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Commotio Cordis Ventricular Fibrillation Triggered by Chest Impact-Induced Abnormalities in Repolarization
... Moreover, the utilization of safety baseballs or tballs, particularly for younger children, represents an additional preventive measure. These balls, being softer and more flexible than standard baseballs, reduce the likelihood of causing significant chest trauma, thereby contributing to injury prevention during athletic activities [15]. ...
... In CC survivors with an idiopathic cardiac etiology, the routine use of ICD for primary transient does not necessarily indicate an underlying arrhythmogenic substrate [15][16]. As a result, ICD implantation in such cases may not offer significant benefit, rather it may expose patients to unnecessary risks that accompany device implantation and management. ...
... As a result, ICD implantation in such cases may not offer significant benefit, rather it may expose patients to unnecessary risks that accompany device implantation and management. While ICDs are not routinely implanted in CC with unknown cardiac cause, a case-by-case basis in patients with documented underlying cardiac abnormalities that increase the risk of SCA may be utilized [15][16]. The decision for ICD implantation in such cases should be made meticulously, balancing the potential benefits against the risks and considering the individual patient's clinical profile and preferences. ...
Ventricular fibrillation (VF) is a life-threatening cardiac arrhythmia characterized by asynchronous and disorganized contractions of the ventricular myocardium, leading to circulatory collapse, and if untreated, death. We present a case of a 30-year-old male who presented with VF following a soccer ball impact, revealing concurrent hypertrophic cardiomyopathy (HCM) and commotio cordis (CC). While both conditions have different mechanisms of action behind VF, management strategies for both encompass lifestyle adjustments, pharmacotherapy, and potential septal reduction procedures. Preventive measures such as safety protocols, implantable cardioverter-defibrillator (ICD) placement, and cardiopulmonary resuscitation (CPR) education are crucial. Overall, managing VF amid the complex interplay of HCM and CC emphasizes the need for tailored, multidisciplinary strategies to optimize patient outcomes.
... C ommotio cordis is a rare and often fatal arrythmia secondary to a blunt nonpenetrating impact over the precordium in the absence of direct structural damage to the heart itself. [1][2][3] Although the precise incidence of commotio cordis remains undetermined, data from the U.S. Commotio Cordis Registry suggest victims are predominantly young and male. 1 Most cases of commotio cordis have been recorded in competitive and recreational sports where it has been suggested to be the second most common cause of death in young athletes. 2 Sudden cardiac death in young athletes is a devastating event, and much of the review literature, experimental studies, and recommendations surrounding commotio cordis have understandably focused on sport-related events. ...
... In sport, this has been partially attributed to higher participation rates in projectile sports among older children and adolescents. 3 The same is likely true in non-sport-related events, considering assaults and MVAs favor younger demographics, 30,31 as would also be expected in "daily events" such as falls and play- Commotio Cordis in Non-Sport-Related Events non-sport-related events affect a wider age demographic outside of the typical child to adolescent demographic associated with sport-related commotio cordis. Future efforts to raise public awareness should be targeted at all age groups. ...
... Genetic sex-related differences in ion channels, sex hormone modification of ion channels, 3 ...
... in commotio cordis and similarities/differences to VF recurrence as a result of CC. The experiments described for CC also bear some similarity to the phenomenon of commotio cordis, in which a blunt impact to the chest causes sudden death in the absence of any previously known cardiac damage (Link, 2012). In commotio cordis, the position(s) of the blunt force impact in humans on the chest (e.g. as a result of a baseball/softball, ice hockey puck, lacrosse ball or knee) and a cross-sectional view of the heart position within the chest with respect to the impact are shown in Fig. 4A (Link, 2012;Quinn & Kohl, 2021). ...
... The experiments described for CC also bear some similarity to the phenomenon of commotio cordis, in which a blunt impact to the chest causes sudden death in the absence of any previously known cardiac damage (Link, 2012). In commotio cordis, the position(s) of the blunt force impact in humans on the chest (e.g. as a result of a baseball/softball, ice hockey puck, lacrosse ball or knee) and a cross-sectional view of the heart position within the chest with respect to the impact are shown in Fig. 4A (Link, 2012;Quinn & Kohl, 2021). The area of impact encompasses the regions where CC are typically administered during CPR in cardiac arrest. ...
... The area of impact encompasses the regions where CC are typically administered during CPR in cardiac arrest. Mechanistic studies using experimental and computational models have shed light on how commotio cordis can potentially trigger VF. Figure 4B shows a global endocardial electrical activation map obtained from in vivo studies carried out in a pig model of commotio cordis (ball hitting the chest of a pig) (Alsheikh-Ali et al., 2008) and highlights the nature of the arrhythmia trigger, which could be a depolarization-induced focal activity and/or a triggered afterdepolarization (Link, 2012;Quinn & Kohl, 2021). A similar pattern has also been reproduced in in vitro studies, where a mechanically-induced stimulation has been shown to elicit electrical activation in an isolated rabbit heart mapped optically (Quinn et al., 2017) (Fig. 4C). ...
Defibrillation remains the optimal therapy for terminating ventricular fibrillation (VF) in out‐of‐hospital cardiac arrest (OHCA) patients, with reported shock success rates of ∼90%. A key persistent challenge, however, is the high rate of VF recurrence (∼50–80%) seen during post‐shock cardiopulmonary resuscitation (CPR). Studies have shown that the incidence and time spent in recurrent VF are negatively associated with neurologically‐intact survival. Recurrent VF also results in the administration of extra shocks at escalating energy levels, which can cause cardiac dysfunction. Unfortunately, the mechanisms underlying recurrent VF remain poorly understood. In particular, the role of chest‐compressions (CC) administered during CPR in mediating recurrent VF remains controversial. In this review, we first summarize the available clinical evidence for refibrillation occurring during CPR in OHCA patients, including the postulated contribution of CC and non‐CC related pathways. Next, we examine experimental studies highlighting how CC can re‐induce VF via direct mechano‐electric feedback. We postulate the ionic mechanisms involved by comparison with similar phenomena seen in commotio cordis. Subsequently, the hypothesized contribution of partial cardiac reperfusion (either as a result of CC or CC independent organized rhythm) in re‐initiating VF in a globally ischaemic heart is examined. An overview of the proposed ionic mechanisms contributing to VF recurrence in OHCA during CPR from a cellular level to the whole heart is outlined. Possible therapeutic implications of the proposed mechanistic theories for VF recurrence in OHCA are briefly discussed. image
... It has been identified as one of the common causes of sudden cardiac death especially in young athletes [2]. Since its establishment in the mid-1990s, National Commotio Cordis Registry has published over 200 confirmed cases of CC [2,22]. The increase in number is attributed to more awareness, hence more reporting rather than increase in the actual incidence of the disease. ...
... Sudden death due to CC is primarily an electrical event, with VF occurring shortly after chest wall impact [22,23]. The two most important variables in the development of VF in cases of CC are a blow directly over the precordium and the timing of chest wall impact within the cardiac cycle [22,24]. ...
... Sudden death due to CC is primarily an electrical event, with VF occurring shortly after chest wall impact [22,23]. The two most important variables in the development of VF in cases of CC are a blow directly over the precordium and the timing of chest wall impact within the cardiac cycle [22,24]. Chest impact occurring during a 10 -20 ms window on the upslope of the T-wave before it reaches its peak has been described as the period when the myocardium is repolarizing and is most susceptible to ventricular arrhythmia development [2,24]. ...
