Temperature affects the kinetic properties of sodium channel: fever itself unmasks the typical electrocardiographic pattern of the Brugada syndrome.

摘要

Clinical and molecular characterization of the Brugada syndrome [1] has progressed rapidly since its initial description [2]. Demonstration of the temperature dependence of the ionic mechanisms of the syndrome [3] was shortly ensued by the first recognition of the development of the electrocardiographic phenotype [4] and the occurrence of arrhythmic storms in Brugada patients [5] during febrile states. A number of conditions may unmask or induce the electrocardiographic Brugada phenotype [1], a transient condition suggested as life-threatening in some cases [6].