• Christopher Madias, Barry J Maron, Stacey Supron, N A Mark Estes, and Mark S Link.
• Cardiac Arrhythmia Center, Tufts Medical Center, Boston, Massachusetts 02111, USA. mlink@tuftsmedicalcenter.org
• J. Cardiovasc. Electrophysiol. 2008 Dec 1;19(12):1304-9.

IntroductionCommotio cordis, sudden cardiac death secondary to blunt nonpenetrating chest blows in sports, is reported with increasing frequency. In a swine model, ventricular fibrillation (VF) is induced by a baseball blow to the chest, and the initiation of VF is related to the peak left ventricular (LV) pressure produced by the blow. LV pressure changes likely result in cell membrane stretch and mechanical activation of ion channels. Disruption of cell cytoskeleton that anchors the cell membrane prior to precordial blows offers the opportunity to explore whether cell membrane deformation is critical to commotio cordis.Methods And ResultsTwelve juvenile swine (mean 12.7 +/- 1.6 kg) were randomized to intravenous normal saline (control, n = 6) or 10 mg of intravenous colchicine (n = 6), which is known to depolymerize microtubules. Animals were given up to six blows timed to the vulnerable portion of the cardiac cycle with a 30 mph baseball on the chest directly over the cardiac silhouette. VF was initiated by 14 of the 29 (48%) impacts in the colchicine-treated animals compared with only 3 of 28 (11%) in the controls (P = 0.002). The peak generated LV pressure did not differ between colchicine animals (405 +/- 61 mmHg) and controls (387 +/- 115) (P = 0.47). However, animals administered colchicine were more likely to have VF generated by the chest blow at all pressures.ConclusionThe initiation of VF by chest blows is significantly increased by selective disruption of the cytoskeleton, suggesting that mechanical deformation of the cell membrane is fundamental to the activation of ion channels and underlies the mechanism of VF in commotio cordis.

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