Atrial fibrillation (AF) is the most common arrhythmia in the world. However, deglutition-induced tachyarrhythmias are exceptionally rare. Diagnosis relies on a documented history, Holter monitoring and echocardiograms. The mechanism underlying deglutition-induced tachycardia remains uncertain, with leading hypotheses suggesting mechanical left atrial stimulation after esophageal distention or activation of the vagus nerve due to increased intra-esophageal pressure. Lifestyle changes, medications (e.g., beta-blockers and antiarrhythmics), and radiofrequency catheter ablation are viable treatment options. First-line treatment is usually beta-blockers, but they have limited effectiveness due to the poorly understood mechanisms behind this pathological condition. Sodium channel blockers targeting vagal motor fibers decrease esophageal muscle contraction force by reducing axonal transmission, supporting the theory that inhibiting rapid sodium channels may mitigate atrial tachycardias. This mechanism presents a promising approach for managing deglutition-induced atrial fibrillation. We present a unique case of a 58-year-old female diagnosed with deglutition-induced atrial fibrillation secondary to esophageal dilation who was successfully treated with the antiarrhythmic propafenone, supporting the vagus nerve hypothesis.
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Trivedi et al. (2024) studied this question.
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