INTRODUCTION — Commotio cordis, which translates from Latin origin as "agitation of the heart," is defined as sudden cardiac death secondary to a blunt, nonpenetrating anterior precordial impact. Sudden death from commotio cordis is a primary arrhythmic event, and, importantly, the chest blow does not inflict direct structural damage to the heart itself. Despite a lack of awareness, commotio cordis is among the more common causes of sudden cardiac death in young athletes (along with hypertrophic cardiomyopathy and congenital anomalies of the coronary arteries) [1-6].
The epidemiology, potential mechanisms, treatment, and primary prevention of commotio cordis will be discussed here. Other common causes of sudden cardiac death are discussed in detail separately. (See "Overview of sudden cardiac arrest and sudden cardiac death" and "Athletes: Overview of sudden cardiac death risk and sport participation" and "Approach to sudden cardiac arrest in the absence of apparent structural heart disease".)
EPIDEMIOLOGY — Reports of sudden cardiac death following chest trauma have appeared in the medical literature since the 1700s [7]. While the exact incidence remains unknown, mostly due to a lack of systematic reporting, commotio cordis has been reported among the most common causes of sudden death in athletics [6].
In the mid-1990s, the National Commotio Cordis Registry was established in the United States (US).
Since the establishment of the Registry, data on over 200 confirmed cases of commotio cordis have been published [3,8]. Some notable findings from the registry include:
●Young persons are most commonly affected (mean age of registry cases was 15 years); only 9 percent of reported cases occurred in those older than 25 years of age.
●95 percent of reported cases have been in males.
●75 percent of cases have occurred during athletics (50 percent during competitive sports, 25 percent during recreational sports).
●Most cases have been reported in sports with blunt projectiles (eg, baseball, lacrosse, hockey) and/or more physical body contact (eg, football).
While the National Commotio Cordis Registry receives reports of cases primarily from the US, 60 cases from outside the US have been reported to the Registry [9,10]. Patient demographics and survival between US and non-US victims were similar, though non-US victims were somewhat older (mean 19 versus 15 years of age), and a significantly greater number of non-US cases occurred during soccer (20 percent versus 3 percent of US cases). In a report of sudden death cases from the Cardiac Risk in the Young Centre for Cardiovascular Pathology in the United Kingdom, 17 cases of commotio cordis were identified [10]. Cases of commotio cordis followed a similar circumstantial and age profile to those reported in the US, with the majority of cases involving a male youth being struck in the chest during sporting activity, including cricket, soccer, and rugby.
MECHANISM — Despite its traumatic appearance, sudden death due to commotio cordis is a primary electrical event, with ventricular fibrillation (VF) occurring immediately upon chest wall impact [8,11,12]. In experimental models, several critical variables appear to influence the likelihood of commotio cordis, including the timing of impact during the cardiac cycle, location of impact, and perhaps the velocity of impact (figure 1).
●Timing of impact – The most important variable in the development of VF in cases of commotio cordis appears to be the timing of chest wall impact within the cardiac cycle. Only impacts occurring during a 20 to 40 millisecond window on the upslope of the T-wave (early ventricular repolarization) will cause VF (figure 2) [2,11].
●Location of impact – Only impacts occurring directly over the cardiac silhouette result in VF [13].
●Velocity of impact – While there is no defined force of chest trauma which results in commotio cordis, the velocity of the projectile at impact appears to be important. In an experimental model, as projectile velocity increases up to 40 miles per hour (mph), the incidence of VF increases to 70 percent [14]. However, at impact velocities greater than 40 mph, the probability of VF decreases, while the frequency of structural damage including myocardial rupture and cardiac contusion increases.
●Hardness of impact object – Harder objects are more likely to cause VF [11,15].
●Shape of impact object – Flat objects have never caused VF in the experimental model, and smaller diameter spheres are more likely to cause VF [16].
Increased dispersion of ventricular repolarization caused by the blow appears to underlie VF in commotio cordis [17]. The ATP-sensitive potassium channel is likely activated by the chest blow and contributes to the development of VF [18]. Conversely, stretch-activated calcium channels and the autonomic nervous system have not been demonstrated to be involved [19,20].
