Reprinted with permission from JOURNAL OF PACING AND CLINICAL ELECTROPHYSIOLOGY, Volume 25, No. 11, November 2002 Copyright© 2002 by Futura Publishing Company, Inc., Armonk, NY 10504-0418. covered a mutation in SCN5A (1795InsD) capable of producing the Brugada and LQT3 phenotypes and Kyndt et al. 23 have recently reported an SCN5A gene mutation capable of producing the Brugada syndrome and progressive conduction disease. SCN5A mutations linked to the Brugada syndrome cause a reduction in the availability of INa secondary to (1) failure of the sodium channel to express,(2) a shift in the voltage and time dependence of INa activation, inactivation, or reactivation,(3) entry of the channel into an intermediate inactivation state from which it recovers more slowly, and/or (4) acceleration of the inactivation of the sodium channel. 4, 5, 9, 14, 20, 22, 24–30

Accelerated inactivation of the sodium channel can be temperature-sensitive. 5 A rise of temperature beyond the physiological range dramatically reduces the charge carried by the sodium channel current (INa) with the T1620M missense mutation. This finding led the present authors to suggest that a febrile state may unmask the Brugada syndrome and/or exacerbate ST-segment elevation and arrhythmogenesis. 5, 31 A number of case reports of fever induced Brugada symptoms have appeared over the past couple of years. 32–34 Two new cases are reported in this issue of PACE. 35, 36 In the report by Porres et al., 35 fever arising secondary to tonsillitis is shown to unmask the Brugada sign and to precipitate episodes of polymorphic ventricular tachycardia (VT) in a 66-year-old male Brugada patient. In the case of Kum et al., 36 fever developing secondary to lobar pneumonia is shown to unmask the Brugada sign in a 39-year-old man.