Atrial Electrophysiologic Remodeling in Canine Heart Failure: Modulation by Atrial Fibrillation

Abstract

Background Heart failure (HF) is a common antecedent to atrial fibrillation (AF). Concomitant HF and AF increases morbidity and mortality over that of either disease alone. AF- and HF-induced atrial electrophysiologic remodeling is known to favor the progression of AF. AF results in accelerated repolarization and reductions in multiple ion currents, including transient outward K + current (I to ), changes associated with AF maintenance. Methods Dogs had tachypacing-induced HF for 10 weeks and then were assigned to 6 weeks of atrial tachypacing (60 seconds of pacing at 10 Hz, repeated every 70 seconds) until sustained AF/atrial flutter was induced (HF+AF, n=3), or continued right ventricular tachypacing (n = 6). Baseline LVFS was reduced ( P to were made at 35° ± 0.5°C. Results HF significantly increased I to vs control, whereas HF+AF significantly reduced I to vs control and HF (Figure A). At 2 Hz, HF shortened action potential durations at 50% repolarization (APD 50 ); HF+AF lengthened APD 50 vs HF alone, and did not differ from control (Figure B). HF shortened APD at 90% repolarization (APD 90 ) vs controls, whereas HF+AF had similar shortening of APD 90 . Conclusions Chronic HF results in increased I to and faster repolarization of left atrial appendage myocytes. The addition of AF to chronic HF reduced I to and lengthened APD 50 without changing APD 90 . The effects of chronic HF and chronic HF+AF on I to and APD morphology are variable, suggesting complex disease-induced effects on the substrate for AF.