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INTRODUCTION AND BACKGROUND

Sudden death due to nonpenetrating chest wall impact in the absence of structural injury to the ribs, sternum and heart is known as commotio cordis. Commotio cordis usually occurs in young athletes when a baseball or other projectile strikes the victim in the precordium. In a report from June of 1996, the US Consumer Product Safety Commission found that there were 38 reported deaths from baseball blows to the chest between 1973 and 1995. (1) Commotio cordis is also reported in hockey, football, lacrosse, softball, karate, and may account for some of the deaths associated with air bag inflation’s in the young. (2-8) With the increased awareness of this condition, over the last 2 years the number of reported cases of commotio has dramatically risen. In a report from January of 1999 the Commotio Registry numbered 70 victims. 8) Currently, however, the Commotio Cordis Registry has over 100 patients. Still, it is probable that the actual number of cases is greater because of underreporting and transient arrhythmias that do not kill.

Commotio cordis principally affects males aged 5 to 16 years. (2) With human commotio victims the initial rhythms reported are predominantly ventricular fibrillation (VF)>. (2-7,9) In the few survivors, precordial ST segment elevation is present. (4,7,10) Commotio cordis victims are unusually refractory to standard resuscitative efforts even in the presence of immediate cardiopulmonary resuscitation. (2,8) At autopsy, no cardiac pathology has been found that would account for the sudden death.

Previous experimental efforts of chest wall trauma are limited by the magnitude of chest wall impact and by the subsequent severity of the cardiac and thoracic damage. In these experiments almost every type of arrhythmia has been reported, from heart block, to atrial fibrillation, to ventricular tachycardia and fibrillation. (11-13) However, severe cardiac and thoracic abnormalities are found in these experiments, pathology not present in commotio cordis victims. In these models, the energies used ranged from 123 to 650 joules (equivalent to a baseball thrown at 123 to 228 mph). Since commotio cordis deaths occur with low velocity projectiles and cardiac or chest wall damage is absent, the aforementioned models do not necessarily reflect the true pathophysiology of commotio cordis.

EXPERIMENTAL DATA

Because there had never been a chest impact study in the range of energy levels seen with clinical commotio cordis, and the pathophysiology of commotio cordis was unknown, we developed an animal model with which further studies elucidating the cellular mechanisms and the prevention and treatment of commotio cordis could be performed. Swine were chosen because of the similarities with human anatomy and because of the previous work with swine and chest wall trauma. (12-14) In our initial 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 (Figure 1). The impact was timed and could strike at any chosen time in the cardiac cycle. Continuous electrocardiographic (EKG) monitoring, baseline and post-impact left ventriculograms, coronary angiography, echocardiograms, and sestamibi scans were performed.

We found that VF was reproducibly produced with chest wall impacts 15 to 30 ms prior to the peak of the T-wave (Table 1 and Figure 2). (15) VF was immediate and was not preceded by ventricular tachycardia, premature ventricular contractions, ST segment elevations or heart block. Impacts at other portions of the cardiac cycle, including other portions of the T-wave, never produced VF. Transient heart block was more often produced by impacts on the QRS, but was also seen at other times of the cardiac cycle. ST elevations and left bundle branch blocks were seen with impacts throughout the cardiac cycle. Apical and distal septal hypokinesis were observed in one-half of the animals. Coronary angiography performed immediately after impact demonstrated no coronary abnormalities. Sestamibi imaging revealed small apical perfusion defects in one quarter of the animals. Autopsies showed no thoracic or cardiac damage.

To evaluate safety (softer than standard) baseballs, 48 additional animals were given up to 3 impacts during the vulnerable period with one of 4 balls differing by hardness. (15) All balls had the same mass (150 grams) and were propelled at the same velocity (30 mph). Highly significant differences in the occurrence of VF were observed between the baseballs tested (Chi-square test for trend p value of < 0.0001) with the softest balls the least likely to cause VF. Because of concern that ball speeds exceeded 30 mph in youth baseball, we also evaluated safety balls delivered at 40 mph. In these experiments, significant differences were also observed between the safety balls and the regulation baseball with the softer balls demonstrating a reduced incidence of VF. (16)

