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.