New-onset atrial fibrillation as first clinical manifestation of latent Brugada syndrome: prevalence and clinical significance

Eur Heart J. 2009 Dec;30(24):2985-92. doi: 10.1093/eurheartj/ehp326.

Abstract

Aims: To evaluate the prevalence, clinical significance, and prognosis of latent Brugada syndrome (BrS) in patients with new-onset atrial fibrillation (AF) unmasked by class 1C antiarrhythmic drugs.

Methods and results: Between January 2000 and June 2008, all consecutive patients with new-onset AF, who after flecainide exhibited typical Brugada ECG pattern, underwent electrophysiologic, pharmacologic, and genetic testing. Among 346 patients [median age 53 years; interquartile range (IQR), 15], 11 (3.2%; median age 51 years; IQR, 19) diagnosed as lone AF exhibited typical Brugada ECG pattern. Genetic testing was negative. Ventricular tachycardia/ventricular fibrillation (VT/VF) was induced by electrophysiologic testing (five patients) or during flecainide infusion (one patient). Six patients with type 1 ECG pattern and inducible VT/VF underwent ICD implantation. During a median follow-up of 31.5 months (range: 10-85) after ICD implantation, three patients developed BrS and one of them experienced VF. Patients without ICD (five patients) remained asymptomatic during a median follow-up of 74 months. Persistent type 1 pattern occurred only in the three patients who developed BrS.

Conclusion: This study, for the first time, reveals the prevalence of latent BrS in patients with new-onset lone AF, which may precede VT/VF. Persistence of type 1 and ventricular tachyarrhythmias inducibility represents a marker of electrical instability leading to sudden death.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Anti-Arrhythmia Agents / therapeutic use
  • Atrial Fibrillation / etiology*
  • Brugada Syndrome / complications*
  • Brugada Syndrome / drug therapy
  • Brugada Syndrome / genetics
  • Electrocardiography
  • Female
  • Flecainide / therapeutic use
  • Genetic Testing
  • Humans
  • Male
  • Middle Aged
  • Muscle Proteins / genetics*
  • Mutation / genetics
  • NAV1.5 Voltage-Gated Sodium Channel
  • Sodium Channels / genetics*

Substances

  • Anti-Arrhythmia Agents
  • Muscle Proteins
  • NAV1.5 Voltage-Gated Sodium Channel
  • SCN5A protein, human
  • Sodium Channels
  • Flecainide