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Cardiology Research and Practice
Volume 2016 (2016), Article ID 5191683, 6 pages
Research Article

L-Type Calcium Channels Do Not Play a Critical Role in Chest Blow Induced Ventricular Fibrillation: Commotio Cordis

1Cardiac Electrophysiology Service, Section of Cardiology, Rush University Medical Center, Chicago, IL, USA
2Cardiac Arrhythmia Center, Division of Cardiology, Tufts Medical Center (TMC), P.O. Box 197, 800 Washington Street, Boston, MA 02111, USA

Received 4 July 2015; Revised 15 October 2015; Accepted 20 October 2015

Academic Editor: Frans Leenen

Copyright © 2016 Christopher Madias et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. In a commotio cordis swine model, ventricular fibrillation (VF) can be induced by a ball blow to the chest believed secondary to activation of mechanosensitive ion channels. The purpose of the current study is to evaluate whether stretch induced activation of the L-type calcium channel may cause intracellular calcium overload and underlie the VF in commotio cordis. Method and Results. Anesthetized juvenile swine received 6 chest wall strikes with a 17.9 m/s lacrosse ball timed to the vulnerable period for VF induction. Animals were randomized to IV verapamil () or placebo (). There was no difference in the observed frequency of VF between verapamil (19/26: 73%) and placebo (20/36: 56%) treated animals (). There was also no significant difference in the combined endpoint of VF or nonsustained VF (21/26: 81% in verapamil versus 24/36: 67% in controls, ). Conclusions. In this experimental model of commotio cordis, verapamil did not prevent VF induction. Thus, in commotio cordis it is unlikely that stretch activation of the L-type calcium channel with resultant intracellular calcium overload plays a prominent role.