7/6/23, 1:36 PM Commotio cordis - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Commotio cordis : Christopher Madias, MD : Peter J Zimetbaum, MD, Mark S Link, MD : Todd F Dardas, MD, MS All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Mar 07, 2023. INTRODUCTION Commotio cordis, which translates from Latin as "agitation of the heart," is defined as sudden cardiac death secondary to a blunt, nonpenetrating precordial impact. The epidemiology, potential mechanisms, treatment, and prevention of commotio cordis will be discussed here. Other causes of sudden cardiac death are discussed in detail separately: (See "Overview of sudden cardiac arrest and sudden cardiac death".) (See "Athletes: Overview of sudden cardiac death risk and sport participation".) (See "Approach to sudden cardiac arrest in the absence of apparent structural heart disease".) EPIDEMIOLOGY While the exact incidence of commotio cordis remains unknown due to a lack of systematic reporting, commotio cordis is among the most common causes of sudden death during athletic participation [1,2]. Commotio cordis can also occur during nonsport activities (eg, impact to the chest during fights) [3]. Commotio cordis is most common among young males and is typically provoked by hard projectiles and high energy physical contact (eg, tackles during football). Commotio cordis https://www.uptodate.com/contents/commotio-cordis/print 1/14 7/6/23, 1:36 PM Commotio cordis - UpToDate caused by blows to the chest by air-filled balls is less common. Younger individuals and males are likely more susceptible to commotio cordis due to a number of factors including more frequent participation in projectile sports. In addition, larger body size and increased stiffness of the chest wall (eg, chest wall maturation) may protect against commotio cordis [4]. Registries are the primary source of information on the epidemiology and risk factors for commotio cordis: The National Commotio Cordis Registry was established in the United States (US) and contains data on over 200 confirmed cases of commotio cordis and cases from other countries [5-8]. Notable findings from the registry include: Young persons are the 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 cases occurred in males. 75 percent of cases 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) or high-energy body contact (eg, football). Survival from commotio cordis has increased over time, likely owing to more rapid response times and wider access to defibrillation (eg, on-site automated external defibrillators), as well as greater public awareness of this condition. In the most recent published data from the Commotio Cordis Registry, survival was up to 58 percent [9]. 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 (UK), 17 cases of commotio cordis were identified [8]. When cases from this registry were compared to the US registry, the circumstances and age profile were similar. In the UK registry, the type of sports included cricket, football (ie, soccer), and rugby. In the F d ration internationale de football association (FIFA) Sudden Death Registry, commotio cordis was confirmed in seven cases and was highly suspected in seven https://www.uptodate.com/contents/commotio-cordis/print 2/14 7/6/23, 1:36 PM Commotio cordis - UpToDate additional cases [10]. In 152 football (ie, soccer) players <35 years old with an episode of sudden death, commotio cordis was the cause in 9 percent of cases. In 11 of 14 cases of commotio cordis, the cause was a ball strike to the chest, while the others were due to a chest blow from an elbow or fist. Six patients survived the episode [10]. MECHANISM Commotio cordis is provoked by the simultaneous occurrence of specific mechanistic elements (eg, timing, location, and velocity of impact) that result in ventricular fibrillation (VF). Thus, despite its traumatic appearance, commotio cordis is primarily an electrical event [6,11,12]. The underlying mechanism is likely increased dispersion of ventricular repolarization caused by the blow, which may activate adenosine triphosphate (ATP)-sensitive potassium channels [13,14]. There are hypotheses that VF may be caused by stretch-activated ion channels (eg, calcium), and the autonomic nervous system, but these hypotheses have not been substantiated [15,16]. In experimental models, several critical variables appear to influence the likelihood of commotio cordis ( figure 1): Timing of impact The most important variable in the development of VF in commotio cordis appears to be the timing of chest wall impact within the