Development of a Biological Model for Commotio Cordis: Use in Evaluating Baseball Injury and Chest Wall Protection

Principal Investigator: Mark S. Link, M.D.
Institution: New England Medical Center, Boston, Massachusetts

Title: Commotio Cordis: Sudden Death Secondary to Low Energy Chest Wall Impact

Abstract: Commotio cordis, sudden death due to low energy nonpenetrating chest wall impact, occurs in young athletes when a baseball or other projectile strikes the victim in the precordium. Death is usually instant and often recalcitrant to standard resuscitative efforts. At autopsy, no cardiac pathology is found. The Commotio Cordis registry recently described 55 cases of commotio cordis.[1]

We have recently developed an animal model of commotio cordis.[2,3] In our model, an object similar in size and weight to a baseball was delivered to the chest wall of juvenile swine at speeds of 30 mph. The impact was timed and varied according to the cardiac cycle. We found that ventricular fibrillation could be reproducibly induced by T-wave strikes occurring 15 to 30 ms prior to the peak of the T-wave. Ventricular fibrillation was immediate and not preceded by other electrophysiologic abnormalities. Strikes at other portions of the cardiac cycle did not produce ventricular fibrillation, but ST segment elevations and occasional heart block. Coronary angiography did not demonstrate coronary artery obstructions or dissections. Technetium 99m perfusion studies showed minor apical perfusion defects in 25% of the animals. Echocardiograms demonstrated transient apical wall motion abnormalities in one half of the animals. Resuscitation, in our model, was critically dependent on early defibrillation.[4] Autopsies did not show thoracic abnormalities or myocardial damage.

With our swine model softer than standard (safety) baseballs were evaluated for the risk of induction of ventricular fibrillation.[5] In these experiments, 48 animals received up to 3 strikes during the vulnerable period for ventricular fibrillation with 1 of 4 different grades of safety baseballs which varied in hardness from a very soft to a regulation baseball. The very soft baseball was found to have a significantly lower incidence of ventricular fibrillation. We have also evaluated whether the energy of the chest wall impact was related to the risk of ventricular fibrillation. Animals received chest impacts of 20, 28, 35, 40, 50 and 60 mph with a regulation baseball. The risk of ventricular fibrillation with chest wall impact increases with baseball velocities up to 40 mph, but then decreases with increased velocities. The limits of vulnerability to ventricular fibrillation with chest wall impacts are defined by energy levels and timing of the cardiac cycle, similar to that seen with the induction of ventricular fibrillation by electrical shocks delivered on the T-wave.

Publications:

1. Maron BJ, Poliac LC, Kyle SB. Clinical profile of commotio cordis: an under-appreciated cause of sudden cardiac death in the young during sporting activities. Circulation 1997; 96:I-755 (Abstract).

2. Link MS, Wang PJ, Pandian NG, Udelson JE, Man-Young L, Vechiotti MA, Vanderbrink BA, Mirra G, Bharati S, Maron BJ, Estes III NAM. A Biological Model of Commotio Cordis: Sudden Death Due to Low Energy Chest Wall Impact. N Engl J Med 1998:In press.

3. Link MS, Wang PJ, Pandian NG, Udelson JE, Man-Young L, Vechiotti MA, Vanderbrink BA, Mirra G, Bharati S, Maron BJ, Estes III NAM. A Biological Model of Commotio Cordis: Sudden Death From Low Energy Chest Wall Impact. J Am Coll Cardiol 1998; 4A. (Abstract).

4. Link MS, Wang PJ, Pandian NG, Man-Young L, Vanderbrink BA, Avelar E, Maron BJ, Estes III NAM. Resuscitation in a Biological Model of Commotio Cordis, Sudden Death From Low Energy Chest Wall Impact. J Am Coll Cardiol 1998; 403A (Abstract).

5. Link MS, Wang PJ, Pandian NG, Man-Young L, Vanderbrink BA, Avelar E, Maron BJ, Estes III NAM. Safety Baseballs Reduce Ventricular Fibrillation and EKG Changes in a Biological Model of Commotio Cordis, Sudden Death From Low Energy Chest Wall Impact. J Am Coll Cardiol 1998; 133A (Abstract).