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 been described in young individuals (commotio cordis). In our previously reported swine model of commotio cordis, ventricular fibrillation (with T-wave strikes) and ST-segment elevation (with QRS strikes) were produced by 30-mph baseball impacts to the precordium. Because activation of the K(+)(ATP) channel has been implicated in the pathogenesis of ST elevation and ventricular fibrillation in myocardial ischemia, we hypothesized that this channel could be responsible for the electrophysiologic findings in our experimental model and in victims of commotio cordis.


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 compared with animals in which no glibenclamide was given. In the second phase, 20 swine were randomized to receive glibenclamide or a control vehicle (in a double-blind fashion), with chest impact delivered just before the T-wave 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 glibenclamide 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 K(+)(ATP) channel reduced the incidence of ventricular fibrillation and the magnitude of ST-segment elevation. Therefore, selective K(+)(ATP) channel activation may be a pivotal mechanism in sudden death resulting from low-energy chest-wall trauma in young people during sporting activities.
Link
M S
MS
Cardiac Arrhythmia Service, New England Medical Center, Tufts University School of Medicine, Boston, MA, USA. Mark.Link@es.NEMC.org
Wang
P J
PJ
VanderBrink
B A
BA
Avelar
E
E
Pandian
N G
NG
Maron
B J
BJ
Estes
N A
NA
D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D016757:Death, Sudden, Cardiac / Q000209:etiology*; D004562:Electrocardiography; D005905:Glyburide / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000378:metabolism*; D013552:Swine; D013898:Thoracic Injuries / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000209:etiology / Q000517:prevention & control; D014949:Wounds, Nonpenetrating / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology
D026902:Potassium Channel Blockers; D015221:Potassium Channels; D000255:Adenosine Triphosphate; D005905:Glyburide