 30 vs 83 ± 24 ml, p = 0.005); a prolonged P-wave duration (122 ± 18 vs 102 ± 11 ms, p = 0.007); a longer right atrial activation time (107 ± 23 vs 85 ± 14 ms, p = 0.02); a prolonged conduction time along the lateral RA (67 ± 4 vs 47 ± 3 ms, p <0.001); a slower mean conduction velocity (1.2 ± 0.2 vs 2.1 ± 0.6 mm/ms, p <0.001); a greater proportion of fractionated electrographic findings (16 ± 4% vs 10 ± 6%, p = 0.006); more frequent abnormal electrographic findings at the crista terminalis (4.1 ± 2.6 vs 1.0 ± 1.1, p = 0.001); a prolonged corrected sinus node recovery time (318 ± 71 vs 203 ± 94 ms, p = 0.02); a trend toward greater effective refractory period (232 ± 29 vs 213 ± 12 ms, p = 0.06); and a lower voltage (2.1 ± 0.5 vs 3.0 ± 0.5 mV, p <0.001). In conclusion, studied remote from arrhythmia, patients with AFL demonstrated significant and diffuse atrial abnormalities characterized by structural changes, conduction abnormalities, and sinus node dysfunction. These persisting abnormalities characterize the substrate underlying typical AFL and may account for the subsequent development of atrial fibrillation.