cardiac cycle. Only impacts that occur during a 20 to 40 millisecond window on the upslope of the T wave (early ventricular repolarization) result in VF [11,17]. Location of impact Only impacts that occur directly over the cardiac silhouette result in VF [18]. Velocity of impact While there is no defined force of chest trauma which results in commotio cordis, the velocity of the projectile appears to be important. In an experimental model, VF did not occur at 20 miles per hour (mph), but, as projectile velocity increased, the likelihood of VF increased (7 percent at 25 mph, 68 percent at 40 mph) [19]. However, at impact velocities greater than 40 mph, the likelihood of VF decreased and the frequency of structural damage including myocardial rupture and cardiac contusion increased. Hardness of impact object Harder objects are more likely to cause VF [11,20]. Shape of impact object Smaller diameter spheres are more likely to cause VF [21]. CHARACTERISTIC CHEST BLOW https://www.uptodate.com/contents/commotio-cordis/print 3/14 7/6/23, 1:36 PM Commotio cordis - UpToDate The types of chest blows that cause commotio cordis vary, but the most common scenario occurs in sports when a dense projectile (eg, baseball, lacrosse ball, hockey puck), impacts the chest wall directly over the heart and the patient collapses within seconds after the impact. (See 'Diagnosis' below.) Notably, approximately one-third of patients who suffered commotio cordis were wearing standard chest protection equipment appropriate for their sport [22]. Thus, the presence of protective gear does not exclude the diagnosis of commotio cordis. (See 'Prevention' below.) EVALUATION FOR HEART DISEASE Survivors of commotio cordis should undergo a comprehensive cardiac evaluation to exclude underlying heart disease such as (see "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Diagnostic evaluation'): Hypertrophic cardiomyopathy. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".) Arrhythmogenic right ventricular dysplasia. (See "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis".) Anomalous coronary arteries. (See "Congenital and pediatric coronary artery abnormalities".) Ion channel gene mutations, such as the long QT syndrome and Brugada syndrome. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management" and "Congenital long QT syndrome: Diagnosis" and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".) Catecholaminergic polymorphic ventricular tachycardia. (See "Catecholaminergic polymorphic ventricular tachycardia".) This evaluation should include a 12-lead electrocardiogram (ECG), ambulatory ECG monitoring, echocardiogram, cardiovascular magnetic resonance imaging, and exercise stress testing. If the presence of a channelopathy (eg, Brugada syndrome, long QT syndrome) is suggested by ECG, further testing for those diseases should be performed. DIAGNOSIS https://www.uptodate.com/contents/commotio-cordis/print 4/14 7/6/23, 1:36 PM Commotio cordis - UpToDate The diagnosis of commotio cordis is based upon the presence of a witnessed blunt chest impact followed by collapse within five to eight seconds, ECG data demonstrating ventricular fibrillation (if available), absence of underlying heart disease, and no evidence (eg, imaging studies, autopsy) of myocardial trauma [12]. Thus, the diagnosis of commotio cordis cannot be established in the presence of an underlying cardiac condition or severe trauma causing myocardial contusion or rupture. (See 'Mechanism' above and "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Cardiac injury'.) MANAGEMENT Immediate resuscitation Following the identification of sudden cardiac arrest, the management of persons with commotio cordis follows the standard basic and advanced life support algorithms. In patients with commotio cordis, ventricular fibrillation (VF) is the most commonly documented arrhythmia. Management should include chest compressions with early defibrillation, as indicated in resuscitation guidelines. (See "Adult basic life support (BLS) for health care providers" and "Pediatric basic life support (BLS) for health care providers".) Postarrest care Similar to other patients who survive cardiac arrest, patients with commotio cordis require comprehensive evaluation for underlying heart disease and appropriate treatment. The approach to management of cardiac arrest is presented separately. (See 'Evaluation for heart disease' above and "Initial assessment and management of the adult post- cardiac arrest patient".) In patients who survive an episode of cardiac arrest attributed to