Deep breathing-triggered atrial fibrillation: An unusual mechanism terminated by focal RF ablation.

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. However, AF mechanisms are not yet well understood. Currently, there are three main hypotheses: multiple randomly propagating wavelets, focal electrical discharges, and localized re-entrant activity with fibrillatory conduction. The development of AF requires a specific “trigger” and anatomic or functional substrate. Paroxysmal discharges of the autonomic nervous system (ANS) have been proposed to be the trigger for anomalous ectopic activity inside and around pulmonary veins (PVs). We report the case of a patient referred for a repeated circumferential pulmonary vein ablation (CPVA) because of symptomatic paroxysmal AF recurrence related to deep inspiration and yawn.

The patient was a 51-year-old male with drug-refractory paroxysmal AF who underwent CPVA in 2009 and cavotricuspid isthmus ablation in 2010. The patient remained free of AF recurrence until 2012. He was referred to our institution because of new-onset palpitations (seconds to hours) related to deep inspiration or yawning, with poor response to antiarrhythmic medications. The clinical symptoms were reproducible when performing these manoeuvres, confirming a diagnosis of AF recurrence; a second CPVA procedure was scheduled. The left PVs were still isolated, whereas the right PVs were found to be reconnected. Provocative manoeuvres were performed during the electrophysiological procedure, triggering an atrial tachycardia that degenerated into self-limited AF (Fig. 1). An activation map of the breathing-triggered AF was obtained while repeatedly performing the provocative manoeuvres. The earliest activation site was localized at the antero-superior aspect of the right superior PV (Fig. 2), where radiofrequency energy was delivered. After ablation, these manoeuvres did not induce any further atrial arrhythmias. The procedure was completed with re-isolation of the right PVs.

Fig. 1

Provocation of atrial tachycardia with deep inspiration (arrow). From superior to inferior: V1 from surface ECG, electrograms recorded from the high right atrium (RA), electrograms recorded with the ablation catheter (Map) located at right inferior PV; and respiration curve (R–C).

Fig. 2

On the left, anterior (Panel A) and posterior (Panel B) views of the left atrium. Panels 1 to 4 (on the right) display the surface ECG (V1 and V6) and the electrograms recorded from the high right atrium (RA) and ablation (Map) catheters at different sites in the left atrium during breathing-induced atrial ectopy (location corresponds to points 1 to 4 in left panels). Panel 1 shows the site with earliest activation at the antero-superior aspect of the right superior pulmonary vein (PV), where radiofrequency application successfully abolished the tachycardia. Panel 2–4 display the activation precocity at the right inferior PV and at the posterior aspect of the left superior and right superior PV antrum. The asterisks indicate the beginning of atrial tachycardia.

The link between the ANS and AF is well established. The cardiac ANS can modulate atrial electrophysiological properties and facilitate both initiation and maintenance of atrial arrhythmias [1]. Both cholinergic and adrenergic stimulation have demonstrated a proarrhythmic effect in atrial myocardium by shortening the refractory period and increasing refractory heterogeneity [2]. Coumel classified paroxysmal AF as either vagal or adrenergic depending on the type of triggers and the temporal distribution of the arrhythmic episodes [3]. The most important triggers described in relation to vagal AF are sleep, postprandial situation, rest after exercise (>30 min post-exercise), ingestion of cool food, coughing, burping and swallowing. On the other hand, adrenergic AF often occurs after physical or emotional stress and in close relationship to exercise (during or immediately after completion). While vagal AF is more common in men, young people and in the absence of structural heart disease, adrenergic AF is more frequent in patients with structural heart disease. Deep breathing increases vagal tone and leads to sinus bradycardia [4]. In the present case, deep breathing induced ectopic beats that triggered AF; this association makes a vagal mechanism more likely. Although this mechanism has not been described as a trigger of AF or atrial tachyarrhythmias, it has been used as a manoeuvre to evaluate the afferent, central and efferent parasympathetic ANS [4]. In this regard, a deep-breathing ratio (maximum heart rate/minimum heart rate) ≥1.2 is considered normal. The link between AF and breathing also might be explained by the anatomical changes and mechanical wall stress of the left atrium and PVs during deep inspiration [5]. This manoeuvre increases the branching angle of the right-sided PVs and leads to a significant reduction in the calibre of the proximal part of the PV. How these anatomic changes might promote the ectopic activity of the right PVs is still not well established. The present case is the first case suggesting a pathogenic link between deep breathing and PV ectopy. However, the precise mechanisms causing breathing-triggered AF have yet to be defined.

Conflict of interest disclosures

None.