SCN5A and Myocardial fibrosis: For example, a study using a haploinsufficient SCN5A+/− mouse model demonstrated fibrotic changes within both ventricles; epicardial activation analysis also showed increased late conducting components.31 Conduction deficits and myocardial fibrosis have been elegantly described in a porcine model of SCN5A deficiency, underscoring the pleotropic nature of sodium channel disease.32