commotio cordis and whose evaluation does not suggest an underlying cardiac etiology (eg, underlying cardiomyopathy, ion channel disorder), implantable cardioverter-defibrillator (ICD) placement is not required to prevent further episodes of commotio cordis. Other indications for ICDs are discussed separately. (See "Implantable cardioverter-defibrillators: Overview of indications, components, and functions", section on 'Indications'.) Return to athletics In individuals who survive a commotio cordis event without cardiac complications and who wish to continue athletics, the decision to return to athletics is individualized. For those who choose to resume athletics, it is prudent to adopt all available measures to reduce the risk of chest wall impact. (See 'Prevention' below.) This approach is similar to the American Heart Association/American College of Cardiology consensus statement on eligibility and disqualification recommendations for competitive https://www.uptodate.com/contents/commotio-cordis/print 5/14 7/6/23, 1:36 PM Commotio cordis - UpToDate athletes, which recommends that athletes can resume training and competition following commotio cordis if the evaluation for cardiac pathology is entirely unrevealing [12]. Our approach is based on the rarity of commotio cordis, which is unlikely to recur in an individual due to its mechanism (see 'Mechanism' above). However, there is insufficient data to determine whether certain individuals may be predisposed to commotio cordis. Rare reports of recurrent commotio cordis include: In an experimental model, a small number of animals were uniquely susceptible to chest blow induction of VF [23]. In addition, there is a case report of an individual who possibly experienced two episodes of commotio cordis [24]. PREVENTION Because many different types of blows to the chest can cause commotio cordis, there is no universal means to reliably prevent commotio cordis. For participants in activities associated with a higher risk of commotio cordis (particularly projectile sports), a combination of safety measures may reduce the risk of commotio cordis: Coaching Coaching measures should encourage athletes to turn away from oncoming projectiles (ie, baseballs, lacrosse balls) whenever possible to avoid contact to the chest [6,12]. Softer and less dense balls Softer and less dense balls should be used whenever possible. As an example, age-appropriate safety baseballs have been shown to decrease the risk of commotio cordis ( figure 2) [11,20]. Protective gear Historically, commercially available chest wall protectors did not clearly prevent commotio cordis during sports participation or in laboratory animal studies [5,22,25,26]. Many of the commotio cordis victims reported to the National Commotio Cordis Registry were wearing protective equipment at the time of their event [5]. The National Operating Committee on Standards for Athletic Equipment has a standard for chest protection, which is based on findings from an experimental animal model that may improve the efficacy of chest protective gear [27]. SOCIETY GUIDELINE LINKS https://www.uptodate.com/contents/commotio-cordis/print 6/14 7/6/23, 1:36 PM Commotio cordis - UpToDate 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 Epidemiology The exact incidence of commotio cordis remains unknown, mostly due to a lack of systematic reporting of cases. Commotio cordis is among the most common causes of sudden death during athletic participation and can also occur during non-sports-related activities (eg, impact to chest during fights). Commotio cordis is most common among young males and is typically provoked by hard projectiles and high-energy physical contact (eg, tackles during football); blows to the chest by soccer balls can also provoke commotio cordis. (See 'Epidemiology' above.) Mechanism Commotio cordis is provoked by the simultaneous occurrence of specific mechanistic elements (eg, timing, location, velocity of impact, shape and hardness of the projectile) that result in ventricular fibrillation (VF) ( figure 1 and figure 2). Thus, despite its traumatic appearance, commotio cordis is primarily an electrical event. The underlying mechanism is likely increased dispersion of ventricular repolarization caused by the blow, which may activate adenosine triphosphate (ATP)-sensitive potassium channels ( figure 1). (See 'Mechanism' above.) Prevention Because many different types of blows to the chest can cause commotio cordis, there is no universal means to reliably prevent commotio cordis. For participants in activities