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C. William Stout, Barry J. Maron, Brian A. Vanderbrink, N. A. Mark Estes III, Mark S. Link
Med Sci Monit 2007; 13(1): BR11-15
Background: Young athletes may die suddenly when they are struck in the chest (commotio cordis). Proposed mechanisms of sudden death in commotio cordis include hypervagatonia and activation of the sympathetic nervous system. In an experimental model of commotio cordis, the importance of the
sympathetic and parasympathetic nervous system in the initiation of ventricular fi brillation was evaluated.
Material/Methods: Juvenile swine weighing between 8 and 12 kg were anesthetized with ketamine and isofl urane and placed prone in a sling. Twenty animals were randomized to pretreatment with placebo or sympathetic
and parasympathetic blockade. Chest blows were guided by echocardiography to the center
of the left ventricle and animals received 1–3 strikes with a regulation baseball propelled at 30 mph and timed to impact 10–30 ms prior to the peak of the T-wave.
Results: With 17 impacts in 10 autonomically blocked animals, 6 episodes of ventricular fi brillation were seen; with 15 impacts in 10 control animals, ventricular fi brillation occurred 6 times. There was also no signifi cant difference between the groups in occurrence of nonsustained polymorphic ventricular tachycardia or ST elevation. Transient complete heart block was less commonly seen in animals treated with autonomic blockade, although this did not achieve statistical signifi cance.
Conclusions: In this experimental model of commotio cordis, autonomic blockade did not affect the frequency of sudden cardiac death, polymorphic ventricular tachycardia or ST segment elevation. Thus, vagotonic
and sympathetic surges likely do not contribute to the syndrome of sudden death due to chest blows in young people and athletes.