36TH BETHESDA CONFERENCE: TASK FORCES
Task Force 11: Commotio cordis
Barry J. Maron, MD, FACC, Chair,
N.A. Mark Estes, III, MD, FACC and
Mark S. Link, MD, FACC
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General considerations
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Sudden and unexpected deaths of young athletes are most frequently the consequence of unsuspected cardiovascular diseases (1). However, participants in organized sports are also subject to another risk for sudden death that occurs in the absence of cardiovascular disease—namely, blunt, non-penetrating, and usually innocent-appearing chest blows, triggering ventricular fibrillation unassociated with structural damage to the ribs, sternum, or heart itself (commotio cordis) (2,3). Although the precise incidence during competitive and recreational sports is unknown, commotio cordis events may be a more frequent cause of sudden death than previously believed, and also more common than many of the cardiovascular diseases that cause these catastrophes (1).
Knowledge of the demographics and clinical profile of commotio cordis is based largely on information from the U.S. Registry (Minneapolis, Minnesota) (2,3). Precordial blows that cause commotio cordis usually are not perceived to be unusual for the sport or activity involved, nor of sufficient magnitude to trigger arrhythmic sudden death. Although reported at a wide range of ages (3 months to 50 years), commotio cordis has a predilection for children and adolescents (mean age 13 years) probably because the young characteristically have narrow, pliable chest walls that facilitate transmission of energy from the chest impact to the myocardium.
Commotio cordis occurs in a wide variety of sports, but most commonly youth baseball (and softball), ice hockey, football, and lacrosse, with death often caused by projectiles that are implements of the competition. Although blows are typically of low energy, projectiles may strike the precordium with a range of velocities—paradoxically, and most commonly, with only modest force such as a pitched baseball striking a batter at 30 to 40 mph, but also with high-velocity blows from hockey pucks or lacrosse balls (up to an estimated 90 mph), and frequently with bodily contact to the precordium such as by karate blows or collisions between outfielders tracking a baseball in-flight. Collapse can be instantaneous or preceded by brief periods of consciousness and physical activity. Despite a structurally normal heart, survival from commotio cordis is uncommon (i.e., only 15%). However, survival from commotio cordis has been reported with increasing frequency associated with prompt cardiopulmonary resuscitation and defibrillation (3). Survivors of commotio cordis should undergo a complete cardiac evaluation including electrocardiogram (ECG), Holter ambulatory monitoring, echocardiogram, and possibly cardiac catheterization to exclude underlying structural cardiac abnormalities.
Also, many deaths from commotio cordis occur around the home or on the playground in informal activities related or unrelated to recreational sports (often involving close relatives) in which the chest impact is delivered in an innocent fashion; for example, such events have occurred as a result of light blows during playful "shadow boxing" or as a remedy for hiccups (3). Unfortunately, some commotio cordis events have even triggered criminal convictions for manslaughter or murder (4).
A swine model that replicates commotio cordis has provided important insights into the mechanisms responsible for the devastating electrophysiologic consequences of these precordial blows (5–7). Determinants of ventricular fibrillation following a chest blow include impact delivered at a wide range of velocities directly over the heart, and timing within a narrow 15-to-30-ms window just prior to the T-wave peak during the vulnerable phase of repolarization (representing only 1% of the cardiac cycle) (5–8). The requirement for such an exquisite confluence of circumstances may largely explain the uncommon occurrence of commotio cordis.
In addition, spontaneously aborted commotio cordis events may occasionally result from blows sustained during the QRS complex (depolarization), which trigger transient complete heart block or nonsustained polymorphic ventricular tachycardia in the animal model (5). Basic cellular mechanisms responsible for commotio cordis are incompletely understood, although selective activation of KATP+ channels may play a pivotal role (9).
