• Christopher Madias, Barry J Maron, Jonathan Weinstock, N A Mark Estes, and Mark S Link.
• Cardiac Arrhythmia Center, Division of Cardiology, Tufts-New England Medical Center, Boston, Massachusetts 02111, USA.
• J. Cardiovasc. Electrophysiol. 2007 Jan 1; 18 (1): 115-22.

AbstractCommotio cordis (CC), sudden death as a result of a blunt, often innocent-appearing chest wall blow, is being reported with increasing frequency. The clinical spectrum is diverse; however, a substantial number of cases occur in youth athletics. In events that occur during sport, victims are struck by projectiles regarded as standard implements of the game. Sudden death is instantaneous and victims are most often found in ventricular fibrillation (VF). Overall survival is poor; however, successful resuscitation can be achieved with early defibrillation. Autopsy is notable for the absence of any significant cardiac or thoracic injury. Development of an experimental model has allowed for substantial insights into the underlying mechanisms of sudden death. In anesthetized juvenile swine, induction of VF is instantaneous following chest wall blows occurring during a vulnerable window before the T wave peak. Crucial variables including the velocity of impact, impact location, and hardness of the impact object have been identified. Rapid left ventricular (LV) pressure rise following chest impact likely results in activation of ion channels via mechano-electric coupling. The generation of inward current via mechano-sensitive ion channels likely results in augmentation of repolarization and nonuniform myocardial activation, and is the cause of premature ventricular depolarizations that are triggers of VF in CC. While softer-than-standard safety baseballs reduce the risk of CC, commercially available chest protectors are ineffective in preventing CC. The development of more effective chest protectors and more widespread use of automated external defibrillators at youth sporting events are needed.

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