In further studies, we evaluated whether the energy of the chest wall impact was related to the risk of VF. (17) Animals received chest impacts of 20 to 70 mph with a regulation baseball at the vulnerable period for VF. With 20 mph impacts, VF was not produced. The risk of VF with chest wall impact increased with baseball velocities up to 40 mph (100% of impacts), but then decreased with increased velocities. (17) Intracardiac pressure monitoring with Millar® pressure catheters demonstrated that peak left ventricular pressures increased as the velocity of the impact was increased up to 50 mph, but then decreased at 60 and 70 mph. The peak left ventricular pressures correlated with transient and long-lasting global left ventricular dysfunction as documented by real-time transesophageal echocardiography during these experiments. (18) Preliminary data with larger animals (20-25 kg) demonstrates again that 40 mph baseballs are the most likely to cause VF. In these experiments, 40 mph baseballs caused VF in 70% of impacts compared to 20% of impacts at 30 mph, 55% of impacts at 50 mph, 50% of impacts at 60 mph, and 40% of impacts at 70 mph. The limits of vulnerability to VF with chest wall impacts are thus defined not only by the timing of the impact, but by the energy of impact, similar to that seen with the induction of VF by electrical shocks delivered on the T-wave.

In our model the site of impact was also demonstrated to be a crucial variable in the risk of VF with baseball impacts. (19) In experiments with impacts at 3 sites over the cardiac silhouette, 2 sites over the left chest wall and 2 sites over the right chest wall, VF was only seen with impacts over the cardiac silhouette. Furthermore, impacts directly over the center of the heart were more deadly (30% incidence of VF) compared to impacts over the base of the heart (13%) and impacts over the apex (4%). In this experiment, peak left ventricular pressures were most marked with impacts over the center of the heart (280 + 36 mmHg) and correlated with the risk of VF (p=0.006). Thus, the chest wall impacts that cause sudden death must occur directly over the heart.

In this model of sudden death, we have also begun to study the cellular mechanisms of VF. Because activation of the K⁺_ATP channel has been implicated in the pathogenesis of ST elevation and possibly arrhythmogenesis in cardiac ischemia, we sought to determine whether activation of this channel was responsible for VF and ST elevation in our chest impact model. In this experiment, animals were given glibenclamide, a selective inhibitor of the K⁺_ATP channel, before chest impact. Animals given glibenclamide had significantly less ST elevation and a decreased incidence of VF. (20) Therefore, K⁺_ATP channel activation may play a pivotal role in the sudden death resulting from low energy chest wall trauma. Whether other cardiac channels are involved in the pathophysiology of VF is not known. Furthermore, it is not clear whether activation of the channel is related to direct mechanical trauma or to acute elevation of left ventricular pressure.

Furthermore, we investigated whether complete autonomic blockade would influence the risk of VF in our model. (21) Twenty animals were randomized to pre-impact administration of control agent or complete sympathetic and parasympathetic blockade (0.4 mg IV atropine and 2 mg IV propanolol). There was no significant difference in the occurrence of VF, ST segment elevation or bundle branch block.

CONCLUSION

Over the last 4 years we have developed a biological model of commotio cordis. The model has received wide acceptance and has allowed us to evaluate the important variables that contribute to the risk of sudden death with chest wall impact. These variables include timing of the impact, hardness of the impact object, energy of the impact object, and location of the impact. Using this model we have evaluated safety baseballs and shown that the softer the baseball the lower the risk of sudden death. We have also begun to explore the cellular mechanisms behind sudden death with baseball impact. This model will continue to be of use in the analysis of chest wall protection, resuscitation and cellular mechanisms of ventricular fibrillation.

