Atrial Tachycardia After Ablation of Persistent Atrial Fibrillation

Abstract

A rrhythmia recurrence after catheter ablation of persistent atrial fibrillation (AF) is not uncommon and frequently requires repeat ablation procedures. [1][2][3] However, the precise arrhythmia that recurs depends on the strategy that was used at the original session. Patients who undergo sole pulmonary vein (PV) isolation usually manifest recurrent AF. Patients who undergo substrate modification, in the form of electrogram based 4 or linear ablation, 5 frequently develop atrial tachycardia (AT) either during or after the procedure. Whether these organized arrhythmias represent underlying driver tachycardias that were responsible for maintaining AF or occur as a result of our intervention (that is, proarrhythmia) remains unresolved. Article see p 1059If we are truly unmasking underlying drivers, then our ablation strategy may be validated because it allows us to map and potentially eliminate sources of AF, which otherwise could not be identified during fibrillatory conduction. Alternatively, it is possible that substrate ablation, especially linear left atrial ablation, may result in macroreentrant ATs that were not present during or responsible for maintaining AF. In this case, either the original source(s) has been eliminated or simply grazed and is now supplanted by organized reentry related to zones of slow conduction created by ablation.The existing literature provides evidence for both hypotheses. A study using spectral analysis showed that the frequency (ie, the cycle length) of the AT that resulted after AF termination matched that of a spectral component that was already present in the baseline periodogram during AF.6 A follow-up study revealed that when linear ablation resulted in complete conduction block, it was accompanied by a decrease in the prevalence of these spectral components.7 These findings suggest that site-specific ATs may be present during ongoing AF, despite the fact that their frequency is lower than the dominant frequency during AF. These studies then support the contention that organized tachycardias are bound to be encountered after elimination of fibrillatory conduction and, therefore, are not brought on by ablation-related slowed conduction. They also imply that these underlying tachycardias may be responsible for maintaining AF in a hierarchical manner.However, there is also significant support for the competing argument that the ablation strategy determines whether organized reentrant arrhythmias will be encountered during or after ablation. For example, macroreentrant ATs using the mitral isthmus or the roof are frequently encountered when patients with paroxysmal AF undergo linear ablation, with 8 or without PV isolation.5 However, these tachycardias are rarely seen after simple antral PV isolation. If these ATs were truly responsible for maintaining AF, why is it possible to eliminate the arrhythmia in 90% of patients with paroxysmal AF 9 without ablation of the left atrial isthmi? An earlier study also showed that virtually all reentrant ATs originated from prior ablation ...