|
|
| HOME | SEARCH | CURRENT ISSUE | PAST ISSUES | COLLECTIONS | HELP |
|
|
|
|
| |||||||||||||||||||||||||||||||||
It is not widely appreciated that nonpenetrating blunt trauma delivered without excessive force to the anterior chest wall can lead to fatal cardiac arrest from concussive injury in the absence of preexisting heart disease or identifiable myocardial damage. Examples discussed by Maron et al.4 include blows to the chest from baseballs and hockey pucks. Unlike other causes of sports-related fatalities involving the heart, commotio cordis usually occurs in young people who have no underlying cardiovascular disease4,5,6 and no evidence of traumatic injury to the pericardium, myocardium, coronary arteries, or great vessels. The absence of myocardial trauma at autopsy distinguishes cardiac concussion (i.e., commotio cordis) from the more common cardiac contusion, in which a portion of the heart muscle is structurally damaged by trauma. The findings of Maron et al.4 raise several salient but currently unanswerable questions regarding the prevalence, mechanisms, and prevention of commotio cordis.
The problem of commotio cordis has not received sufficient attention, perhaps in part because it tends to occur in children and younger adolescents engaged in amateur sports.4,5,6 If it were more common in highly visible professional athletes, the media attention would lead to prompt widespread awareness of the problem. There remains no comprehensive registry to reveal the prevalence of sudden death from cardiac arrest in the younger population. However, for over two decades the U.S. Consumer Product Safety Commission has tabulated deaths from commotio cordis and continues to study the problem.6,7,8 One should bear in mind that deaths from commotio cordis represent only a very small fraction of the annual traumatic deaths in children and adolescents. Although effective preventive measures, such as the use of seat belts, bicycle helmets, and safety measures for home firearms, are now known for many types of accidental deaths in children, preventive measures for commotio cordis have not yet been rigorously established. The report by Maron et al.4 should encourage discourse and stimulate research to define the pathophysiologic basis for this form of instantaneous death.
The mechanisms of cardiac arrest in commotio cordis remain uncertain. However, both investigational9,10,11 and clinical observations after chest-wall trauma document that either ventricular fibrillation or acute bradyarrhythmias2,5,6 may result from nonpenetrating chest trauma. Previous research on the effects of blunt impact in porcine models of thoracic trauma have documented ventricular fibrillation or bradycardia as the usual terminal arrhythmia.9,10,11 Biomechanical observations suggest that during rapid, high-level acceleration of the sternum, the elastic skeletal structures attain a velocity that approximates that of the impacting object.9,10,11 Children and adolescents seem to be at particular risk, because they have thin, compliant chests,5,6,9,10,11 a situation that enhances the transmission of force to the heart. Studies using external chest-wall stimulators in humans have demonstrated that it is possible to introduce ventricular beats reliably into the cardiac cycle with mechanical premature stimulation of the chest wall with as little as 0.04 J.12,13 It is also well known that sufficient energy can be transmitted to the myocardium with a precordial thump to terminate ventricular tachycardia. The hypothesis that mechanical energy transmitted to the myocardium can generate enough electrical energy during the vulnerable period of repolarization to cause fatal ventricular arrhythmias, although plausible, has not been subjected to rigorous scientific evaluation. Tests of implantable cardioverter–defibrillators have demonstrated electrophysiologically that ventricular fibrillation can be reproducibly initiated by the intracardiac delivery of as little as 0.1 J during the electrically vulnerable period of repolarization near the peak of the T wave on the electrocardiogram. However, neither the zone of vulnerability nor the fibrillation threshold for mechanical stimulation is known. The fact that the patients described by Maron et al. could not be resuscitated may suggest an alternative mechanism. It is usually possible to terminate ventricular fibrillation in a normal heart, as long as there is no excessive delay in administering cardiopulmonary resuscitation and defibrillation. Other possible mechanisms that should be investigated are temporary alterations of coronary-blood distribution or a transient reactive vascular reflex,14,15 an extreme vasovagal response, electromechanical dissociation, damage to the conduction system detectable only with specialized histochemical techniques, and apnea.
Systematic evaluation of the mechanisms of commotio cordis with the development of an appropriate biologic model is critical to identifying protective devices and strategies. Unnecessarily restricting athletic activities on the basis of unfounded fears would be an inappropriate response to this rare event. Strategies incorporating chest protectors, modified baseballs, or other safety equipment should be implemented only when such equipment has been subjected to rigorous, standardized, and independent testing of its ability to reduce or eliminate the risk of commotio cordis.16 Although further epidemiologic studies and a comprehensive prospective registry would help define the magnitude of risk in various sports, such efforts are more likely to be useful in monitoring the efficacy of protective measures than in identifying preventive techniques and strategies. Appropriate models for defining the electrophysiologic basis of commotio cordis, by contrast, will allow testing of protective devices. Once mechanisms are defined, a scientific basis for adequate prevention should ensue. The complex issues related to the cost of preventing a rare but catastrophic event deserve thoughtful analysis. Formulating acceptable cost-effective preventive strategies, establishing compliance, and assessing efficacy represent major challenges. Despite considerable advances in our knowledge about sudden death in athletes, the report by Maron et al.4 shows that much remains unknown. Effective measures to prevent sports-related sudden death from commotio cordis and other cardiovascular causes are likely to be developed only if recognition of the problem stimulates support for and intensification of applied research. In the meantime, individual players, along with their parents and coaches, will have to decide for themselves whether to wear chest protectors during sports such as youth hockey and baseball.
N.A. Mark Estes, III, M.D.
Tufts University School of
Medicine
Boston, MA 02111
References
| |||||||||||||||||||||||||||||||||
Related Letters:
Sudden Death during
Sports Activities
Dixon A. E., Shulman S., Fontaine G.,
Fontaliran F., Sinclair J. B., Maron B. J.
Extract | Full Text
N Engl J Med 1995; 333:1784-1785, Dec 28, 1995. Correspondence
This article has been cited by other articles:
|
HOME | SEARCH | CURRENT ISSUE | PAST ISSUES | COLLECTIONS | HELP Comments and questions? Please contact us. The New England Journal of Medicine is owned, published, and copyrighted © 2006 Massachusetts Medical Society. All rights reserved. |
Previous
.gif){kind=spacer}