Takotsubo cardiomyopathy (TCM), also known as stress cardiomyopathy or "broken heart syndrome", is characterized by acute transient regional left ventricular systolic dysfunction in the absence of obstructive coronary artery disease or acute plaque rupture. Atypical forms and rare anatomical variants can have different presentations; hence, recognition becomes more important. Prognosis is much more favorable if managed appropriately. An equally infrequent cause of cardiac arrest is commotio cordis (CC). This is defined as sudden cardiac death secondary to a blunt chest wall impact leading to ventricular arrhythmias. We report a case with findings of TCM and/or CC in a patient with a blunt chest trauma in the setting of motor vehicle accident.
... Commotio cordis is defined as sudden cardiac arrest secondary to blunt, nonpenetrating trauma to the chest wall. An important distinction between commotio cordis and cardiac contusion is that commotio cordis is due to blunt chest wall trauma that does not cause structural cardiac damage but instead leads to an electrical event [1,2]. ...
... The most frequent arrhythmia occurring with commotio cordis is ventricular fibrillation (VF), however polymorphic ventricular tachycardia and heart block have also been reported [1]. Higher energy impacts directly over the precordium are more likely to cause VF with ST segment elevation mediated by an increase in potassium current across the cell membrane via potassium ATP channel [3][4][5][6][7]. ...
... The mean age of individuals affected by this condition is 14 years old, with 78% < 18 years of age. The most frequently affected athletes are those participating in baseball, softball, hockey, and lacrosse [1,4]. We present a case of a 33-year-old male who suffered a blow to the chest while playing soccer that led to VF arrest and was subsequently found to have cardiomyopathy. ...
Background
Commotio cordis is an event in which a blunt, non-penetrating blow to the chest occurs, triggering a life-threatening arrhythmia and often sudden death. This phenomenon is often seen in young, male athletes and has become increasingly well-known over the past few decades. We present a unique case in which ventricular fibrillation occurs in an older male athlete after blunt trauma.
Case presentation
Patient with no known medical history was brought to the ER after being found unconscious after a soccer ball kick to the chest. He was found to be in ventricular fibrillation and successfully resuscitated on the soccer field. Patient was admitted to the hospital and lab workup and initial imaging were unremarkable, except elevated troponin and lactate, which returned to normal levels. An echocardiogram showed global left ventricular systolic dysfunction with a visually estimated ejection fraction of 45–50%. Coronary showed angiographically nonobstructive coronary arteries. The patient was diagnosed with commotio cordis and discharged from the hospital in stable condition. Follow-up echocardiogram continued to show low ejection fraction and event monitor demonstrated frequent polymorphic ventricular tachycardia with periods of asystole.
Conclusion
This case is unique in that blunt trauma to the chest from a soccer ball immediately triggered ventricular fibrillation in a patient with a possible cardiomyopathy. It is possible that the blunt trauma caused primary commotio cordis that led to cardiomyopathy in a previous healthy man, or that an underlying cardiomyopathy made it more likely for this to occur. Overall, increased awareness and prevention efforts of blunt chest trauma are required to reduce the high mortality associated life-threatening arrhythmias. There is limited data regarding the interplay between these two entities.
... In swine, ventricular fibrillation could be induced by mechanical impact delivered in the period of 40-1 ms before the peak of the Twave [Link (2003;2012)]. During this period, the authors reported a clear increase in impact-induced arrhythmia, even though impacts during the QRS or ST segment could occasionally cause nonsustained ventricular tachycardia. ...
... In the present study, only models with E SAC less than or equal to −40 mV, representing a considerable contribution from SAC K , gave rise to reentry due to early repolarization. The vulnerability window for these reentries were near or coinciding with the QRS complex, whereas experimental evidence has typically pointed to the T-wave as the most vulnerable period for arrhythmia Quinn and Kohl, 2011;Link, 2012). ...
Background
The electrophysiological mechanism connecting mitral valve prolapse (MVP), premature ventricular complexes and life-threatening ventricular arrhythmia is unknown. A common hypothesis is that stretch activated channels (SACs) play a significant role. SACs can trigger depolarizations or shorten repolarization times in response to myocardial stretch. Through these mechanisms, pathological traction of the papillary muscle (PM), as has been observed in patients with MVP, may induce irregular electrical activity and result in reentrant arrhythmia.
Methods
Based on a patient with MVP and mitral annulus disjunction, we modeled the effect of excessive PM traction in a detailed medical image-derived ventricular model by activating SACs in the PM insertion region. By systematically varying the onset of SAC activation following sinus pacing, we identified vulnerability windows for reentry with 1 ms resolution. We explored how reentry was affected by the SAC reversal potential ( E SAC ) and the size of the region with simulated stretch (SAC region). Finally, the effect of global or focal fibrosis, modeled as reduction in tissue conductivity or mesh splitting (fibrotic microstructure), was investigated.
Results
In models with healthy tissue or fibrosis modeled solely as CV slowing, we observed two vulnerable periods of reentry: For E SAC of −10 and −30 mV, SAC activated during the T-wave could cause depolarization of the SAC region which lead to reentry. For E SAC of −40 and −70 mV, SAC activated during the QRS complex could result in early repolarization of the SAC region and subsequent reentry. In models with fibrotic microstructure in the SAC region, we observed micro-reentries and a larger variability in which times of SAC activation triggered reentry. In these models, 86% of reentries were triggered during the QRS complex or T-wave. We only observed reentry for sufficiently large SAC regions ( > = 8 mm radius in models with healthy tissue).
Conclusion
Stretch of the PM insertion region following sinus activation may initiate ventricular reentry in patients with MVP, with or without fibrosis. Depending on the SAC reversal potential and timing of stretch, reentry may be triggered by ectopy due to SAC-induced depolarizations or by early repolarization within the SAC region.
... As of July 2012, there were 216 cases of CC in the NCCR, with all cases meeting the following inclusion criteria: (1) a witnessed blunt, nonpenetrating blow to the precordium followed immediately by cardiovascular collapse, (2) detailed documentation of events, (3) no evidence of structural damage to the heart on autopsy in nonsurvivors, and (4) absence of underlying cardiovascular abnormalities [6]. Approximately 10-20 cases have historically been reported to the NCCR each year [11,17]. Over the last few years, there has been a decline in the number of reported cases to the NCCR, which may be due to a decrease in the incidence of these events and/or a reduction in the number of sporting events in the setting of the COVID-19 pandemic [18]. ...
... In the swine model, impacts occurring only during a narrow (15 ms) window of ventricular repolarization (the upstroke of the T wave, which accounts for only 1% of the cardiac cycle duration) resulted in VF [32]. A six-lead electrocardiogram showing the electrocardiographic change from sinus rhythm to VF following impact in the swine model is seen in Figure 2 of reference 17 (not published here due to copyright) [17]. During this narrow interval of the swine cardiac cycle, there was increased The percentages shown reflect reported cases described in references [6,11,12,16,23,24] heterogeneity of repolarization across the myocardium, and any incidence of premature ventricular depolarization in this brief time period could lead directly to VF [31]. ...
