Clinical Relevance
Our study included a relatively large cohort of AF ablation patients
with a unique characteristic – the use of amiodarone in the
pre-ablation period for purposes of rhythm control. We were able to use
this substantial cohort of amio-treated patients to investigate whether
therapeutic response to the drug predicted ablation outcomes with
standard ablation approaches (a predominantly PVI-based strategy;
irrigated, force-sensing RF or second-generation cryoballoon cathters).
Previous studies of AAD use before AF ablation have focused on three
main ideas: response to AADs as a test to predict ablation outcome; AAD
maintenance of sinus rhythm to allow atrial reverse remodeling prior to
ablation; and AAD therapy to minimize non-PV foci targeted during the
ablation procedure.
Miyazaki and colleagues analyzed the relationship between pre-ablation
response to bepridil (a calcium-blocking anti-anginal) and ablation
outcomes in 82 patients with persAF exclusively (7). Their study found
that post-ablation AF freedom was greater in the patients who
cardioverted pharmacologically with the bepridil (no electrical
cardioversion performed) than in the patients who did not cardiovert
with bepridil therapy. Kang and colleagues conducted an analogous study
investigating pre-ablation electrical cardioversion efficacy in AF
patients. They found that those persAF patients (94) who were more
easily cardioverted pre-ablation (lower energy; fewer shocks) had
improved ablation outcomes as compared to patients who were more
difficult to cardiovert (11).
Our study tests a similar idea to the one investigated by Miyazaki and
Kang: does pre-procedure response to a rhythm-control strategy (AAD or
cardioversion) predict response to catheter ablation for AF? Unlike the
previous reports mentioned, we found that pre-procedure response to
amiodarone was not a reliable predictor of post-ablation outcomes. We
were able to study a large cohort of patients relative to these previous
reports. All patients were restored to sinus rhythm (unlike the Miyazaki
study) prior to ablation, making ours more an investigation of trigger
suppression rather than termination of ongoing AF. Finally, and
importantly, most of our patients received what many would consider
standard therapy for patients with PAF or persAF (PVI only), rather than
extensive (and often pro-arrhythmic) supplemental ablation beyond PVI.
A second type of study, focusing on atrial structural and electrical
remodeling with AAD therapy to maintain NSR in the pre-ablation window,
is supported by pre-clinical investigations of amiodarone on atrial
electrophysiology. Amiodarone therapy in canine models of AF prevents
action potential shortening, depressed conduction velocity, interstitial
fibrosis deposition, and AF inducibility (12,13). Based on that idea of
pre-ablation conditioning with amiodarone, Benak and colleagues
investigated 62 persAF patients treated with amiodarone and
cardioversion three months prior to anticipated PVI (9). They selected
the patients who maintained NSR on amiodarone and performed PVI, finding
comparable ablation results to a matched cohort of patients with PAF.
They did not perform ablation in the group of persAF patients who did
not maintain NSR on amiodarone. Our investigation extends the findings
of the Benak study, in which patients who failed amiodarone therapy were
not allowed to undergo PVI; our results suggest that this group should
not have ablation therapy denied them solely because of failure to
respond to amiodarone treatment.
Finally, a number of studies have demonstrated that pre-treatment with
amiodarone limits the number of non-PV targets seen at the time of
ablation, allowing for reduced procedural and ablation times (14,15,16).
These investigations used an extensive ablation approach for patients
with persAF, with routine lesion application targeting non-PV sites. We
believe that the ablation approach in our investigation reflects broad
trends in the field of catheter ablation for both persAF and PAF, with
an emphasis on PVI and a de-emphasis on the routine application of
potentially pro-arrhythmic lesion sets (lines, low-voltage
homogenization, etc.) (17).