Biatrial Electrical and Structural AtrialChanges in Heart Failure: Electroanatomic Mapping in Persistent Atrial Fibrillation inHumans.

Abstract

This study sought to characterize the biatrial substrate in heart failure (HF) and persistent atrial fibrillation(PeAF). Atrial fibrillation (AF) and HF frequently coexist; however, the contribution of HF to the biatrial substratein PeAF is unclear. Consecutive patients with PeAF and normal left ventricular (NLV) systolic function (left ventricular ejection fraction [LVEF] >55%) or idiopathic cardiomyopathy (LVEF≤45%) undergoing AF ablation were enrolled. In AF, pulmonaryvein (PV) cycle length (PVCL) was recorded via a multipolar catheter in each PV and in the left atrial appendage for 100 consecutive cycles. After electrical cardioversion, biatrial electroanatomic mapping was performed. Complex electrograms, voltage, scarring, and conduction velocity were assessed. Forty patients, 20 patients with HF (mean age: 62 ± 8.9 years; AF duration: 15 ± 11 months; LVEF: 33 ± 8.4%) and 20 with NLV (mean age: 59 ± 6.7 years; AF duration: 14 ± 9.1 months; p= 0.69; mean LVEF: 61 ± 3.6%; p<0.001), were enrolled. HF reduced biatrial tissue voltage (p< 0.001) with greater voltage heterogeneity (p< 0.001). HF was associated with significantly more biatrial fractionation (left atrium [LA]: 30% vs. 9%; p< 0.001; right atrium [RA]: 28% vs. 11%; p< 0.001), low voltage (<0.5 mV) (LA: 23% vs. 6%; p= 0.002; RA: 20% vs 11%; p= 0.006), and scarring (<0.05mV) in the LA (p= 0.005). HF was associated with a slower average PVCL (185 vs. 164 ms; p= 0.016), which correlated significantly with PV antral bipolar voltage (R=-0.62; p< 0.001) and fractionation (R= 0.46; p=0.001). HF is associated with significantly reduced biatrial tissue voltage, fractionation, and prolongation of PVCL. Advanced biatrial remodeling may have implications for invasive and noninvasive rhythm control strategies in patients with AF and HF.