INTRODUCTION: Commotio 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 RESULTS: Twelve 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.
CONCLUSION: The 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.