Brugada syndrome caused by a large deletion in SCN5A only detected by multiplex ligation-dependent probe amplification

J Cardiovasc Electrophysiol. 2011 Sep;22(9):1073-6. doi: 10.1111/j.1540-8167.2010.02003.x. Epub 2011 Feb 2.

Abstract

A 14-year-old boy presented with atrial flutter. His ECG showed Brugada changes, first-degree AV block and major sinus pauses. Polymorphic VT was inducible at electrophysiology study. A pacemaker defibrillator was placed. Classic sequencing for SCN5A was normal. Multiplex ligation-dependent probe amplification, however, detected a major deletion in SCN5A. It is predicted that this deletion would result in haploinsufficiency. The report is the first description of a large-scale rearrangement of the SCN5A gene and supports the association between the molecular pathology and the phenotypic expression.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Brugada Syndrome / diagnosis
  • Brugada Syndrome / genetics*
  • Brugada Syndrome / pathology
  • Gene Deletion*
  • Genetic Association Studies / methods
  • Humans
  • Male
  • NAV1.5 Voltage-Gated Sodium Channel
  • Nucleic Acid Amplification Techniques / methods
  • Sodium Channels / genetics*

Substances

  • NAV1.5 Voltage-Gated Sodium Channel
  • SCN5A protein, human
  • Sodium Channels