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|Title:||Effect of chronic right atrial stretch on atrial electrical remodeling in patients with an atrial septal defect|
|Citation:||Circulation, 2003; 107(13):1775-1782|
|Publisher:||Lippincott Williams & Wilkins|
|Joseph B. Morton, Prashanthan Sanders, Jitendra K. Vohra, Paul B. Sparks, John G. Morgan, Steven J. Spence, Leeanne E. Grigg, and Jonathan M. Kalman|
|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 (42+/-10 years old; RA volume, 65+/-16 mL) and 17 normal control subjects (44+/-11 years old; RA volume, 38+/-8 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 (8.3+/-5.6 months), follow-up echo studies (n=12) and electrophysiological study (n=4) 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 (47+/-12 mL; P<0.01 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.|
|Keywords:||remodeling; fibrillation; defects|
|Description:||© 2003 American Heart Association, Inc.|
|Appears in Collections:||Medicine publications|
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