Since the nationally televised cardiac arrest of American National Football League player Damar Hamlin in January 2023, commotio cordis has come to the forefront of public attention. Commotio cordis is defined as sudden cardiac arrest due to direct trauma to the precordium resulting in ventricular fibrillation or ventricular tachycardia. While the precise incidence of commotio cordis is not known due to a lack of standardized, mandated reporting, it is the third most common cause of sudden cardiac death in young athletes, with more than 75% of cases occurring during organized and recreational sporting events. Given that survival is closely tied to how quickly victims receive cardiopulmonary resuscitation and defibrillation, it is crucial to raise awareness of commotio cordis so that athletic trainers, coaches, team physicians, and emergency medical personnel can rapidly diagnose and treat this often-fatal condition. Broader distribution of automated external defibrillators in sporting facilities as well as increased presence of medical personnel during sporting events would also likely lead to higher survival rates.
... An analysis of the US Commotio Cordis Registry revealed a 95% male predominance [8]. The male preponderance has been postulated to be related to the participation of males in sports in which commotio cordis occurs, but it is also speculated that there may be some sex-related as well as genetic susceptibility, as the number of women participating in competitive sports has increased without a change in the condition's incidence among them [9]. The mechanisms of injury include motor vehicle accidents, traumatic falls, explosions, and projectile impacts during sporting activities such as baseball, football, and lacrosse [10]. ...
... This phenomenon arises due to sudden high-energy, blunt impact to the chest wall, evoking fatal arrhythmia resulting in SCD. Ventricular fibrillation is known to be the most frequent arrhythmia associated with commotio cordis, but studies have also reported polymorphic ventricular tachycardia, heart block, and atrial fibrillation [9,21]. ...
Sudden cardiac death (SCD) is one of the leading causes of cardiovascular mortality, and it is caused by a diverse array of conditions. Among these is commotio cordis, a relatively infrequent but still significant cause, often seen in young athletes involved in competitive or recreational sports. It is known to be caused by blunt trauma to the chest wall resulting in life-threatening arrhythmia (typically ventricular fibrillation). The current understanding pertains to blunt trauma to the precordium, with an outcome depending on factors such as the type of stimulus, the force of impact, the qualities of the projectile (shape, size, and density), the site of impact, and the timing of impact in relation to the cardiac cycle.
In the management of commotio cordis, a history of preceding blunt chest trauma is usually encountered. Imaging is mostly unremarkable except for ECG, which may show malignant ventricular arrhythmias. Treatment is focused on emergent resuscitation with the advanced cardiac life support protocol algorithm, with extensive workup following the return of spontaneous circulation. In the absence of underlying cardiovascular pathologies, implantable cardiac defibrillator insertion is not beneficial, and patients can even resume physical activity if the workup is unremarkable. Proper follow-up is also key in the management and monitoring of re-entrant ventricular arrhythmias, which are amenable to ablative therapy. Prevention of this condition involves protecting the chest wall against blunt trauma, especially with the use of safety balls and chest protectors in certain high-risk sporting activities.
This study aims to elucidate the current epidemiology and clinical management of SCD with a particular focus on a rarely explored etiology, commotio cordis.
... Defined as a cardiac concussion, commotio cordis shows no signs of structural damage to the heart post-impact (Maron et al. 1995;Pearce 2005). According to the US Commotio Cordis Registry (USCCR) in Minneapolis, there are currently over 200 confirmed cases worldwide (Maron and Estes 2010;Link 2012). Although the occurrence rate of commotio cordis is low, most cases are fatal (Drewniak et al. 2007). ...
... With reference to impact location, our most damaging case depicts an impact over the cardiac silhouette, specifically over the center and base of the LV ( Figure 5B). Previous studies have identified in swine models that baseball impacts over the LV induce VF during the repolarization phase of the cardiac cycle (Link et al. 2001;Garan et al. 2005;Link 2012). Most interestingly, the same study that identified which velocities were most likely to induce VF, reported that it occurred mostly with blows directly over the center of the cardiac silhouette (30% of impacts) compared to those over the LV base (13%) or apex (4%) from a swine model (Madias et al. 2007). ...
Commotio cordis is a sudden death mechanism that occurs when the heart is impacted during the repolarization phase of the cardiac cycle. This study aimed to investigate commotio cordis injury metrics by correlating chest force and rib deformation to left ventricle strain and pressure. We simulated 128 chest impacts using a simulation matrix which included two initial velocities, 16 impact locations spread across the transverse and sagittal plane, and four baseball stiffness levels. Results showed that an initial velocity of 17.88 m/s and an impact location over the left ventricle was the most damaging setting across all possible settings, causing the most considerable left ventricle strain and pressure increases. The impact force metric did not correlate with left ventricle strain and pressure, while rib deformations located over the left ventricle were strongly correlated to left ventricle strain and pressure. These results lead us to the recommendation of exploring new injury metrics such as the rib deformations we have highlighted for future commotio cordis safety regulations.
... Commotio cordis («сотрясение сердца», «волнение сердца», «возбуждение сердца») -феномен, характеризующийся жизнеугрожающими нарушениями ритма, в частности, ФЖ, чаще всего приводящей к ВСС, вызванной тупым, непроникающим ударом в прекардиальную область без повреждения костной структуры грудной клетки или сердца (при отсутствии другого кардиоваскулярного заболевания) [19][20]. Желудочковые нарушения ритма, включая желудочковую тахикардию (ЖТ) и ФЖ являются редкими осложнениями ЗТС. ...
Trauma remains a leading global cause of mortality, particularly in the young population. Cardiac damage is a predictor for poor outcome after multiple traumas, with a poor prognosis and prolonged in-hospitalization. Cardiac injury encompasses a spectrum of pathologies ranging from clinically silent, transient arrhythmias to deadly cardiac wall rupture. Of diagnosed cardiac injuries cardiac contusion (blunt cardiac injury) and commotio cordis are most common. Timely diagnosis of this category of victims is a key aspect of successful treatment and emergency care both at the pre-hospital stage and in a specialized medical institution. This narrative review focuses on the main types, etiopathology, as well as classification of cardiac trauma. It explains the main histopathological difference between blunt cardiac injury and myocardial infarction.
... Удар найчастіше наноситься тупим предметом, таким як м'яч, кулак, лікоть або Рис. 6. ЕКГ пацієнта із синдромом Вольфа-Паркінсона-Вайта [33] шолом. Бейсбол -вид спорту з найвищою частотою випадків Commotio cordis [28]. ...
Deaths of children during physical education classes occur every year not only in Ukraine but also around the world, and these are always events that receive wide publicity. According to the Centers for Disease Control and Prevention (CDC), every year in the United States, about 2,000 young, apparently healthy people under the age of 25 die from sudden cardiac arrest. Aim - to analyze the causes of sudden cardiac arrest (SCA) in children and adolescents during physical activities and to identify the main ways to prevention of SCA, providing family physicians with practical and relevant information on the strategy of screening, assessment and management of the risk of developing SCA in children during physical activities. Primary care physicians (PCPs), who see patients from infancy to adolescence and have a long-term relationship with the child and family play a key role in preventing sudden cardiac arrest in children. They conduct a medical examination and Rufier test for all children before they enter school and determine the group of activities for physical education classes to prevent these tragic events. The authors declare that they have no conflict of interest.
... To choose the best course of therapy for the disease, a precise diagnosis of the condition is necessary. An electrocardiogram (ECG) may be performed by a healthcare practitioner to evaluate the cardiac rhythm of a patient and spot any irregularities, such as PR prolongation [7]. ...