REFERENCES

1. Adler P, Monticone RCJ. Injuries and deaths related to baseball. In: Kyle SB, ed. Youth Baseball Protective Equipment Project Final Report. Washington, D. C.: United States Consumer Product Safety Commission, 1996:1-43.
2. Maron BJ, Poliac LC, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. The New England Journal of Medicine 1995;333:337-42.
3. Kaplan JA, Karofsky PS, Volturo GA. Commotio cordis in two amateur ice hockey players despite the use of commercial chest protectors: case reports. The Journal of Trauma 1993;34:151-3.
4. Abrunzo TJ. Commotio cordis, the single, most common cause of traumatic death in youth baseball. The American Journal of Diseases of Children 1991;145:1279-82.
5. Dickman GL, Hassan A, Luckstead EF. Ventricular fibrillation following baseball injury. The Physician and Sports Medicine 1978;6:85-6.
6. Maron BJ, Strasburger JF, Kugler JD, Bell BM, Brodkey FD, Poliac LC. Survival following blunt chest impact induced cardiac arrest during sports activities in young athletes. The American Journal of Cardiology 1997;79:840-1.
7. Link MS, Ginsburg SH, Wang PJ, Kirchhoffer JB, Estes NAM, Parris YM. Commotio cordis: cardiovascular manifestations of a rare survivor. Chest 1998;114:326-8.
8. Maron BJ, Link MS, Wang PJ, Estes NAM. Clinical profile of commotio cordis: an under-appreciated cause of sudden death in the young during sports and other activities. Journal of Cardiovascular Electrophysiology 1999;10:114-20.
9. Deady B, Innes G. Sudden death of a young hockey player: case report of commotio cordis. The Journal of Emergency Medicine 1999;17:459-62.
10. Morikawa M, Hirose K, Mori T, Kusukawa J, Tomioka N, Watanabe Y. Myocardial contusion caused by a baseball. Clinical Cardiology 1996;19:831-3.
11. Liedtke AJ, Gault JH, Demuth WE. Electrographic and hemodynamic changes following nonpenetrating chest trauma in the experimental animal. American Journal of Physiology 1974;226:377-82.
12. Cooper GJ, Pearce BP, Stainer MC, Maynard RL. The biomechanical response of the thorax to nonpenetrating impact with particular reference to cardiac injuries. The Journal of Trauma 1982;22:994-1008.
13. Viano DC, Andrzejak DV, Polley TZ, King AI. Mechanism of fatal chest injury by baseball impact: development of an experimental model. Clinical Journal of Sports Medicine 1992;2:166-71.
14. Howe BB, Fehn PA, Pensinger RR. Comparative anatomical studies of the coronary arteries of canine and porcine hearts. Acta Anat 1968;71:13-21.
15. Link MS, Wang PJ, Pandian NG, et al. An experimental model of sudden death due to low energy chest wall impact (commotio cordis). The New England Journal of Medicine 1998;338:1805-11.
16. Link MS, Wang PJ, VanderBrink BA, Maron BJ, Estes NAMI. Reduced risk of death with safety balls in an experimental model of commotio cordis: sudden death from low energy chest wall impact. Journal of the American College of Cardiology 1999;33:534 (abstract).
17. Link MS, Wang PJ, Pandian NG, et al. Upper and lower energy limits of vulnerability to sudden death with chest wall impact (commotio cordis). Circulation 1998;98:I-51 (abstract).
18. Link MS, Avelar E, Wang PJ, et al. Global and transient cardiac stunning in an experimental model of sudden death with low energy chest wall impact-evidence from real time transesophageal echocardiography. Journal of the American College of Cardiology 1999;33:405 (abstract).
19. Link MS, Maron BJ, VanderBrink BA, et al. Impact directly over the cardiac silhouette is necessary to produce sudden death in an experimental model of commotio cordis. Journal of the American College of Cardiology 2000; 35: 161A.
20. 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;100:413-8.
21. Link MS, VanderBrink BA, Wang PJ, et al. Lack of correlation between the autonomic nervous system and cardiac arrhythmias in an experimental model of sudden death from low energy chest wall impact. Journal of the American College of Cardiology 1999:submitted (abstract). 22 1996;94:2534-4.

Table1: Incidence of ventricular fibrillation with impacts at different segments of the cardiac cycle.

	QRS	ST	-40 to -31 ms to T-peak	-30 to -21 ms to T-peak	-20 to -10 ms to T-peak	-9 to -1 ms to T-peak	T- down-slope
Total impacts	59	89	46	287	196	17	34
VF induced	0	0	2	77	65	2	0
% VF	0%	0%	4%	27%	33%	11%	0%

PUBLICATION LIST

PUBLISHED PEER REVIEWED JOURNAL ARTICLES

Link MS, Wang PJ, Pandian NG, Udelson JE, Lee MY, Vecchiotti MA, Vanderbrink B, Mirra G, Bharati S, Maron BJ, Estes NAM. An Experimental Model of Sudden Death Due to Low Energy Chest Wall Impact (Commotio Cordis). The New England Journal of Medicine. 1998; 338: 1805-1811.

Maron BJ, Link MS, Wang PJ, Estes NAM. Clinical Profile of Commotio Cordis: An Underappreciated Cause of Sudden Death in the Young During Sports and Other Activities. Journal of Cardiovascular Electrophysiology. 1999; 10: 114-120.

