# Unmasking Type 1 Brugada Pattern Following Pilsicainide Administration for Paroxysmal Atrial Fibrillation: A Case Report

## TL;DR

A 79-year-old man developed a drug-induced Brugada ECG pattern after taking pilsicainide for atrial fibrillation, highlighting the need for vigilance when using sodium channel blockers.

## Contribution

This case report adds to the understanding of drug-induced Brugada patterns in asymptomatic patients without a family history of the condition.

## Key findings

- Pilsicainide induced a type 1 Brugada ECG pattern in a patient with no prior symptoms or family history.
- ECG changes resolved within 3 days after discontinuing the drug.
- The patient remained asymptomatic with no arrhythmic events over 6 months of follow-up.

## Abstract

Brugada syndrome is a genetic arrhythmia characterized by coved ST-segment elevation in the right precordial leads, predisposing individuals to sudden cardiac death due to fatal ventricular arrhythmias. Currently, a type 1 Brugada electrocardiographic (ECG) pattern can be used to diagnose the condition; however, diagnosis is difficult because normal intercostal spaces do not always allow for the detection of a type 1 Brugada ECG. Sodium channel blockers, including pilsicainide, a class Ic antiarrhythmic agent, cause Brugada-type ECG patterns. We report the case of a 79-year-old man with no prior syncope or family history of Brugada syndrome who developed a drug-induced type 1 Brugada ECG pattern after treatment for paroxysmal atrial fibrillation with pilsicainide. The patient presented with palpitations and atrial fibrillation, for which pilsicainide and rivaroxaban were administered. ECG performed after symptom resolution revealed a coved-type ST-segment elevation characteristic of type 1 Brugada ECG. The patient remained asymptomatic, and pilsicainide was immediately discontinued. Subsequent ECGs normalized within 3 days. No ventricular arrhythmias were observed during >6 months of follow-up, and an implantable cardiac monitor was placed for ongoing surveillance.

This case highlights the importance of recognizing drug-induced Brugada-type ECG patterns, particularly in asymptomatic patients treated with sodium channel blockers. Although the presence of a type 1 ECG pattern is diagnostic of Brugada syndrome, its prognostic significance in drug-induced asymptomatic cases remains uncertain. Existing data suggest that asymptomatic patients with drug-induced type 1 ECGs and no family history of or prior arrhythmic events generally have a favorable prognosis and do not require implantable cardioverter-defibrillator placement. This case highlights that even patients with normal ECGs may present with drug-induced Brugada-type patterns. Clinicians should always be alert to ECG changes when prescribing sodium channel blockers for atrial fibrillation.