Paroxysmal Lone Atrial Fibrillation Is Associated With an Abnormal Atrial Substrate: Characterizing the “Second Factor”
Received 15 August 2008; received in revised form 3 November 2008; accepted 26 November 2008.
Objectives
The purpose of this study was to determine whether patients with paroxysmal “lone” atrial fibrillation (AF) have an abnormal atrial substrate.
Background
While “AF begets AF,” prompt termination to prevent electrical remodeling does not prevent disease progression.
Methods
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.
Results
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).
Conclusions
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.
Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital, and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia
Reprint requests and correspondence: Dr. Prashanthan Sanders, Cardiovascular Research Centre, Department of Cardiology, Level 5 McEwin Building, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia
Dr. Stiles is supported by the National Heart Foundation of New Zealand and the Dawes Scholarship from the Royal Adelaide Hospital. Dr. John is supported by the Biosense-Webster Electrophysiology Scholarship from the University of Adelaide. Mr. Wong is supported by a Student Research Scholarship from the National Heart Foundation of Australia. Dr. Brooks is supported by the Mary Overton Award from the Royal Adelaide Hospital. Dr. Lau is supported by a post-graduate medical scholarship from the National Health and Medical Research Council of Australia, the Earl Bakken Electrophysiology Scholarship from the University of Adelaide, and a Kidney Health Australia Biomedical Research Scholarship. Dr. Dimitri is supported by post-graduate medical scholarships from the Cardiac Society of Australia and New Zealand, and jointly by the National Heart Foundation of Australia and the National Health and Medical Research Council of Australia. Dr. Roberts-Thomson is supported by a post-graduate medical scholarship from the National Health and Medical Research Council of Australia. Dr. Sanders is supported by the National Heart Foundation of Australia; and has served on the advisory board of and received lecture fees and research funding from Bard Electrophysiology, Biosense-Webster, Medtronic, and St. Jude Medical.
ABSTRACT