Several strategies for prevention of commotio cordis events, including innovations in the design of sports equipment, have been considered. Softer-than-normal ("safety") baseballs reduce risk for ventricular fibrillation under laboratory conditions (5,7). Although such projectiles do not provide absolute protection from sudden death on the baseball field (3), nevertheless there is sufficient reason to encourage the use of such baseballs in organized play at appropriate ages (10). Chest barriers with proven efficacy for youth sports (e.g., baseball, lacrosse, and hockey) have not yet been developed, and many of the commercially available products offer no or only incomplete protection against provoked arrhythmias (3,11). The continued reports of commotio cordis events during organized and recreational sports emphasize the importance of more timely resuscitative efforts, including immediate access to automated external defibrillators (AEDs) (12,13), and also development of preventive strategies including design of effective chest barriers (11).
Recommendations:
- 1 Age-appropriate safety baseballs are recommended for use in children up to 13 years of age.
- 2 Although chest wall protectors may prevent traumatic injury in goalies and baseball catchers, insufficient evidence is available to recommend universal use of commercially available chest barriers for all participants in sports, specifically to prevent commotio cordis events.
- 3 AEDs should be available within 5 min after participant collapse at sporting events.
- 4 Survivors of a commotio cordis with ventricular fibrillation (or a presumed aborted event without documented ventricular fibrillation) should undergo a thorough cardiac evaluation, including at least 12-lead ECG, ambulatory Holter monitoring, and echocardiogram. Standard electrophysiologic testing and an implantable cardioverter-defibrillator are not usually recommended.
- 5 Because data are lacking with regard to the susceptibility for recurrent events, eligibility for returning to competitive sports in survivors is at present a decision left to individual clinical judgment.
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Appendix 1
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References
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- Maron BJ. Sudden death in young athletes N Engl J Med 2003;349:1064-1075.[Free Full Text]
- Maron BJ, Poliac LC, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities N Engl J Med 1995;333:337-342.[Abstract/Free Full Text]
- Maron BJ, Gohman TE, Kyle SB, Estes III NAM, Link MS. Clinical profile and spectrum of commotio cordis JAMA 2002;287:1142-1146.[Abstract/Free Full Text]
- Maron BJ, Mitten MJ, Greene BC. Criminal consequences of commotio cordis Am J Cardiol 2002;89:210-213.[CrossRef][ISI][Medline]
- Link MS, Wang PJ, Pandian NG, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis) N Engl J Med 1998;338:1805-1811.[Abstract/Free Full Text]
- Link MS, Maron BJ, VanderBrink BA, et al. Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis J Am Coll Cardiol 2001;37:649-654.[Abstract/Free Full Text]
- Link MS, Maron BJ, Wang PJ, Pandian NG, VanderBrink BA, Estes III NAM. Reduced risk of sudden death from chest wall blows (commotio cordis) with safety baseballs Pediatrics 2002;109:873-877.[Abstract/Free Full Text]
- Link MS, Maron BJ, Wang PJ. Upper and lower limits of vulnerability to sudden arrhythmic death with chest wall impact (commotio cordis) J Am Coll Cardiol 2003;41:99-104.[Abstract/Free Full Text]
- Link MS, Wang PJ, VanderBrink BA, et al. Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (commotio cordis) Circulation 1999;100:413-418.[Abstract/Free Full Text]
- Kyle SB. Youth Baseball Protective Equipment Project Final Report. Washington, DC: United States Consumer Product Safety Commission; 1996.
- Weinstock J, Maron BJ, Song C, Mane PP, Estes III NAM, Link MS. Commercially available chest wall protectors fail to prevent ventricular fibrillation induced by chest wall impact (commotio cordis) (abstr) Heart Rhythm 2004;1:692.
- Strasburger JF, Maron BJ. Images in clinical medicinecommotio cordis. N Engl J Med 2002;347:1248.[Free Full Text]
- Link MS, Maron BJ, Stickney RE, et al. Automated external defibrillator arrhythmia detection in a model of cardiac arrest due to commotio cordis J Cardiovasc Electrophysiol 2003;14:83-87.[CrossRef][ISI][Medline]
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General considerations
Appendix 1