associated with a higher risk of commotio cordis (particularly projectile sports), coaching to avoid chest blows and softer balls and equipment may reduce the risk. Commercially available chest wall protectors may reduce the risk of commotio cordis but are not uniformly effective. (See 'Prevention' above.) Characteristic chest blow The types of chest blows that cause commotio cordis vary, but the most common scenario occurs in sports when a dense projectile (eg, baseball, lacrosse ball, hockey puck), impacts the chest wall directly over the heart and the patient collapses within seconds after the impact. (See 'Diagnosis' above.) Evaluation for heart disease Survivors of commotio cordis should undergo a comprehensive cardiac evaluation to exclude underlying heart disease such as (see https://www.uptodate.com/contents/commotio-cordis/print 7/14 7/6/23, 1:36 PM Commotio cordis - UpToDate 'Evaluation for heart disease' above and "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Diagnostic evaluation'): Hypertrophic cardiomyopathy Arrhythmogenic right ventricular dysplasia Anomalous coronary arteries Ion channel gene mutations such as the long QT syndrome and Brugada syndrome Catecholaminergic polymorphic ventricular tachycardia Diagnosis The diagnosis of commotio cordis is based upon the presence of a witnessed blunt chest impact followed by collapse within five to eight seconds, ECG data demonstrating VF (if available), absence of underlying heart disease, and no evidence (eg, imaging studies, autopsy) of myocardial trauma. Management Immediate resuscitation Following the identification of sudden cardiac arrest, the management of persons with commotio cordis follows standard basic and advanced life-support algorithms. (See "Adult basic life support (BLS) for health care providers" and "Pediatric basic life support (BLS) for health care providers".) Postarrest care Similar to other patients who survive cardiac arrest, patients with commotio cordis require comprehensive evaluation for underlying heart disease and appropriate treatment. (See 'Evaluation for heart disease' above and "Initial assessment and management of the adult post-cardiac arrest patient".) Return to athletics In individuals who survive a commotio cordis event without cardiac complications and who wish to continue athletics, the decision to return to athletics is individualized. For those who choose to resume athletics, it is prudent to adopt all available measures to reduce the risk of chest wall impact. (See 'Return to athletics' above and 'Prevention' above.) In patients who survive an episode of cardiac arrest attributed to commotio cordis and whose evaluation does not suggest an underlying cardiac etiology (eg, underlying cardiomyopathy, ion channel disorder), implantable cardioverter-defibrillator (ICD) placement is not required to prevent further episodes of commotio cordis. Other indications for ICDs are discussed separately. (See "Implantable cardioverter- defibrillators: Overview of indications, components, and functions", section on 'Indications'.) https://www.uptodate.com/contents/commotio-cordis/print 8/14 7/6/23, 1:36 PM Commotio cordis - UpToDate Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Maron BJ, Doerer JJ, Haas TS, et al. Historical observation on commotio cordis. Heart Rhythm 2006; 3:605. 2. Maron BJ. Sudden death in young athletes. N Engl J Med 2003; 349:1064. 3. Maron BJ, Link MS. Don't Forget Commotio Cordis. Am J Cardiol 2021; 156:134. 4. Madias C, Maron BJ, Dau N, et al. Size as an Important Determinant of Chest Blow-induced Commotio Cordis. Med Sci Sports Exerc 2018; 50:1767. 5. Maron BJ, Estes NA 3rd. Commotio cordis. N Engl J Med 2010; 362:917. 6. Link MS. Commotio cordis: ventricular fibrillation triggered by chest impact-induced abnormalities in repolarization. Circ Arrhythm Electrophysiol 2012; 5:425. 7. Maron BJ, Ahluwalia A, Haas TS, et al. Global epidemiology and demographics of commotio cordis. Heart Rhythm 2011; 8:1969. 8. Cooper S, Woodford NW, Maron BJ, et al. A Lethal Blow to the Chest as an Underdiagnosed Cause of Sudden Death in United Kingdom Sports (Football, Cricket, Rugby). Am J Cardiol 2019; 124:808. 9. Maron BJ, Haas TS, Ahluwalia A, et al. Increasing survival rate from commotio cordis. Heart Rhythm 2013; 10:219. 10. Egger F, Scharhag J, K stner A, et al. FIFA Sudden Death Registry (FIFA-SDR): a prospective, observational study of sudden death in worldwide football from 2014 to 2018. Br J Sports Med 2022; 56:80. 11. 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. 