Correspondence

Sudden Death Due to Low-Energy Chest-Wall Impact (Commotio Cordis)

N Engl J Med 1998; 339:1398-1399November 5, 1998

Article

To the Editor:

Link et al. (June 18 issue)1 developed an animal model of commotio cordis. Ventricular fibrillation was reproducibly and instantaneously initiated by impacts to the chest during a narrow temporal window on the upstroke of the T wave in young pigs under general anesthesia.

Swine may have a low threshold for ventricular fibrillation as a species-specific characteristic. Radio-frequency ablation in humans rarely leads to ventricular fibrillation.2 However, in a study of the long-term effects of this procedure,3 all 10 young German Landrace pigs (mean [±SD] weight, 13.9±2.1 kg) had ventricular fibrillation when radio-frequency current was delivered to the left ventricular myocardium (unpublished data). In these pigs, surface electrocardiograms obtained under general anesthesia showed a mean QT interval of 449±62.9 msec (range, 360 to 470) and a mean QT interval corrected for heart rate (QTc) of 558.3±47.5 msec (range, 460 to 630). Similar findings have been reported.4

No base-line electrocardiographic characteristics are reported by Link et al. Measuring the QTc in the two electrocardiograms included in their paper (Figure 1 and Figure 2), we found values of 445 and 522 msec. These values are well above the upper limit of normal for the QTc of 440 msec in humans.5 In humans, prolongation of the QTc correlates with the risk of ventricular arrhythmias.5 By analogy, the species-specific prolongation of the QT interval may put swine at increased risk for ventricular fibrillation.

Regina Bökenkamp, M.D.
Thomas Paul, M.D.
Hannover Medical School, 30623 Hannover, Germany

5 References

1
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
Full Text | Web of Science | Medline

2
Hendricks G. The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. Eur Heart J 1993;14:1644-1653
CrossRef | Web of Science | Medline

3
Paul T, Bokenkamp R, Mahnert B, Trappe H-J. Coronary artery involvement early and late after radiofrequency current application in young pigs. Am Heart J 1997;133:436-440
CrossRef | Web of Science | Medline

4
Hamlin RL, Burton RR, Leverett SD, Burns JW. The electrocardiogram from miniature swine recorded with the McFee-axial reference program. J Electrocardiol 1974;7:155-162
CrossRef | Web of Science | Medline

5
Garson A Jr, Dick M II, Fournier A, et al. The long QT syndrome in children: an international study of 287 patients. Circulation 1993;87:1866-1872
Web of Science | Medline

To the Editor:

The elegant study by Link et al. proves that relatively low energy blows delivered to the precordium during a narrow temporal window on the upstroke of the T wave not only reliably produce ventricular fibrillation, but also do so with the next heartbeat. Energy arriving at the myocardium outside the 15-msec period of vulnerability occasionally caused unsustained polymorphic ventricular tachycardia, whereas transient complete heart block was sometimes observed when the impact occurred during the QRS complex.

Why, then, after being hit in the chest by a puck or a baseball, do some athletes remain briefly conscious, even active, before cardiac arrest?1-3 The theory invoked to explain this phenomenon — that the impact may initially produce ventricular tachycardia that deteriorates to ventricular fibrillation1,2 — was not supported by the results of Link et al. There is, however, evidence that prolonged periods of apnea may occur after blunt trauma to the chest and that latent ventricular fibrillation can occur in such cases.4 Perhaps Link et al. did not observe a delay in the onset of ventricular fibrillation because all the animals were ventilated.

Brian Deady, M.D.
Royal Columbian Hospital, New Westminster, BC V3L 3W7, Canada

4 References

1
Deady B, Innes G. Sudden death of a young hockey player: case report of commotio cordis. J Emerg Med (in press).

2
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
Full Text | Web of Science | Medline

3
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. Am J Cardiol 1997;79:840-841
CrossRef | Web of Science | Medline

4
Viano DC, Andrzejak DV, Polley TZ, King AI. Mechanism of fatal chest injury by baseball impact: development of an experimental model. Clin J Sport Med 1992;2:166-171
CrossRef

To the Editor:

On August 1, 1970, a healthy, athletic 42-year-old man collapsed immediately after being struck in the chest by a cricket ball during a match in Louisville, Kentucky. A team member who was a physician immediately began cardiopulmonary resuscitation, and the patient was transported to a nearby hospital and pronounced dead on arrival. The autopsy showed no evident cause of death, which was presumed to be secondary to cardiac arrhythmia. I suspect that death was due to the then-unrecognized condition of commotio cordis.

