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Circulation. 2003;108:1461-1468
Published online before print September 2, 2003, doi: 10.1161/01.CIR.0000090688.49283.67
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(Circulation. 2003;108:1461.)
© 2003 American Heart Association, Inc.


Clinical Investigation and Reports

Electrical Remodeling of the Atria in Congestive Heart Failure

Electrophysiological and Electroanatomic Mapping in Humans

Prashanthan Sanders, MBBS; Joseph B. Morton, MBBS; Neil C. Davidson, MBBS, MD; Steven J. Spence; Jitendra K. Vohra, MD; Paul B. Sparks, MBBS, PhD; Jonathan M. Kalman, MBBS, PhD

From the Department of Cardiology, Royal Melbourne Hospital, and the Department of Medicine, University of Melbourne, Melbourne, Australia.

Correspondence to Professor Jonathan M. Kalman, Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia. E-mail jon.kalman{at}mh.org.au

Received February 24, 2003; revision received July 9, 2003; accepted July 10, 2003.

Background— Atrial fibrillation (AF) frequently complicates congestive heart failure (CHF). However, the electrophysiological substrate for AF in humans with CHF remains unknown. We evaluated the electrophysiological and electroanatomic characteristics of the atria in patients with CHF.

Methods and Results— Twenty-one patients (aged 53.7±13.6 years) with symptomatic CHF (left ventricular ejection fraction 25.5±6.0%) and 21 age-matched controls were studied. The following were evaluated: effective refractory periods (ERPs) from the high and low lateral right atrium (LRA), high septal right atrium, and distal coronary sinus (CS); conduction time along the CS and LRA; corrected sinus node recovery times; P-wave duration; and conduction at the crista terminalis. In a subset, electroanatomic mapping was performed to determine atrial activation, regional conduction velocity, double potentials, fractionated electrograms, regional voltage, and areas of electrical silence. Patients with CHF demonstrated an increase in atrial ERP with no change in the heterogeneity of refractoriness, an increase of atrial conduction time along the LRA and the CS, prolongation of the P-wave duration and corrected sinus node recovery times, and greater number and duration of double potentials along the crista terminalis. Electroanatomic mapping demonstrated regional conduction slowing with a greater number of electrograms with fractionation or double potentials, associated with areas of low voltage and electrical silence (scar). Patients with CHF demonstrated an increased propensity for AF with single extrastimuli, and induced AF was more often sustained.

Conclusions— Atrial remodeling due to CHF is characterized by structural changes, abnormalities of conduction, sinus node dysfunction, and increased refractoriness. These abnormalities may be responsible in part for the increased propensity for AF in CHF.


Key Words: arrhythmia • atrium • electrophysiology • heart failure • remodeling




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