Commotio Cordis 

Sudden unexpected cardiac death that occurs in young people during sports participation is usually associated with previously diagnosed or undiagnosed structural or primary electrical cardiac abnormalities. Examples of such abnormalities include hypertrophic cardiomyopathy, anomalous origin of a coronary artery, arrhythmogenic right ventricular cardiomyopathy, and primary electrical disorders, such as congenital prolongation of the QTc interval and catecholaminergic, polymorphic ventricular tachycardia. Sudden death due to ventricular fibrillation may also occur when a projectile (eg, baseball, lacrosse ball, hockey puck) strikes the precordium of an individual with no underlying cardiac disease. This is termed commotio cordis (CC).

Much of the understanding of the clinical and pathophysiologic aspects of commotio cordis is the result of work by N.A. Mark Estes III, MD, and Mark S. Link, MD, from the New England Cardiac Arrhythmia Center at the Tufts University School of Medicine in Boston, Massachusetts and data derived from the National Commotio Cordis Registry (Minneapolis, Minnesota).

Recent data from the registry of the Minneapolis Heart Institute Foundation show that commotio cordis is one of the leading cause of sudden cardiac death in young athletes, exceeded only by hypertrophic cardiomyopathy and congenital cornoary artery abnormalities.^[1]

Commotio cordis typically involves young, predominantly male, athletes in whom a sudden, blunt, nonpenetrating and innocuous-appearing trauma to the anterior chest results in immediate cardiac arrest and sudden death from ventricular fibrillation. The rate of resuscitation is low but improving. Although commotio cordis usually involves impact from a baseball, it has also been reported during hockey, softball, lacrosse, karate, and other sports activities in which a relatively hard and compact projectile or bodily contact caused impact to the person's precordium. Nearly 250 cases have been reported to the National Commotio Cordis Registry.^{[2, 3]} Despite a recent increase in registry cases because of increased awareness, the entity is still probably underreported.

Although reported more often in recent years, commotio cordis remains a relatively rare event. This is based, in part, on the pathophysiology of the disorder, which requires precise synchronization of numerous relevant variables. In a series of studies using a swine model of commotio cordis, investigators identified the critical timing and location of blunt chest trauma required to induce ventricular fibrillation and sudden death. See the image below.

Ventricular fibrillation can be triggered by chest wall impact only over the heart, and predominantly occurs with impact over the center of the left ventricle. Impact over other precordial sites causes ventricular fibrillation less often. Nonsustained polymorphic ventricular tachycardia, ST-segment elevation, transient complete heart block, left bundle-branch block, and left ventricular wall motion abnormalities occurred in the absence of ventricular fibrillation only following impact over the cardiac silhouette in the swine model. Chest wall impact that did not overlie the heart failed to produce ventricular fibrillation or any other ECG abnormalities.

During experimental studies in which the precordial impacts were timed to occur during various points in the cardiac cycle, the electrophysiologic consequences were determined to be critically dependent on impact timing. The highest incidence of ventricular fibrillation produced by striking the precordium with a wooden object similar in size and weight to a baseball occurred when the impact was delivered within a 20-millisecond window that occurred 10-30 milliseconds before the T-wave peak. This window represents only about 4% of the cardiac cycle in an individual engaged in activities who has a heart rate of 120 beats per minute. Ventricular fibrillation was not preceded by ventricular tachycardia, conduction abnormalities, or ischemic ST changes; this suggests that the mechanism was related to a primary electrical phenomenon, not to myocardial ischemia.

Impacts delivered outside the period of vulnerability on the T-wave upstroke or during other portions of the electrical cycle rarely resulted in ventricular fibrillation; however, such impacts occasionally caused polymorphic ventricular tachycardia, complete heart block, left bundle-branch block, or ST-segment elevation, all of which were transient. In vivo studies have suggested that impact-related premature ventricular depolarizations together with elevated ventricular pressure-related activation of mechanosensitive ion channels (particularly the ATP-dependent K⁺ channel) probably provide the basis for ventricular fibrillation and sudden death following blunt thoracic trauma, as well as the ischemic-like ECG changes noted in those rare individuals who survive commotio cordis.

A wide variation in individual vulnerability to ventricular fibrillation from appropriately timed strikes has been noted during animal studies. Animals with a higher susceptibility to ventricular fibrillation had, in general, longer QRS and QTc durations at baseline.^[4] More research is clearly indicated to verify these observations and the potential relevance to human subjects.

Other studies using the commotio cordis swine model showed a "bell-shaped" curve relating simulated baseball strike velocity and the induction of ventricular fibrillation, with the highest incidence of fibrillation (approximately 70% of strikes) occurring at a velocity of 40 mph. Also, the hardness of the object that strikes the chest was shown to be directly related to ventricular fibrillation. Softer-than-normal baseballs reduced the risk of ventricular fibrillation with very soft baseballs having the lowest incidence.

Frequency

United States

As many as 20 commotio cordis events are thought to occur in the United States each year,^[5] but the actual incidence is unkonwn because commotio cordis as a diagnosis is still under-appreciated and underreported.

Mortality/Morbidity

According to the National Commotio Cordis Registry, approximately 25% of persons with commotio cordis have been resuscitated.^[5] Over the past decade, resuscitative efforts have been successful in 30% of cases, thereby doubling the survival compared with the previous decade.

Race

According to data collected by the National Commotio Cordis Registry, nearly 80% of cases of commotio cordis are in whites.^[3]

Sex

According to data collected by the National Commotio Cordis Registry, 95% of cases of commotio cordis occur in males.^[3]

Age

Although reported in a wide range of ages (6 wk to 50 y), commotio cordis occurs most frequently in male children aged 10-18 years, with a mean age of 15 ± 9 years. Data from the National Commotio Cordis Registry show that 26% are younger than 10 years and that only about 10% are older than 25 years.^[3]