Although blows from hockey pucks and baseballs and other direct, firm blows to the chest are recognized risks, cricket balls have only infrequently been mentioned as responsible for commotio cordis, perhaps because of the limited popularity of cricket in the United States.1-3 Cricket is played with a very firm ball, similar to a baseball but made of rubber with layers of cork and a leather covering, measuring 3 in. in diameter and weighing 5.5 oz. The ball is hit with a wooden bat at high impact, as is true in baseball. Cricket players typically do not wear padding over the chest.

As sporting authorities consider recommendations to reduce the risks of commotio cordis from sports-related injuries, cricket balls should be identified as posing a risk and cricket players should consider wearing precordial padding to reduce the risk of death from this rare but tragic injury.

Cynthia L. Haq, M.D.
University of Wisconsin–Madison Medical School, Madison, WI 53715

3 References

1
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
Full Text | Web of Science | Medline

2
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
Full Text | Web of Science | Medline

3
Curfman GD. Fatal impact -- concussion of the heart. N Engl J Med 1998;338:1841-1843
Full Text | Web of Science | Medline

To the Editor:

The last paragraph of the editorial on commotio cordis by Dr. Curfman (June 18 issue)1 contains an ambiguity that may be misinterpreted. The phrase “at an instant when the heart is suspended in diastole” may refer to electrical diastole, but the more commonly used term is (mechanical) systole, as is clearly shown in Figure 1 of the article by Link et al.

Ludwig Klein, M.D.
Cornell University Medical Center, New York, NY 10021

1 References

1
Curfman GD. Fatal impact -- concussion of the heart. N Engl J Med 1998;338:1841-1843
Full Text | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: The use of an animal model to explain a human condition has potential limitations. Bökenkamp and Paul suggest that ventricular fibrillation may be more easily induced in swine than in humans. Although this may be true, we observed ventricular fibrillation with chest impact only during a 15-to-30-msec window on the upslope of the T wave. Ventricular fibrillation was never observed with impacts during other portions of the cardiac cycle, during the placement of left ventricular catheters, or during coronary angiography. Although the absolute risk in humans associated with an impact to the chest during this window of vulnerability during repolarization cannot be determined from this experiment, our study does support the concept that timing is a critical component. Validation of our model in other species would be welcome.

Deady asks about the mechanism of collapse in athletes who are hit in the chest and have an intervening period before final collapse. In the initial report of 25 victims by Maron et al., instantaneous collapse was noted in 12, whereas the others had a short period of consciousness before collapsing.1 In our model, we did not observe ventricular tachycardia degenerating into ventricular fibrillation. Perhaps the short period of conscious activity before collapse in clinical circumstances can be better explained by the occurrence of briefly tolerated ventricular fibrillation. In patients with implantable cardioverter–defibrillators, there are documented instances of ventricular fibrillation occurring for up to 20 seconds without loss of consciousness. In our model, the animals were not ventilated and thus apnea causing ventricular fibrillation would have been theoretically possible. However, this phenomenon was never observed.

Haq comments on a death that was probably due to commotio cordis caused by a cricket ball. Although this is the first such case of commotio cordis of which we are aware, the physical characteristics of the cricket ball are similar to those of a baseball, and thus, cases of commotio cordis due to a cricket ball are plausible. We agree that the low incidence of sudden death among cricket players is most likely explained by the limited popularity of cricket in this country.

Mark S. Link, M.D.
Tufts–New England Medical Center, Boston, MA 02111

Barry J. Maron, M.D.
Minneapolis Heart Institute Foundation, Minneapolis, MN 55407

N.A. Mark Estes, III, M.D.
Tufts–New England Medical Center, Boston, MA 02111

1 References

1
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
Full Text | Web of Science | Medline