scholarly journals Mechanically Induced Ectopy via Stretch-Activated Cation-Nonselective Channels Is Caused by Local Tissue Deformation and Results in Ventricular Fibrillation if Triggered on the Repolarization Wave Edge (Commotio Cordis)

Author(s):  
T. Alexander Quinn ◽  
Honghua Jin ◽  
Peter Lee ◽  
Peter Kohl
Heart Rhythm ◽  
2011 ◽  
Vol 8 (10) ◽  
pp. 1578-1581 ◽  
Author(s):  
John Kalin ◽  
Christopher Madias ◽  
Alawi A. Alsheikh-Ali ◽  
Mark S. Link

2001 ◽  
Vol 37 (2) ◽  
pp. 649-654 ◽  
Author(s):  
Mark S Link ◽  
Barry J Maron ◽  
Brian A VanderBrink ◽  
Masaaki Takeuchi ◽  
Natesa G Pandian ◽  
...  

2008 ◽  
Vol 19 (12) ◽  
pp. 1304-1309 ◽  
Author(s):  
CHRISTOPHER MADIAS ◽  
BARRY J. MARON ◽  
STACEY SUPRON ◽  
N. A. MARK ESTES ◽  
MARK S. LINK

Heart Rhythm ◽  
2008 ◽  
Vol 5 (9) ◽  
pp. 1355-1356 ◽  
Author(s):  
Alawi A. Alsheikh-Ali ◽  
Christopher Akelman ◽  
Christopher Madias ◽  
Mark S. Link

2007 ◽  
Vol 23 (4) ◽  
pp. 282-288 ◽  
Author(s):  
Elizabeth I. Drewniak ◽  
David B. Spenciner ◽  
Joseph J. Crisco

Sudden death resulting from ventricular fibrillation (VF) caused by a nonpenetrating chest wall impact, known as commotio cordis (CC), is the second leading cause of death among young athletes. To date, seven young athletes wearing chest protectors have died from CC. The purpose of this study was to determine whether a relationship exists between mechanical properties of chest protectors and occurrence of VF, previously determined by Weinstock et al., using an established swine model. A servo-hydraulic material tester was used to determine properties of the chest protectors, including displacement, permanent deformation, stiffness, and area of pressure distribution. These properties were then compared with the occurrence of VF. We found that a decreased proportion of hits resulting in VF was significantly associated (R2 = 0.59, p = 0.001) with an increase in the area of pressure distribution. These findings are a limited, but crucial, first step in understanding the prevention of this complex and perplexing phenomenon.


Heart Rhythm ◽  
2007 ◽  
Vol 4 (4) ◽  
pp. 529-532 ◽  
Author(s):  
Mark S. Link ◽  
N.A. Mark Estes

Circulation ◽  
2010 ◽  
Vol 122 (24) ◽  
pp. 2499-2504 ◽  
Author(s):  
Alawi A. Alsheikh-Ali ◽  
Christopher Madias ◽  
Stacey Supran ◽  
Mark S. Link

The Lancet ◽  
2014 ◽  
Vol 383 (9925) ◽  
pp. 1358 ◽  
Author(s):  
Ryan J Spencer ◽  
Hariharan Sugumar ◽  
Elizabeth Jones ◽  
Omar Farouque

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Christopher Madias ◽  
Ann C. Garlitski ◽  
John Kalin ◽  
Mark S. Link

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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