Besides direct pro-arrhythmic effects of INa-L activation, the increased INa-L may potentially contribute to the development dilated cardiomyopathy since increased influx of Na+ due to gain-of-function mutations in SCN5A and SCN10 (genes encoding Na+ channels) has been implicated in the development of heart failure in rodents [49] and was associated with dilated cardiomyopathy [54] as well as sudden cardiac death [55,56]. This evidence concerns the gene SCN5A and dilated cardiomyopathy.