Younger individuals are likely more susceptible to commotio cordis due to a number of factors. Among these is more frequent participation in projectile sports by younger individuals. In addition, there is evidence to suggest that larger size and possibly increased stiffness of the chest wall with biologic maturation might have a protective effect [21].
CLINICAL MANIFESTATIONS AND DIAGNOSIS — While the reported nature of chest blows causing commotio cordis have varied, the most common scenario occurs in sports in which a dense projectile, such as a baseball, a lacrosse ball, or a hockey puck results in blunt chest wall impact directly over the heart. Smaller, spherical objects are more likely to induce ventricular arrhythmias rather than larger spheres and nonspherical objects [16]. Commotio cordis is almost never caused by pneumatic objects such as soccer balls and tennis balls. Notably, of the victims in the United States National Commotio Cordis Registry who were participating in competitive sports, approximately one-third suffered commotio cordis despite wearing the standard chest protection equipment for that sport [22]. (See 'Prevention' below.)
The diagnosis of commotio cordis is presumptively made based upon the clinical scenario (ie, a witnessed blunt chest impact followed by almost instantaneous collapse), available electrocardiographic (ECG) data demonstrating ventricular fibrillation, and the absence of structural heart disease or myocardial trauma on imaging studies (ie, echocardiogram, computed tomography of the chest) or autopsy. In patients in whom autopsies have been performed, there has been no note of anomalous coronary arteries or premature atherosclerotic disease.
All commotio cordis survivors should undergo a thorough evaluation assessing for structural heart disease, in particular including arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy and anomalous coronary arteries, and ion channel gene mutations such as the long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Diagnostic evaluation'.)
While blunt chest blow is required as the trigger for ventricular arrhythmias in victims of commotio cordis, any structural damage to the body from this impact is confined to the chest wall. This is an important point in distinguishing sudden cardiac death due to commotio cordis from more severe trauma, which may lead to a cardiac contusion or myocardial rupture, both of which are associated with high rates of death. (See 'Mechanism' above and "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Cardiac injury'.)
OUTCOMES/RESUSCITATION — Commotio cordis is a primary electrical event, with ventricular fibrillation being the initial documented arrhythmia in most victims. Survival in commotio cordis has historically been poor, with no reported survival in the initial 25 patients in the National Commotio Cordis Registry [3]. However, more recent data show improving survival, with 58 percent survival of reported cases between 2006 and 2012 [23]. These improvements in survival presumably relate to earlier recognition and activation of emergency medical services, increased bystander cardiopulmonary resuscitation, and earlier defibrillation, often by lay bystanders using automated external defibrillators. (See "Automated external defibrillators".)
Following the identification of sudden cardiac arrest, the management of persons with commotio cordis follows the standard basic and advanced life support algorithms. Management should include chest compressions with early defibrillation, as indicated in resuscitation guidelines. Incorporation of basic life support and automated external defibrillator concepts has led to an improvement in survival for not only athletes, but also entire populations [24,25]. (See "Adult basic life support (BLS) for health care providers" and "Pediatric basic life support (BLS) for health care providers" and "Advanced cardiac life support (ACLS) in adults" and "Pediatric advanced life support (PALS)".)
PREVENTION — Because of its reported occurrence in a vast array of situations, there is no universal means available to prevent all commotio cordis. However, due to its association with sports involving hard, dense projectiles and/or physical contact, one means of preventing commotio cordis is to avoid involvement in higher-risk (in relative terms) activities. For participants who choose to continue with activities associated with a higher risk of commotio cordis (particularly projectile sports), a combination of safety measures including coaching to avoid chest wall impact and protective equipment might decrease the associated risks [8,12]. In 2017, the National Operating Committee on Standards for Athletic Equipment approved a mechanical surrogate for the evaluation of chest wall protectors to prevent or reduce the risk of commotio cordis [26].
●Coaching measures should encourage athletes to turn away from oncoming projectiles (ie, baseballs, lacrosse balls) whenever possible to avoid contact to the chest.
●Softer and less dense balls should be used whenever possible without changing the nature of the game. As an example, age-appropriate safety baseballs have been shown to decrease the risk of commotio cordis (figure 3) [11,15].
●Surprisingly, commercially available chest wall protectors have not been shown to effectively prevent commotio cordis, both in the clinical arena and in laboratory animal studies [3,22,27,28]. Many of the commotio cordis victims reported to the National Commotio Cordis Registry were wearing protective equipment at the time of their event [3].