An injury inflicted by a blunt object, such as a car, a fist, or a bat, is referred to as blunt trauma. Usually, it causes tissue damage and discomfort. It also has the tendency to fracture bones. Blunt trauma can happen to the chest, head, abdomen, limbs, and other regions of the body. Lacerations (cuts), concussions (brain injuries), contusions (bruises), fractures (broken bones), and internal injuries are examples of blunt trauma injuries. The location of the trauma, the impact's force, and the victim's general health all got affected according to the severity of the damage. Blunt trauma to the chest can result in cardiac arrest or the abrupt blockage of the heart's pumping activity. Because the heart is a muscular organ, it needs oxygen to beat continuously. Blunt chest trauma can stop the heart from beating because of a lack of oxygen or blood supply, or because the heart muscle has been physically harmed. Pulmonary contusions (bruising of the lung tissue), rib fractures, injury to the heart or blood vessels, and other injuries caused by blunt trauma can result in cardiac arrest.
... 45 There were only 2 cases of commotio cordis over the 20-year time period, although cases are thought to occur more frequently in pediatric athletes given a more compliant chest wall and participation in sports with a firm projectile. 46 Limitations This study has several limitations that warrant discussion. First, there is no mandatory reporting system throughout the United States, so it is possible that cases of SCD may have been missed, which would make incidence rates higher than reported. ...
Background: The incidence and causes of sudden cardiac death (SCD) among young competitive athletes impact prevention strategies yet remain incompletely understood.
Methods: National Collegiate Athletic Association (NCAA) athlete deaths from 7/1/2002-6/30/2022 were identified through 4 independent databases/search strategies. Autopsy reports and medical history were reviewed by an expert panel to adjudicate causes of SCD. Poisson regression was used to calculate incidence rate ratios (IRR) for 5-year intervals over the 20-year study.
Results: A total of 143 SCD cases were identified among 1102 athlete deaths and 9,106,516 athlete-years (AYs). The incidence of SCD among NCAA athletes was 1:63,682 AYs [95% CI 1:54,065, 1:75,010]. Incidence was higher in males compared to females (1:43,348 vs. 1:164,504 AYs) and Black compared to White athletes (1:27,217 vs. 1:74,581 AYs). The highest incidence of SCD was among Division 1 male basketball players (1:8,188; White 1:5,848; Black 1:7,696 AYs). The incidence rate for SCD decreased over the study period (5-year IRR 0.71 [95% CI 0.61,0.82]), whereas the rate of non-cardiovascular deaths remained stable (5-year IRR 0.98 [95% CI 0.94,1.04]; Figure 1A ). Autopsy-negative sudden unexplained death (AN-SUD, 19.5%) was the most common post-mortem exam finding, followed by idiopathic left ventricular hypertrophy/possible cardiomyopathy (CM, 16.9%) and hypertrophic CM (12.7%) in cases with enough information for adjudication (118/143, Figure 1B ). There were 8 cases of myocarditis, with none attributed to COVID-19 infection. SCD events occurred most commonly during exertion among athletes with coronary artery anomalies (100%) and arrhythmogenic CM (83%), whereas AN-SUD and hypertrophic CM had a higher proportion of non-exertional SCD (44% and 40%, respectively).
Conclusions: The incidence of SCD in college athletes has decreased. Male sex, Black race, and basketball are associated with a higher incidence of SCD.
... 45 There were only 2 cases of commotio cordis over the 20-year time period, although cases are thought to occur more frequently in pediatric athletes given a more compliant chest wall and participation in sports with a firm projectile. 46 Limitations This study has several limitations that warrant discussion. First, there is no mandatory reporting system throughout the United States, so it is possible that cases of SCD may have been missed, which would make incidence rates higher than reported. ...
Background: Understanding the incidence, causes, and trends of sudden cardiac death (SCD) among young competitive athletes is critical to inform preventive policies.
Methods: This study included National Collegiate Athletic Association athlete deaths during a 20-year time frame (July 1, 2002, through June 30, 2022). Athlete deaths were identified through 4 separate independent databases and search strategies (National Collegiate Athletic Association resolutions list, Parent Heart Watch database and media reports, National Center for Catastrophic Sports Injury Research database, and insurance claims). Autopsy reports and medical history were reviewed by an expert panel to adjudicate causes of SCD.
Results: A total of 143 SCD cases in National Collegiate Athletic Association athletes were identified from 1102 total deaths. The National Collegiate Athletic Association resolutions list identified 117 of 143 (82%), the Parent Heart Watch database or media reports identified 89 of 143 (62%), the National Center for Catastrophic Sports Injury Research database identified 63 of 143 (44%), and insurance claims identified 27 of 143 (19%) SCD cases. The overall incidence of SCD was 1:63682 athlete-years (95% CI, 1:54065–1:75010). Incidence was higher in male athletes than in female athletes (1:43348 [95% CI, 1:36228–1:51867] versus 1:164504 [95% CI, 1:110552–1:244787] athlete-years, respectively) and Black athletes compared with White athletes (1:26704 [1:20417–1:34925] versus 1:74581 [1:60247–1:92326] athlete-years, respectively). The highest incidence of SCD was among Division I male basketball players (1:8188 [White, 1:5848; Black, 1:7696 athlete-years]). The incidence rate for SCD decreased over the study period (5-year incidence rate ratio, 0.71 [95% CI, 0.61–0.82]), whereas the rate of noncardiovascular deaths remained stable (5-year incidence rate ratio, 0.98 [95% CI, 0.94–1.04]). Autopsy-negative sudden unexplained death (19.5%) was the most common postmortem examination finding, followed by idiopathic left ventricular hypertrophy or possible cardiomyopathy (16.9%) and hypertrophic cardiomyopathy (12.7%), in cases with enough information for adjudication (118 of 143). Eight cases of death were attributable to myocarditis over the study period (1 case from January 1, 2020, through June 30, 2022), with none attributed to COVID-19 infection. SCD events were exertional in 50% of cases. Exertional SCD was more common among those with coronary artery anomalies (100%) and arrhythmogenic cardiomyopathy (83%).
Conclusions: The incidence of SCD in college athletes has decreased. Male sex, Black race, and basketball are associated with a higher incidence of SCD.
... Treatment options for Commotio cordis are limited and involve foremost defibrillation. Using porcine model studies [26,32], a series of conditions were established that must be met simultaneously for Commotio cordis to ensue: (i) the impact occurs over or near the cardiac silhouette, (ii) the impact speed ranges from 30 to 50-mph, and (iii), the impact occurs during the so-called vulnerable window of cardiac excitation which denotes the time interval of 30 to 10 ms before the peak of the T-wave [23]. These findings in pigs were reproduced by 2D and 3D simulation studies that showed impacts causing Commotio cordis to be a function of both the time in the cardiac electrical cycle and the impact location [12,22]. ...
Commotio cordis is one of the leading causes of sudden cardiac death in youth baseball. Currently, there are chest protector regulations regarding the prevention of Commotio cordis in baseball and lacrosse; however, they are not fully optimized. For the advancement of Commotio cordis safety, it is vital to include various age groups and a variety of impact angles in the testing process. This study employed finite element models and simulated Commotio cordis-inducing baseball collisions for different velocities, impact angles, and age groups. Commotio cordis risk response was characterized in terms of left ventricular strain and pressure, chest band and rib deformation, and force from impact. Normalized rib and chest band deformation when correlated with left ventricular strain resulted in R2 = 0.72, and R2 = 0.76, while left ventricular pressure resulted in R2 = 0.77, R2 = 0.68 across all velocities and impact angles in the child models. By contrast, the resultant reaction force risk metric as used by the National Operating Committee on Standards for Athletic Equipment (NOCSAE) demonstrated a correlation of R2 = 0.20 in the child models to ventricular strain, while illustrating a correlation to pressure of R2 = 0.74. When exploring future revisions to Commotio cordis safety requirements, the inclusion of deformation-related risk metrics at the level of the left ventricle should be considered.
