Dissociation Between Ionic Remodeling and Ability to Sustain Atrial Fibrillation During Recovery From Experimental Congestive Heart Failure

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Abstract
Background— Congestive heart failure (CHF) downregulates atrial transient outward ( I to ), slow delayed rectifier ( I Ks ), and L-type Ca 2+ ( I Ca,L ) currents and upregulates Na + -Ca 2+ exchange current ( I NCX ) (ionic remodeling) and causes atrial fibrosis (structural remodeling). The relative importance of ionic versus structural remodeling in CHF-related atrial fibrillation (AF) is controversial. Methods and Results— We measured hemodynamic and echocardiographic parameters, mean duration of burst pacing–induced AF (DAF), and atrial-myocyte ionic currents in dogs with CHF induced by 2-week ventricular tachypacing (240 bpm), CHF dogs allowed to recover without pacing for 4 weeks (REC), and unpaced controls. Left ventricular ejection fraction averaged 58.6±1.2% (control), 36.2±2.3% (CHF, P I to density by ≈65% ( P I Ca,L density by ≈50% ( P I Ks density by ≈40% ( P I NCX density by ≈110% ( P P P P =NS versus CHF). Conclusions— With reversal of CHF, there is complete recovery of ionic remodeling, but the prolonged-AF substrate and structural remodeling remain. This suggests that structural, not ionic, remodeling is the primary contributor to AF maintenance in experimental CHF.