●A new standard for the evaluation of chest wall protectors to prevent commotio cordis has been adapted by the United States National Commotio Cordis Registry [29].
RETURN TO PLAY — Commotio cordis is a rare event, likely due to the number of specific mechanistic elements that need to be realized (eg, timing, location, and velocity of impact). The issue of return to play raises the matter of individual susceptibility to commotio cordis. In the experimental model, a small number of animals were uniquely susceptible to chest blow induction of ventricular fibrillation [30]. In addition, there is a case report of an individual who likely experienced two episodes of commotio cordis [31]. There is also a case report of commotio cordis occurring in an adolescent with a heterozygous mutation for the CACNA1C gene that has been associated with a phenotype of long QT syndrome [32]. Despite these reports, it remains unclear if there is individual predisposition to commotio cordis; however, reducing the potential risk of chest wall impact would be prudent for individuals who survive a commotio cordis event.
Survivors of commotio cordis should undergo a comprehensive cardiac evaluation to exclude structural heart disease. This evaluation should include a 12-lead ECG, ambulatory ECG monitoring, echocardiogram, cardiac magnetic resonance imaging, and exercise stress testing. Testing for primary electrical diseases (eg, Brugada syndrome, long QT syndrome) might also be considered if suggested by other ECG parameters. In 2015, the American Heart Association/American College of Cardiology consensus statement on eligibility and disqualification recommendations for competitive athletes recommended that athletes can resume training and competition following commotio cordis if the evaluation for cardiac pathology is entirely unrevealing [12].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Ventricular arrhythmias".)
SUMMARY AND RECOMMENDATIONS
●Commotio cordis, defined as sudden cardiac death secondary to ventricular fibrillation (VF) as a result of nontraumatic chest wall impact, is one of the more common causes of sudden cardiac death in young athletes. (See 'Introduction' above.)
●While commotio cordis has been reported from a large variety of blunt chest blows, the most common scenario occurs in sports in which a dense projectile, such as a baseball, a lacrosse ball, or a hockey puck results in chest wall impact directly over the heart. (See 'Clinical manifestations and diagnosis' above.)
●The exact incidence of commotio cordis remains unknown, mostly due to a lack of systematic reporting of cases. However, since the United States National Commotio Cordis Registry was established, data have revealed that commotio cordis occurs more frequently in younger males participating in sports involving projectiles and/or physical contact. (See 'Epidemiology' above.)
●Several critical variables appear to influence the likelihood of commotio cordis occurring, including the timing of impact during the cardiac cycle, location of impact, and the velocity of impact (figure 1). (See 'Mechanism' above.)
●The diagnosis of commotio cordis is presumptively made based upon the clinical scenario (ie, a witnessed blunt chest impact followed by almost instantaneous collapse), available electrocardiographic data demonstrating VF, and the absence of structural heart damage on imaging studies (ie, echocardiogram, computed tomography of the chest) or autopsy. (See 'Clinical manifestations and diagnosis' above.)
●While blunt chest blow is required as the trigger for ventricular arrhythmias in victims of commotio cordis, any structural damage to the body from this impact is confined to the chest wall. This is an important point in distinguishing sudden cardiac death due to commotio cordis from more severe trauma, which may lead to a cardiac contusion or myocardial rupture. (See 'Clinical manifestations and diagnosis' above.)
●Following the identification of sudden cardiac arrest, the management of persons with commotio cordis follows standard basic and advanced life-support algorithms. Management should include chest compressions with early defibrillation, as indicated in resuscitation guidelines. (See 'Clinical manifestations and diagnosis' above and "Adult basic life support (BLS) for health care providers" and "Pediatric basic life support (BLS) for health care providers" and "Advanced cardiac life support (ACLS) in adults" and "Pediatric advanced life support (PALS)".)
●For participants in activities where commotio cordis is seen more frequently, a combination of safety measures, including coaching and protective equipment, might decrease the associated risks. (See 'Prevention' above.)
●Patients may return to competitive athletics following commotio cordis assuming that no cardiac pathology is discovered following a comprehensive cardiac evaluation. However, prudence would suggest that sports with a higher likelihood of chest wall impact should be avoided. (See 'Return to play' above.)
