Transcranial Magnetic Stimulation as an Antidepressant Alternative in a Patient With Brugada Syndrome and Recurrent Syncope

Abstract

Brugada syndrome (BrS) is a common occult cause of sudden cardiac arrest in otherwise healthy-appearing adults. The pathognomonic electrocardiographic pattern may be unmasked only by certain medications, many of which are unknown. We report a case of a depressed but otherwise healthy man with an asymptomatic right bundle branch block on electrocardiography who experienced antidepressant-induced BrS and ultimately recovered with transcranial magnetic stimulation (TMS). After an initial trial of nortriptyline, the patient's depressive symptoms improved; however, he experienced a syncopal event and was subsequently diagnosed as having BrS. Cross titration to bupropion, which had not previously been known to exacerbate BrS, was followed by another cardiac event. As a result, the patient was referred for TMS as a substitute for pharmacotherapy. After 31 TMS sessions over 8 weeks, the patient demonstrated significant improvement by subjective report and objective reduction in his Patient Health Questionnaire-9 scores from 10 (moderate) to 1 (minimal). Transcranial magnetic stimulation is a Food and Drug Administration-approved nonpharmacologic treatment for depression. Given the potential lethality of BrS with known and unknown psychopharmacologic agents, providers should consider TMS as first-line therapy in this patient population. Bupropion should be added to the list of agents known to exacerbate this disease.

Atrial arrhythmias in inherited arrhythmogenic disorders

“…Therefore, the involvement of a sex predilection for the development of AF in patients with BrS is not clear [1] . Clinical AFL has been anecdotally reported either in young patients (<20 years old) as an isolated arrhythmia, or coexisting with AF in adults, or as a part of atrial myopathy and progressive cardiac conduction disorder in patients with BrS [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] .…”

“…Genetic mutations, particularly, loss-of-function mutations and/or deletions in I Na channel α-subunit (SCN5A), have been identified in patients with both BrS and AFL [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] .…”