Effect of Chronic Right Atrial Stretch on Atrial Electrical Remodeling in Patients With an Atrial Septal Defect

Abstract

Background-Adults with an atrial septal defect (ASD) frequently develop late atrial arrhythmias. We sought to characterize the pattern and persistence of atrial electrical remodeling caused by chronic right atrial (RA) stretch in this group. Methods and Results-Thirteen ASD patients without atrial arrhythmia (42Ϯ10 years old; RA volume, 65Ϯ16 mL) and 17 normal control subjects (44Ϯ11 years old; RA volume, 38Ϯ8 mL) had electrophysiological study to measure (1) atrial effective refractory period (AERP) from the low lateral/high lateral/high septal RA and distal coronary sinus (CS), (2) dispersion of AERP, (3) lateral-RA and CS conduction time during constant pacing, (4) conduction delay across the crista terminalis measuring the number of crista catheter bipoles (0 -10) recording discrete double potentials during pacing, (5) corrected sinus node recovery time, and (6) P-wave duration. After ASD closure (8.3Ϯ5.6 months), follow-up echo studies (nϭ12) and electrophysiological study (nϭ4) were performed. The low-lateral AERP, P-wave duration, sinus node recovery time, and extent of conduction delay across the crista terminalis were significantly greater in ASD patients. No differences were found for other measured electrophysiological study parameters. At follow-up, there was incomplete resolution of RA volume (47Ϯ12 mL; PϽ0.01 versus before surgery), a trend toward shortening of the AERP at the lateral RA and an increase at the distal CS and high septal RA, but persisting extensive, widely split crista double potentials. Conclusions-Chronic RA stretch because of ASD causes electrical remodeling with modest increases in RA ERP, conduction delay at the crista terminalis, and sinus node dysfunction. Conduction delay at the crista terminalis persists beyond ASD closure and may contribute to the long-term atrial arrhythmia substrate in this condition. (Circulation.

Analysis of maximum P-wave duration and dispersion after percutaneous closure of atrial septal defects: Comparison of two septal occluders

“…Thus, one can only speculate about the possible mechanisms of new-onset atrial arrhythmias after patent foramen ovale closure, by which a deployed occlude device, potentially causes atrial fibrillation. Conduction delay at the atrial septum may persist beyond secundum ASD closure due to atrial septal stretching and may contribute to the long-term atrial arrhythmia substrate in this condition (18). The effects of acute stretch in studies have shown abnormal conduction slowing in response to atrial premature depolarization (19,20).…”

Sinus Node and Atrial Arrhythmias

“…26 Similarly, even in the absence of atrial arrhythmias, patients with conditions associated with atrial remodeling and atrial stretch (eg, congestive heart failure) exhibit altered SN function. [27][28][29][30][31] In clinical practice, prolongation of SN recovery time has been noted after conversion of atrial arrhythmias to sinus rhythm by electric cardioversion or catheter ablation. 32 Furthermore, patients with prolonged postcardioversion sinus pauses are more likely to experience AF recurrence after catheter ablation.…”

Prediction of early-onset atrial tachyarrhythmia after successful trans-catheter device closure of atrial septal defect

“…Even many years after correction, this may result in conduction disturbances in the atrial myocardium. [22–26] According to Morton et al [27] , chronic right atrial stretch causes electrical remodeling with modest increases in the right atrial effective refractory period, and the right atrial remodeling persists after ASD closure and contributes to long-term atrial arrhythmia. Roberts-Thomson et al [28] also reported that ASDs are associated with chronic left atrial stretch, resulting in remodeling characterized by LA enlargement, loss of myocardium, and electrical scarring, which produce widespread conduction abnormalities, but do not lead to changes or increases in the effective refractory period.…”