Link MS, Wang PJ, Vanderbrink BA, Avelar E, Pandian NG, Maron BJ, Estes NAM. 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.

BOOK CHAPTERS/INVITED REVIEWS

Link MS, Maron BJ, Estes III NA. Commotio Cordis. in Sudden Cardiac Death and the Athlete, Futura, Armonk, NY. edited by Estes III, NA, Salem, DN, Wang, PJ. 1997; 515-528.

Link MS, Wang PJ, Maron BJ, Estes NAM. What is commotio cordis? Cardiology in Review. 1999; 7: 265-269.

Link MS, Maron BJ, Wang PJ. Estes NAM. Sudden Death and other Cardiovascular Manifestations of Chest Wall Trauma in Sports. In Textbook of Exercise and Sports Cardiology, Edited by Paul Thompson.

Link MS, Wang PJ, Homoud MK, Estes NAM. Commotio Cordis: Sudden Death due to chest wall trauma. Giornale Italiano di Cardiologia. 2000: 29: S134-S137.

EDITORIALS

Link MS. Commotio Cordis, Sudden Death Due to Chest Wall Impact in Sports. Heart. 1999; 81: 109-110.

CASE REPORTS

Link MS, Ginsburg SH, Wang PJ, Kirchhoffer JB, Berul CI, Estes III NAM, Parris YM. Commotio Cordis: Cardiovascular Manifestations of a Rare Survivor. Chest. 1998; 114: 326-328.

PUBLISHED ABSTRACTS

Link MS, Wang PJ, Pandian NG, Udelson JE, Lee MY, Vecchiotti MA, Vanderbrink B, Mirra G, Bharati S, Maron BJ, Estes NAM. A Biological model of commotio cordis: sudden death from low energy chest wall impact. Journal of the American College of Cardiology . 1998;31:4A.

Link MS, Wang PJ, Pandian NG, Lee MY, VanderBrink B, Avelar E, Maron BJ, Estes NAM. Safety baseballs reduce ventricular fibrillation and EKG changes in a biological model of commotio cordis, sudden death from low energy chest wall impact. Journal of the American College of Cardiology . 1998;31:133A.

Link MS, Wang PJ, Pandian NG, Lee MY, VanderBrink B, Avelar E, Maron BJ, Estes NAM. Resuscitation in a biological model of commotio cordis, sudden death from low energy chest wall impact. Journal of the American College of Cardiology. 1998;31:403A.

Link MS, Wang PJ, VanderBrink B, Avelar E, Pandian NG, Maron BJ, Estes NAM. Upper and lower limits of vulnerability to sudden death with chest wall impact (Commotio Cordis). Circulation. 1998; 98: I-51.

Link MS, Wang PJ, VanderBrink B, Maron BJ, Estes NAM. Reduced Risk of Death with Safety Balls in an Experimental Model of Commotio Cordis: Sudden Death from Low Energy Chest Wall Impact. Journal of the American College of Cardiology. 1999; 33: 534A.

            Link MS, Avelar E, Wang PJ, VanderBrink BA, Maron BJ, Estes NAM, Pandian NG. Global and Transient Cardiac Stunning in an Experimental Model of Sudden Death with Low Energy Chest Wall Impact-Evidence from Real Time Transesophageal Echocardiography. Journal of the American College of Cardiology. 1999; 33: 405A

Link MS, Wang PJ, VanderBrink BA, Takeuchi M, Maron BJ, Estes NAM. Timing of chest impact is critical for the vulnerability to ventricular fibrillation and sudden death in an experimental model of commotio cordis. Circulation. 1999; 100: 4612.

Link MS, Maron BJ, VanderBrink BA, Takeuchi M, Pandian NG, Wang PJ, Estes NAM. Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis. Journal of the American College of Cardiology. 2000; 35: 161A.

Link MS, Wang PJ, VanderBrink BA, Zhu W, Takeuchi M, Pandian NG, Maron BJ, Estes NAM. Importance of early defibrillation in commotio cordis, sudden death due to low energy chest wall trauma in sports. Journal of the American College of Cardiology. 2000; 35: 400A.

Link MS, VanderBrink BA, Wang PJ, Takeuchi M, Bharati S, Pandian NG, Maron BJ, Estes NAM. Lack of Correlation Between the Autonomic Nervous System and Cardiac Arrhythmias in an Experimental Model of Sudden Death From Low Energy Chest Wall Impact (Commotio Cordis) PACE. 2000; 23: 622A.

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