Left atrial remodeling in patients with atrial septal defects
Presented in part at the 28th Annual Scientific Sessions of the Heart Rhythm Society, Denver, Colorado, May 2007, and published in abstract form (Heart Rhythm 2007;4:S347).
Received 15 February 2008; accepted 25 March 2009. published online 02 April 2009.
Background
Information regarding left atrial (LA) substrate in conditions predisposing to atrial fibrillation (AF) is limited.
Objective
This study sought to characterize the left atrial remodeling that results from chronic atrial stretch caused by atrial septal defect (ASD).
Methods
Eleven patients with hemodynamically significant ASDs and 12 control subjects were studied. The following were evaluated using multipolar catheters: effective refractory period (ERP) at 7 sites, P-wave duration (PWD), conduction time, and inducibility of AF. LA electroanatomic maps were created to determine atrial activation, and regional conduction and voltage abnormalities.
Results
Patients with ASDs showed significant LA enlargement (P <0.001), unchanged or prolonged atrial ERPs, increase in LA conduction times (P = 0.03), prolonged PWD (P <0.001), regional conduction slowing (P <0.001), greater number of double potentials or fractionated electrograms (P <0.0001), reduced atrial voltage (P <0.001), and more frequent electrical scar (P = 0.005) compared with control subjects. In addition, patients with ASDs showed a greater propensity for sustained AF with single extrastimuli (4 of 11 vs. 0 of 12, P = 0.04).
Conclusion
ASDs are associated with chronic left atrial stretch, which results in remodeling characterized by LA enlargement, loss of myocardium, and electrical scar that results in widespread conduction abnormalities but with no change or an increase in ERP. These abnormalities were associated with a greater propensity for sustained AF.
⁎Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital, and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia
†Department of Cardiology, Royal Melbourne Hospital, and the Department of Medicine, University of Melbourne, Melbourne, Australia
Address reprint requests and correspondence: Dr. Prashanthan Sanders, Cardiovascular Research Centre, Department of Cardiology, Level 5, McEwin Building, Royal Adelaide Hospital, Adelaide, SA 5000, Australia
This study was supported in part by a Grant-in-Aid (G 08A 3646) from the National Heart Foundation of Australia and New Zealand. Dr. Roberts-Thomson is the recipient of a Postgraduate Research Scholarship from the National Health and Medical Research Council of Australia. Dr. John is supported by the Biosense-Webster Electrophysiology Scholarship, University of Adelaide. Dr. Brooks is supported by a Postdoctoral Fellowship from the National Heart Foundation of Australia. Dr. Stiles is supported by the National Heart Foundation of New Zealand and the Dawes Scholarship, Royal Adelaide Hospital. Dr. Lau is supported by the Earl Bakken Electrophysiology Scholarship, University of Adelaide, a Kidney Health Australia Biomedical Research Scholarship, and a Postgraduate Research Scholarship from the National Health and Medical Research Council of Australia. Dr. Sanders is supported by the National Heart Foundation of Australia.
Dr. Sanders has served on the advisory board of and has received lecture fees and research funding from St Jude Medical, Medtronic, Bard Electrophysiology, and Biosense-Webster.
ABSTRACT