Why the study?
Does IV verapamil prevent ventricular fibrillation in a commotio cordis swine model?
Does IV verapamil prevent ventricular fibrillation in a commotio cordis swine model?
IV verapamil does not prevent ventricular fibrillation in a commotio cordis swine model, suggesting stretch activation of L-type calcium channels is not the primary mechanism.
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Does not support IV verapamil for VF prevention in this model; leaves open L-type calcium channel mechanisms in commotio cordis.
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 (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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Madias et al. (2016) studied this question.
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