Selective activation of the K-ATP(+) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (commotio cordis)

Background-Sudden death due to relatively innocent chest-wall impact has be en described in young individuals (commotio cordis). In our previously repo rted swine model of commotio cordis, ventricular fibrillation (with T-wave strikes) and ST-segment elevation (with QRS strikes) were produced by 30-mp h baseball impacts to the precordium. Because activation of the K-ATP(+) ch annel has been implicated in the pathogenesis of ST elevation and ventricul ar fibrillation in myocardial ischemia, we hypothesized that this channel c ould be responsible for the electrophysiologic findings in our experimental model and in victims of commotio cordis. Methods and Results-In the initial experiment, 6 juvenile swine were given 0.5 mg/kg IV glibenclamide, a selective inhibitor of the K-ATP(+) channel, and chest impact was given on the QRS. The results of these strikes were co mpared with animals in which no glibenclamide was given. In the second phas e, 20 swine were randomized to receive glibenclamide or a control vehicle ( in a double-blind fashion), with chest impact delivered just before the T-w ave peak. With QRS impacts, the maximal ST elevation was significantly less in those animals given glibenclamide (0.16+/-0.10 mV) than in controls (0. 35+/-0.20 mV; P=0.004), With T-wave impacts, the animals that received glib enclamide had significantly fewer occurrences of ventricular fibrillation ( 1 episode in 27 impacts; 4%) than controls (6 episodes in 18 impacts; 33%; P=0.01). Conclusions-In this experimental model of commotio cordis, blockade of the KC, channel reduced the incidence of ventricular fibrillation and the magni tude of ST-segment elevation. Therefore, selective K-ATP(+) channel activat ion may be a pivotal mechanism in sudden death resulting from low-energy ch est-wall trauma in young people during sporting activities.