... 21 Extreme stimuli, such as commotio cordis and electrocution, can also initiate VF in the normal heart. 22,23 Our study suggests that for some patients with idiopathic VF and no further events during the follow up period, their substrate assessment (at least by standard methods and V-CoS) is within the normal range. It is possible that these patients have no underlying myocardial abnormalities and were the victims of a rare external initiating stimulus. ...
Background
Idiopathic ventricular fibrillation (VF) is a diagnosis of exclusion following normal cardiac investigations. We sought to determine if exercise‐induced changes in electrical substrate could distinguish patient groups with various ventricular arrhythmic pathophysiological conditions and identify patients susceptible to VF.
Methods and Results
Computed tomography and exercise testing in patients wearing a 252‐electrode vest were combined to determine ventricular conduction stability between rest and peak exercise, as previously described. Using ventricular conduction stability, conduction heterogeneity in idiopathic VF survivors (n=14) was compared with those surviving VF during acute ischemia with preserved ventricular function following full revascularization (n=10), patients with benign ventricular ectopy (n=11), and patients with normal hearts, no arrhythmic history, and negative Ajmaline challenge during Brugada family screening (Brugada syndrome relatives; n=11). Activation patterns in normal subjects (Brugada syndrome relatives) are preserved following exercise, with mean ventricular conduction stability of 99.2±0.9%. Increased heterogeneity of activation occurred in the idiopathic VF survivors (ventricular conduction stability: 96.9±2.3%) compared with the other groups combined (versus 98.8±1.6%; P =0.001). All groups demonstrated periodic variation in activation heterogeneity (frequency, 0.3–1 Hz), but magnitude was greater in idiopathic VF survivors than Brugada syndrome relatives or patients with ventricular ectopy (7.6±4.1%, 2.9±2.9%, and 2.8±1.2%, respectively). The cause of this periodicity is unknown and was not replicable by introducing exercise‐induced noise at comparable frequencies.
Conclusions
In normal subjects, ventricular activation patterns change little with exercise. In contrast, patients with susceptibility to VF experience activation heterogeneity following exercise that requires further investigation as a testable manifestation of underlying myocardial abnormalities otherwise silent during routine testing.
... assessed 01/18/2023). 10,21,23 Commotio cordis is caused by a low-energy, blunt-force trauma to the chest that initiates cardiac arrest, and affected individuals may not survive without timely cardiopulmonary resuscitation and defibrillation. Commotio cordis is likely under-reported with ~20 to 30 cases a year, but the incidence started to increase in the late 1990s due to awareness from high profile review articles. ...
... In the current study, traffic accidents were the most frequent kind of trauma in the cases that were included (76.5 percent), falling from height in 21 cases (13.7%), and assault in 15 cases (9.8%). This agreed with Link (13) , who demonstrated that high-speed car collisions were the most common reported cause of blunt chest injuries, followed by falls from a height or 6683 instances involving crushing. Also, in accordance with our results, Emet et al. (14) showed that motor vehicle accidents (MVAs) and falls from a height were the most frequent causes of trauma (71 percent each), with other causes accounting for the remainder of the cases (6 percent). ...
... Low-energy, nonpenetrating impacts to the chest, such as those found in children's baseball games, may lead to incidences of commotio cordis [2]. Identified as the second leading cause of sudden cardiac death in youth athletes [3], this rare sudden death mechanism is a result of the heart going into ventricular fibrillation due to the combination of multiple variables: impact speed (30-50 mph), impact location (impacts over the precordium), and timing of impact relative to the cardiac cycle (repolarization phase during the upslope of the T-wave) [3,4]. ...
Commotio cordis is the second leading cause of sudden cardiac death in young athletes. Currently available chest protectors on the market are ineffective in preventing cases of commotio cordis in young athletes that play baseball. This study focused on using contour maps to identify specific baseball impact locations to the chest that may result in instances of commotio cordis to children during baseball games. By identifying these vulnerable locations, we may design and develop chest protectors that can provide maximum protection to prevent commotio cordis in young athletes. Simulation cases were run using the validated CHARM-10 chest model, a detailed finite element model representing an average 10-year-old child's chest. A baseball model was developed in company with the chest model, and then used to impact the chest at different locations. An 7x8 impact location matrix was designed with 56 unique baseball impact simulations. Left ventricle strain and pressure, reaction force between the baseball and chest, and rib deformations were analyzed. Left ventricle strain was highest from baseball impacts directly over the left ventricle (0.34) as well as impacts slightly lateral and superior to the cardiac silhouette (0.34). Left ventricle pressure was highest with impacts directly over the left ventricle (82.94 kPa). We have identified the most dangerous impact locations resulting in high left ventricle strain and pressure. This novel study provided evidence of where to emphasize protective materials for establishing effective chest protectors that will minimize instances of commotio cordis in young athletes.
... Still, other variables like speed, location of impact, shape, and hardness of the impact structure are relevant contributors based on animal models. 4 For example, impact energy superior to 50 joules will likely cause structural damage (contusio cordis). It is questionable if there is a component of individual susceptibility that might be modulated by gender, chest wall pliability, or genetics. ...
... [8] Deduced from histologic studies, resultant microhemorrhages, inflammatory infilt- rate with subsequent cardiac cell necrosis, and interstitial edema may contribute to cell injury. [9] The inflammation surrounding the vessels and potential intravascular rouleaux formation may also lead to local microvascular cardiac ischemia. [6] Additionally, the trauma force may start a reflex catecholamine surge that can further induce a tachyarrhythmia. ...
BACKGROUND
The heart’s mechanical state feeds back to its electrical activity, potentially contributing to arrhythmias. Mechano-arrhythmogenesis has been mechanistically explained during electrical diastole, when cardiomyocytes are at their resting membrane potential. During electrical systole, cardiomyocytes are refractory right after the onset of depolarization, while during repolarization in physiological conditions, they seem to be protected from systolic mechano-arrhythmogenesis by near-simultaneous restoration of resting membrane potential and cytosolic calcium concentration ([Ca ²⁺ ] i ): repolarization-relaxation coupling (RRC). Yet, late-systolic mechano-arrhythmogenesis has been reported in ischemic myocardium, with unclear underlying mechanisms. We hypothesize that ischemia-induced alteration of RRC gives rise to a vulnerable period for mechano-arrhythmogenesis.
METHODS
Acute left ventricular regional ischemia was induced by coronary artery ligation in Langendorff-perfused rabbit hearts, with mechanical load controlled by an intraventricular balloon. Mechanical activity was assessed by echocardiography and arrhythmia incidence by ECG. Single left ventricular cardiomyocytes were exposed to simulated ischemia or pinacidil (ATP-sensitive potassium channel opener). Stretch was applied in diastole or late systole using carbon fibers. Stretch characteristics and arrhythmia incidence were assessed by sarcomere length measurement. In both models, RRC was assessed by simultaneous voltage-[Ca ²⁺ ] i fluorescence imaging and mechano-arrhythmogenesis mechanisms were pharmacologically tested.