12. Link MS, Estes NA 3rd, Maron BJ, American Heart Association Electrocardiography and Arrhythmias Committee of Council on Clinical Cardiology, Council on Cardiovascular Disease in Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and American College of Cardiology. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 13: Commotio Cordis: A Scientific Statement From the American Heart Association and American College of Cardiology. Circulation 2015; 132:e339. 13. Bode F, Franz MR, Wilke I, et al. Ventricular fibrillation induced by stretch pulse: implications for sudden death due to commotio cordis. J Cardiovasc Electrophysiol 2006; 17:1011. https://www.uptodate.com/contents/commotio-cordis/print 9/14 7/6/23, 1:36 PM Commotio cordis - UpToDate 14. 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. 15. Garan AR, Maron BJ, Wang PJ, et al. Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis). J Cardiovasc Electrophysiol 2005; 16:433. 16. Stout CW, Maron BJ, Vanderbrink BA, et al. Importance of the autonomic nervous system in an experimental model of commotio cordis. Med Sci Monit 2007; 13:BR11. 17. Madias C, Maron BJ, Weinstock J, et al. Commotio cordis sudden cardiac death with chest wall impact. J Cardiovasc Electrophysiol 2007; 18:115. 18. 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. 19. Link MS, Maron BJ, Wang PJ, et al. Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis). J Am Coll Cardiol 2003; 41:99. 20. Link MS, Maron BJ, Wang PJ, et al. Reduced risk of sudden death from chest wall blows (commotio cordis) with safety baseballs. Pediatrics 2002; 109:873. 21. Kalin J, Madias C, Alsheikh-Ali AA, Link MS. Reduced diameter spheres increases the risk of chest blow-induced ventricular fibrillation (commotio cordis). Heart Rhythm 2011; 8:1578. 22. Doerer JJ, Haas TS, Estes NA 3rd, et al. Evaluation of chest barriers for protection against sudden death due to commotio cordis. Am J Cardiol 2007; 99:857. 23. Alsheikh-Ali AA, Madias C, Supran S, Link MS. Marked variability in susceptibility to ventricular fibrillation in an experimental commotio cordis model. Circulation 2010; 122:2499. 24. Maron BJ, Link MS. Recurrent commotio cordis: D j vu. HeartRhythm Case Rep 2015; 1:249. 25. Weinstock J, Maron BJ, Song C, et al. Failure of commercially available chest wall protectors to prevent sudden cardiac death induced by chest wall blows in an experimental model of commotio cordis. Pediatrics 2006; 117:e656. 26. Drewniak EI, Spenciner DB, Crisco JJ. Mechanical properties of chest protectors and the likelihood of ventricular fibrillation due to commotio cordis. J Appl Biomech 2007; 23:282. 27. McCalley E, Dau N, Kumar KR, et al. Development and Validation of a Mechanical Surrogate to Assess the Ability of Chest Protectors to Prevent Commotio Cordis, Sudden Cardiac Death With Chest Wall Impact. Circulation 2016; 134:A17799. https://www.uptodate.com/contents/commotio-cordis/print 10/14 7/6/23, 1:36 PM Commotio cordis - UpToDate Topic 15853 Version 20.0 https://www.uptodate.com/contents/commotio-cordis/print 11/14 7/6/23, 1:36 PM Commotio cordis - UpToDate GRAPHICS Mechanisms of commotio cordis From: Link MS, Estes NA. Athletes and arrhythmis. J Cardiovasc Electrophysiol 2010; 21:1184. Copyright 2010. Reproduced with permission of John Wiley & Sons, Inc. Graphic 52268 Version 2.0 https://www.uptodate.com/contents/commotio-cordis/print 12/14 7/6/23, 1:36 PM Commotio cordis - UpToDate Chest wall trauma causes ventricular fibrillation Differences in the frequency with which ventricular fibrillation resulted from chest-wall impact at 30 miles per hour during the period of cardiac cycle vulnerable to induction of ventricular fibrillation, ie, from 30 to 15 ms before T- wave peak. p<0.03 for the differences between regulation baseball and very soft baseball. p<0.01 for the differences between wooden object and each type of baseball. Data from: 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. Graphic 61105 Version 5.0 https://www.uptodate.com/contents/commotio-cordis/print 13/14 7/6/23, 1:36 PM Commotio cordis - UpToDate Contributor Disclosures Christopher Madias, MD No relevant financial relationship(s) with ineligible companies to disclose. Peter J Zimetbaum, MD Consultant/Advisory Boards: Abbott Medical [Lead extraction]. All of the relevant financial relationships listed have been mitigated. Mark S Link, MD No relevant financial relationship(s) with ineligible companies to disclose. Todd F Dardas, MD, MS No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. 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