In this context, mild hypothermia has been described as an antiarrhythmic factor that maintains myocardial conduction during prolonged ischemia by sustaining Nav1.5 and Cx43 function [326], whereas hyperthermia has been described as a proarrhythmic factor, especially in combination with SCN5A mutations as is the case in Brugada syndrome [327,328,329,330]. Here, SCN5A is linked to Brugada syndrome.