Low room temperature can trigger ventricular fibrillation in J wave syndromes

Recently, much attention has been focused on early repolarization and what has been called the “J wave syndrome,” based on the association between the early repolarization patterns observed in electrocardiograms (ECGs) and the risk of idiopathic ventricular fibrillation (VF), as reported by several researchers. The triggering mechanisms underlying J wave syndromes have not been fully elucidated. As for the causative genes for J wave syndromes, various genetic mutations related to sodium, calcium, and potassium channels have been reported to date. Also, triggering factors for VF, such as certain autonomic nervous system activity, hypokalemia, ischemia, febrile illnesses, use of certain drugs, and hypothermia, have been reported. Osborn J waves were initially described in experimental hypothermia. Although J waves are frequently observed in hypothermic therapy, few reports have discussed the lethal ventricular arrhythmias associated with J waves. Current guidelines recommend mild therapeutic hypothermia to prevent neurologic damage following cardiac arrest. However, several recent case reports have described J-wave augmentation and subsequent VF episodes induced by hypothermic therapy or hypothermia in early repolarization syndrome. To date, the mechanisms underlying hypothermia-induced J waves and arrhythmogenesis remain unclear. By using a canine arterially perfused right ventricular wedge preparation, which mimics Brugada syndrome, Fish and Antzelevitch demonstrated that hypothermia results in an enhanced action potential spike-and-dome morphology and the loss of the epicardial action potential dome. Similarly, using a canine left ventricular wedge preparation mimicking early repolarization syndrome, Gurabi et al demonstrated that hypothermia causes accentuation of the epicardial action potential notch, leading to loss of the action potential dome at some sites,