Abstract 1078: Atrial Ionic Remodeling in Chronic Non-ischemic Heart Failure
Congestive heart failure (HF) is associated with increased incidence of atrial fibrillation (AF). Many studies have used short term (4 – 6 weeks) ventricular tachypacing to study HF and atrial electrophysiology and have reported electrophysiological remodeling. We hypothesized that chronic (>18 weeks) heart failure (HF) would result in a distinct form of atrial electrophysiologic remodeling.
METHODS: Dogs underwent right ventricular tachypacing for ≥18 weeks, at a heart rate of 180 bpm for the final 10 weeks. Left atrial appendage myocytes were studied using perforated whole cell patch clamp at 36°C.
RESULTS: All HF dogs had LV fractional shortening <18%. Chronic HF shortened the action potential duration (APD) at all frequencies tested (At 2 Hz, APD50: 27±5ms vs. 11±2 ms, APD90: 152 ±15 vs. 97±10ms in Control and HF myocytes respectively, p<0.05, Panel A). Resting membrane potential was reduced (p<0.05) in HF (-65±2.9mV) vs. Control (-73.2±2.5 mV). HF reduced IK1 (-0.4±0.07 (HF) vs. -2.21±0.4 pA/pF (Control) at -80 mV, p<0.05). Transient outward K+ current (Ito) was increased (p<0.05, Panel B). Sustained outward K+ current was reduced (9.6±1.2 (Control) vs. 4.3±0.3 pA/pF (HF), p<0.05); the slow component of the delayed rectifier current (IKs) was reduced in HF (p<0.05). In separate experiments we found that sustained persistent AF (>4 weeks) was easily induced during chronic HF.
CONCLUSIONS: Chronic HF significantly shortens the left atrial APD which is attributable to increases in Ito. These findings differ significantly from changes reported in shorter-term tachypacing HF, and suggest that HF duration is an important mediator of the electrophysiologic substrate for AF.