RESULTS
In whole hearts, acute regional ischemia leads to systolic stretch and disturbed RRC at the ischemic border. These electro-mechanical changes were associated with waves of arrhythmias, which could be reduced by mechanical unloading, electro-mechanical uncoupling, or buffering of [Ca ²⁺ ] i . In left ventricular cardiomyocytes, physiological RRC is associated with a low incidence of systolic mechano-arrhythmogenesis, while a vulnerable period emerged by prolonged RRC during ischemia. The increase in systolic mechano-arrhythmogenesis was reduced by restoring RRC, chelating [Ca ²⁺ ] i , blocking mechano-sensitive TRPA1 (transient receptor potential ankyrin 1) channels, or buffering reactive oxygen species levels.
CONCLUSIONS
Prolonged RRC allows for late-systolic mechano-arrhythmogenesis in acute ischemia, involving contributions of elevated [Ca ²⁺ ] i , TRPA1 activity, and reactive oxygen species, which represent potential antiarrhythmic targets.
Collaborators
Larry A. Allen, MD, MHS, FAHA, FACC; Mats Börjesson, MD, PhD, FACC; Alan C. Braverman, MD, FACC; Julie A. Brothers, MD; Silvia Castelletti, MD, MSc, FESC; Eugene H. Chung, MD, MPH, FHRS, FAHA, FACC; Timothy W. Churchill, MD, FACC; Guido Claessen, MD, PhD; Flavio D’Ascenzi, MD, PhD; Douglas Darden, MD; Peter N. Dean, MD, FACC; Neal W. Dickert, MD, PhD, FACC; Jonathan A. Drezner, MD; Katherine E. Economy, MD, MPH; Thijs M.H. Eijsvogels, PhD; Michael S. Emery, MD, MS, FACC; Susan P. Etheridge, MD, FHRS, FAHA, FACC; Sabiha Gati, BSc (Hons), MBBS, PhD, MRCP, FESC; Belinda Gray, BSc (Med), MBBS, PhD; Martin Halle, MD; Kimberly G. Harmon, MD; Jeffrey J. Hsu, MD, PhD, FAHA, FACC; Richard J. Kovacs, MD, FAHA, MACC; Sheela Krishnan, MD, FACC; Mark S. Link, MD, FHRS, FAHA, FACC; Martin Maron, MD; Silvana Molossi, MD, PhD, FACC; Antonio Pelliccia, MD; Jack C. Salerno, MD, FACC, FHRS; Ankit B. Shah, MD, MPH, FACC; Sanjay Sharma, BSc (Hons), MBChB, MRCP (UK), MD; Tamanna K. Singh, MD, FACC; Katie M. Stewart, NP, MS; Paul D. Thompson, MD, FAHA, FACC; Meagan M. Wasfy, MD, MPH, FACC; Matthias Wilhelm, MD
This American Heart Association/American College of Cardiology scientific statement on clinical considerations for competitive sports participation for athletes with cardiovascular abnormalities or diseases is organized into 11 distinct sections focused on sports-specific topics or disease processes that are relevant when considering the potential risks of adverse cardiovascular events, including sudden cardiac arrest, during competitive sports participation. Task forces comprising international experts in sports cardiology and the respective topics covered were assigned to each section and prepared specific clinical considerations tables for practitioners to reference. Comprehensive literature review and an emphasis on shared decision-making were integral in the writing of all clinical considerations presented.
BACKGROUND
Motorcycle and equestrian accidents can share similar trauma mechanisms and can result in serious injuries.
OBJECTIVE
This study aims to analyze variations in injuries and safety standards through types, severity, and outcomes of traumatic injuries in both motorcycle and equestrian riders.
METHODS
Using the 2020 ACS TQIP database, we split patients into two groups based on their primary injury. We chose codes V28 and V80.0 to identify non-collision fall or throw injuries for motorcycle and equestrian accidents respectively. A total of 17,730 motorcycle and 5,461 equestrian patients were identified.
RESULTS
Motorcyclists were more likely to experience external/superficial injuries (41.34% vs. 29.08%, p < .001) and chest trauma (5.15% vs. 3.18%, p < .001), while equestrian trauma resulted in more injuries to the abdomen and pelvic content (24.07% vs. 15.75%, p < .001), extremities and pelvic girdle (9.85% vs. 4.98%, p < .001), and head/neck (15.57% vs. 12.16%, p < .001) comparatively. Motorcyclists also had a higher average length of inpatient stay (6.06 (8.03) vs. 4.32 (4.23) days, p < .001). Helmet use was more common among motorcyclists than horseback riders (57.79% vs. 24.24%, p < .001). The average injury severity score between the two groups was not significantly different.
CONCLUSION
These data show the different injuries observed between both activities and the need for increased safety equipment, especially in the case of hip and pelvic injuries among equestrians. The low rate of helmet, especially among equestrian riders, is concerning despite broad education regarding their benefits.
Introduction
Commotio cordis is a rare event that occurs following blunt, non-penetrating trauma to the chest, precipitating a ventricular arrhythmia. Commotio cordis requires immediate medical attention through cardiopulmonary resuscitation and defibrillation, often resulting in death. Commotio cordis is most common condition among young male athletes. The purpose of this study was to describe the incidents and patterns of commotio cordis among young athletes participating in organised sports in the USA from academic years 1982-1983 through 2022-2023.
Methods
This was a retrospective, descriptive epidemiology study using surveillance data from the National Center for Catastrophic Sport Injury Research. The study included all commotio cordis incidents captured in the database. We calculated descriptive statistics (counts and proportions) overall and stratified by outcome and athlete sport.
Results
Over the study period, 64 incidents of commotio cordis were captured. The majority occurred among males (n=60) and were caused by contact with an object/apparatus (n=39) or contact with another player (n=20). The most common sports were baseball (n=20), lacrosse (n=17) and football (n=13). Over half of these incidents resulted in death (n=34), although survival from commotio cordis increased over the study period. A higher proportion of fatal incidents occurred among football athletes and were caused by contact with another player.
Conclusions
Commotio cordis remains most common among young male athletes who participate in organised baseball, lacrosse and football. Although survival has improved over time, greater awareness and emergency preparedness for commotio cordis in an organised sport are needed to facilitate prompt recognition and intervention.
BACKGROUND
Commotio cordis, sudden cardiac death (SCD) caused by relatively innocent impact to the chest, is one of the leading causes of SCD in sports. Commercial chest protectors have not been demonstrated to mitigate the risk of these SCDs.
METHODS
To develop a standard to assess chest protectors, 4 phases occurred. A physiological commotio cordis model was utilized to assess variables that predicted for SCD. Next, a surrogate model was developed based on data from the physiological model, and the attenuation in risk was assessed. In the third phase, this model was calibrated and validated. Finally, National Operating Committee on Standards for Athletic Equipment adopted the standard and had an open review process with revision of the standard over 3 years.
RESULTS
Of all variables, impact force was the most robust at predicting SCD. Chest wall protectors which could reduce the force of impact to under thresholds were predicted to reduce the risk of SCD. The correlation between the experimental model and the mechanical surrogate ranged from 0.783 with a lacrosse ball at 30 mph to 0.898 with a baseball at 50 mph. The standard was licensed to National Operating Committee on Standards for Athletic Equipment which initially adopted the standard in January 2018, and finalized in July 2021.
