Variability in local action potential durations, dispersion of repolarization and wavelength restitution in aged wild-type and Scn5a+/- mouse hearts modeling human Brugada syndrome.

Abstract

Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na+ channel. In affected individuals, the risk of developing malignant ventricular arrhythmias and sudden cardiac death are increased.[1] Two leading theories, the depolarization and repolarization hypotheses, have been put forward to explain the underlying electrophysiological mechanisms[2] with the use of mouse models providing much insight into this controversial area. The monophasic action potential (MAP) recording technique has been extensively used to examine electrophysiology at the whole heart level.[3] This letter attempts to provide a brief overview to illustrate the importance of understanding the limitations of experimental methods and the need to appraise experimental data.