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


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

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 calciumchannelmay cause intracellular calciumoverload and underlie the VF in commotio cordis. Method and Results: Anesthetized juvenile swine received 6 chest wall strikes with a 17.9m/s lacrosse ball timed to the vulnerable period for VF induction. Animals were randomized to IV verapamil (n = 6) or placebo (n = 6). There was no difference in the observed frequency of VF between verapamil (19/26: 73%) and placebo (20/36: 56%) treated animals (p = 0.16). 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, p = 0.22). 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.
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  • L-Type Calcium Channels Do Not Play a Critical Role in Chest Blow Induced Ventricular Fibrillation: Commotio Cordis

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Authors

Christopher Madias
Cardiac Electrophysiology Service, Section of Cardiology, Rush University Medical Center, Chicago, IL, United States
Ann C. Garlitski
Cardiac Arrhythmia Center, Division of Cardiology, Tufts Medical Center (TMC), P.O. Box 197, 800Washington Street, Boston, MA 02111, United States
John Kalin
Cardiac Arrhythmia Center, Division of Cardiology, Tufts Medical Center (TMC), P.O. Box 197, 800Washington Street, Boston, MA 02111, United States
Mark S. Link
Cardiac Arrhythmia Center, Division of Cardiology, Tufts Medical Center (TMC), P.O. Box 197, 800Washington Street, Boston, MA 02111, United States

Abstract


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 calciumchannelmay cause intracellular calciumoverload and underlie the VF in commotio cordis. Method and Results: Anesthetized juvenile swine received 6 chest wall strikes with a 17.9m/s lacrosse ball timed to the vulnerable period for VF induction. Animals were randomized to IV verapamil (n = 6) or placebo (n = 6). There was no difference in the observed frequency of VF between verapamil (19/26: 73%) and placebo (20/36: 56%) treated animals (p = 0.16). 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, p = 0.22). 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.