CONCLUSIONS
An effective mechanical surrogate based on physiological data from a well-established model of commotio cordis predicts the reduction in SCD with chest protectors. A greater reduction in force provides a great degree of protection from commotio cordis. This new National Operating Committee on Standards for Athletic Equipment standard for chest protectors should result in a significant reduction in the risk of commotio cordis on the playing field.
The complexity of cardiac electrophysiology, involving dynamic changes in numerous components across multiple spatial (from ion channel to organ) and temporal (from milliseconds to days) scales makes an intuitive or empirical analysis of cardiac arrhythmogenesis challenging. Multiscale mechanistic computational models of cardiac electrophysiology provide precise control over individual parameters, and their reproducibility enables a thorough assessment of arrhythmia mechanisms. This review provides a comprehensive analysis of models of cardiac electrophysiology and arrhythmias. from the single cell to the organ level, and how they can be leveraged to better understand rhythm disorders in cardiac disease and to improve heart patient care. Key issues related to model development based on experimental data are discussed and major families of human cardiomyocyte models and their applications are highlighted. An overview of organ-level computational modeling of cardiac electrophysiology and its clinical applications in personalized arrhythmia risk assessment and patient-specific therapy of atrial and ventricular arrhythmias is provided. The advancements presented here highlight how patient-specific computational models of the heart reconstructed from patient clinical data have achieved success in predicting risk of sudden cardiac death and guiding optimal treatments of heart rhythm disorders. Finally, an outlook towards potential future advances, including the combination of mechanistic modeling and machine learning / artificial intelligence, is provided. As the field of cardiology is embarking on a journey towards precision medicine, personalized modeling of the heart is expected to become a key technology to guide pharmaceutical therapy, deployment of devices, and surgical interventions.
The wooden club (clava) is rarely associated with the image of Roman soldiers, perhaps because it was considered an unconventional weapon with ethnic attributes and/or specific combat roles. Nonetheless, it is attested in the archaeological record and some ancient texts. The panoply and the military career of the soldiers represented on the tombstones of Catavignus son of Ivomagus (1st century AD) and Marcus Aurelius Alexis (early 3rd century AD) offered us the possibility to reconsider the use of the club as an offensive weapon within the Imperial Roman army. The authors made a replica of the clava using historical tools and manufacturing techniques. A series of tests have then been performed to investigate the use of the club in combat. The possible traumas on human targets were also evaluated with a forensic anthropological approach. The results suggest the essential role of flexion and rotation of the kinetic chain «hip/shoulder/ arm» in wielding the clava. This movement requires a much more mobile combat style that can prove very effective against heavily armoured targets due to the weapon's high-impact force and a more extended reach than more conventional Roman sidearms.
This chapter outlines pertinent embryology, anatomy, physiology, diagnosis and treatment of traumatic injuries.KeywordsBlunt traumaPenetrating traumaShock
Background:
Commotio cordis is an increasingly recognized cause of sudden cardiac death. Although commonly linked with athletes, many events occur in non-sport-related settings.
Objectives:
The goal of this study was to characterize and compare non-sport-related vs sport-related commotio cordis.
Methods:
PubMed and Embase were searched for all cases of commotio cordis from inception to January 5, 2022.
Results:
Of 334 commotio cordis cases identified, 121 (36%) occurred in non-sport-related contexts, which included assault (76%), motor vehicle accidents (7%), and daily activities (16%). Projectiles were implicated significantly less in non-sport-related events (5% vs 94%, respectively; P < 0.001). Nonprojectile etiologies in non-sport-related events mostly consisted of impacts with body parts (79%). Both categories affected similar younger aged demographic (P = 0.10). The proportion of female victims was significantly higher in non-sport-related events (13% vs 2%, respectively; P = 0.025). Mortality was significantly higher in non-sport-related events (88% vs 66%, respectively; P < 0.001). In non-sport-related events, rates of cardiopulmonary resuscitation (27% vs 97%, respectively; P < 0.001) and defibrillation (17% vs 81%, respectively; P < 0.001) were both lower and resuscitation was more commonly delayed beyond 3 min (80% vs 5%, respectively; P < 0.001).
Conclusions:
Commotio cordis occurs across a spectrum of non-sport-related settings including assault, motor vehicle accidents, and daily activities. Both categories affected a younger and male-predominant demographic. Mortality is higher in non-sport-related commotio cordis, likely owing to lower rates of cardiopulmonary resuscitation, defibrillation, automated external defibrillator availability, and extended time to resuscitation. Increased awareness of non-sport-related commotio cordis is essential to develop a means of prevention and mortality reduction, with earlier recognition and prompt resuscitation measures.
Background: Men’s and women’s lacrosse operate with significantly different rules, equipment, and contact. Previous studies have assessed injury rates (IRs) in either men’s or women’s lacrosse, but a few studies have compared injury patterns in the National Collegiate Athletic Association (NCAA) men’s and women’s lacrosse. Purpose: We sought to examine whether there were differences in injury type, mechanism, setting, and time loss in men and women playing lacrosse in the NCAA. Methods: We performed a retrospective case-control study using data collected by the NCAA Injury Surveillance Program (ISP) during a 10-season period (2004–2005 to 2013–2014). The data were assessed for potential differences in injuries between male and female lacrosse players and analyzed to obtain descriptive statistics through calculations of rates, percentages, and confidence intervals (CIs). Main outcomes measured were IRs per 1000 athletic exposures (AEs) and injury rate ratios (IRRs) with 95% CIs. Results: The IRs were 5.19 per 1000 AEs in women’s lacrosse and 6.52 per 1000 AEs in men’s lacrosse. Men had more injuries overall than women in competitions and practices and in preseason, regular season, and postseason play. Preseason IRs were higher than the regular season, and competition injuries were greater than practice injuries in both sexes. Women had more injuries to the head/face, knee, lower leg, and foot. Sprains, strains, concussions, and contusions were the most common types of injuries in both sexes. Overuse/gradual onset, cartilage, concussion, inflammation, and tendinosis injuries were more common in women than men. Injuries in men resulted in time loss more often than injuries in women. Conclusions: Our retrospective study’s findings suggest that there were differences in injury patterns between men’s and women’s lacrosse. Future prospective research should assess whether these disparities are due to differences in equipment and rules and whether changes to these factors can reduce injuries.
Shock is a life-threatening condition of circulatory failure leading to inadequate organ perfusion and tissue oxygenation. In a trauma patient, shock may be due to hypovolemia, cardiogenic, obstructive or distributive causes individually or in combination. The physiological response to major hemorrhage is dependent on a variety of autonomic reflexes, mechanism of injury, bleeding source, and baseline physiology of the patient. This article discusses the common causes of shock and the accompanying physiology, how clinical assessment can support the diagnosis and effective treatment of shock, and the common pitfalls in trauma patients.
Introduction
Albeit described since 1763, cardiac contusions is still an under-recognised clinical condition in the acute care setting. This evidence-based review aims to provide an overview of the topic by focusing on etiopathogenesis, classification and clinical presentation of patients with cardiac contusions, as well as on the diagnostic work-up and therapy options available for this subset population in the acute care setting.
Methods
A targeted research strategy was performed using PubMed, MEDLINE, Embase and Cochrane Central databases up to June 2022. The literature search was conducted using the following keywords (in Title and/or Abstract): (“cardiac” OR “heart” OR “myocardial”) AND (“contusion”). All available high-quality resources written in English and containing information on epidemiology, etiopathogenesis, clinical findings, diagnosis and management of cardiac contusions were included in our research.
