Poor rhythm outcomes in patients with LVAs
Patients with LVAs demonstrated a higher AF/AT recurrence rate during the long-term follow-up period than those without LVAs, even after multiple ablations. This in turn suggests that durable PVI, and ablation targeting non-PV AF triggers and induced regular ATs does not sufficiently suppress arrhythmogenic substrate in patients with LVAs. Furthermore, transformation from the paroxysmal to persistent form of AF and late recurrence of AF/AT were more often observed in patients with LVAs. These findings suggest that atrial arrhythmogenic substrate progresses after the ablation procedure. The generation of LVAs in paroxysmal AF is relatively dependent on upstream factors causing atrial remodeling, such as aging, female gender, and elevated atrial pressure rather than AF burden.6-8 These upstream factors would likely to continue to remodel the atrium even after ablation.
In addition, ablation targeting LVAs did not reduce AF/AT recurrence. Two hypotheses may explain why LVA ablation failed to suppress AF episodes. First, not all arrhythmogenic substrate is included within LVAs, although LVAs themselves indicate the presence of extra-PV arrhythmogenic substrate. Several studies have suggested that preserved-voltage areas may also serve as arrhythmogenic substrate.9,10 Second, arrhythmogenic substrate might progress even after ablation, as mentioned above, and ablation of LVAs at the time of the ablation procedure does not mean eternal LVA modification.