Results
Biochemical samples of cardiac troponins together with a 12‑lead ECG appear to be sufficient screening tools in hemodynamically stable subjects, while cardiac ultrasound provides a further diagnostic clue for patients with hemodynamic instability or those more likely to have a significant cardiac contusion.
Conclusions
The management of patients with suspected cardiac contusion remains a challenge in clinical practice. For this kind of patients a comprehensive diagnostic approach and a prompt emergency response are required, taking into consideration the degree of severity and clinical impairment of associated traumatic injuries.
Specific body systems have focused examinations. In this article the cardiovascular history and assessment is discussed. Building on from the previous article – Clinical History Taking, this article will guide the reader into the requirements of how to assess a patient with a cardiovascular presentation, how to clinically focus when presented with the multitude of possibilities and what information is required to establish a differential diagnosis. History taking and clinical examination is discussed in detail to allow the reader to develop their assessment skills to an advanced practice level.
The review describes a rarely occurring state of commotio cordis (CC) — ventricular fibrillation (VF), associated with unintentional blunt impact on the anterior thoracic wall in the absence of structural damage to the heart. The development of VF is based on the coincidence of the time of a closed breast trauma with a vulnerable period during early repolarization (the so-called "vulnerability window"). More often, death occurs instantly or in the coming minutes of a post-traumatic period. CC is more common in male adolescents and seems to be the second leading cause of sudden death in young athletes. It is possible to save the victim with cardiorespiratory resuscitation or defibrillation only in 25–28 % of cases. High mortality is explained by the fact that victims often do not have time to receive immediate medical care. It is necessary to inform the population, medical community and athletes about importance to avoid hitting the heart. As a preventive measure in some sports, chest protectors are used. Information about the potential danger of blows to the heart area should be provided to the attention of athletes involved, since even an unintentional mild blow can provoke a life-threatening arrhythmia. Having access to defibrillators at sporting events, teaching people to use them and to realize the cardio-pulmonary resuscitation measures can improve the survival of the CC victims.
Traumatic injuries can and often do lead to cardiac arrest. While many injury patterns can lead to this final pathway, the treatment and outcomes for this condition vary greatly depending on the cause. This chapter considers medical and surgical causes of cardiac arrest in trauma and discusses how they should be managed with reference to the MABCD approach employed elsewhere in this textbook. The indications for and conduct of resuscitative thoracotomy are explored, and an overview of some of the forensic aspects that may come into play are discussed.
Blunt cardiac injury (BCI), defined as injury to the heart from blunt force trauma, ranges from minor to life-threatening. The majority of BCIs are due to motor vehicle accidents; however, injuries caused by falls, blasts, and sports-related injuries can also be sources of BCI. A significant proportion of patients with BCI do not survive long enough to receive medical care, succumbing to their injuries at the scene of the accident. Additionally, patients with blunt trauma often have coexisting injuries (brain, spine, orthopedic) that can obscure the clinical picture; therefore, a high degree of suspicion is often required to diagnose BCI. Traditionally, hemodynamically stable injuries suspicious for BCI have been evaluated with electrocardiograms and chest radiographs, whereas hemodynamically unstable BCIs have received operative intervention. More recently, computed tomography and echocardiography have been increasingly utilized to identify injuries more rapidly in hemodynamically unstable patients. Transesophageal echocardiography can play an important role in the diagnosis and management of several BCIs that require operative repair. Close communication with the surgical team and access to blood products for potentially massive transfusion also play key roles in maintaining hemodynamic stability. With proper surgical and anesthetic care, survival in cases involving urgent cardiac repair can reach 66%-75%. This narrative review focuses on the types of cardiac injuries that are caused by blunt chest trauma, the modalities and techniques currently used to diagnose BCI, and the perioperative management of injuries that require surgical correction.
The overall incidence of sudden cardiac death is considerably lower among women than men, reflecting significant and often under-recognized sex differences. Women are older at time of sudden cardiac death, less likely to have a prior cardiac diagnosis, and less likely to have coronary artery disease identified on postmortem examination. They are more likely to experience their death at home, during sleep, and less likely witnessed. Women are also more likely to present in pulseless electrical activity or systole rather than ventricular fibrillation or ventricular tachycardia. Conversely, women are less likely to receive bystander cardiopulmonary resuscitation or receive cardiac intervention post-arrest. Underpinning sex disparities in sudden cardiac death is a paucity of women recruited to clinical trials, coupled with an overall lack of prespecified sex-disaggregated evidence. Thus, predominantly male-derived data form the basis of clinical guidelines. This review outlines the critical sex differences concerning epidemiology, cause, risk factors, prevention, and outcomes. We propose 4 broad areas of importance to consider: physiological, personal, community, and professional factors.
There are multiple conditions that can make children prone to having a sudden cardiac arrest (SCA) or sudden cardiac death (SCD). Efforts have been made by multiple organizations to screen children for cardiac conditions, but the emphasis has been on screening before athletic competition. This article is an update of the previous American Academy of Pediatrics policy statement of 2012 that addresses prevention of SCA and SCD. This update includes a comprehensive review of conditions that should prompt more attention and cardiology evaluation. The role of the primary care provider is of paramount importance in the evaluation of children, particularly as they enter middle school or junior high. There is discussion about whether screening should find any cardiac condition or just those that are associated with SCA and SCD. This update reviews the 4 main screening questions that are recommended, not just for athletes, but for all children. There is also discussion about how to handle post-SCA and SCD situations as well as discussion about genetic testing. It is the goal of this policy statement update to provide the primary care provider more assistance in how to screen for life-threatening conditions, regardless of athletic status.
Sudden cardiac arrest in an athlete is often attributable to physical activity that is, paradoxically, endured to enhance the strength and survivability of the athlete. This paradox beckons a more comprehensive collective understanding of the impact exercise imparts on health. While rare, sudden cardiac arrest and subsequent sudden cardiac death present within several subsets of athletes. This chapter reviews the incidence and known leading causes of sudden cardiac death among athletes. With worldwide consensus among experts remaining elusive, this chapter concisely summarizes all available data on the efficacy of pre-competition screening aimed to identify at-risk athletes to prevent the occurrence of sudden cardiac arrest/death. Beyond detection, management strategies for prompt resolution of these cardiac events, such as the implementation of emergency response system protocols and the use of automated external defibrillators, will similarly be reviewed and summarized herein.
Although optimizing sleep with the goal of optimizing athletic performance is gaining support among the athletic community, sleep and its disorders remain under-recognized and underappreciated. This is critically important as athletic performance is impaired by the presence of inadequate sleep and untreated sleep disorders. Athletes are uniquely at a higher risk for certain sleep disorders such as obstructive sleep apnea, including those in collision sports where athletes with larger body mass and neck size have a distinct advantage.
Commotio cordis is one of the leading causes of sudden cardiac death in young athletes. In commotio cordis, blunt, non-penetrating chest trauma triggers ventricular fibrillation that leads to sudden cardiac death. Victims are predominantly young adolescent males involved in sports. In order to induce sudden cardiac death, the blow must be delivered in a narrow 20 msec window during cardiac repolarization. Additional factors such as location of the impact, velocity, shape, and firmness of the object alter the probability of inducing ventricular fibrillation. On a cellular level, the chest wall impact during a vulnerable time window triggers activation of a mechanosensitive KATP⁺ channel and leads to inhomogeneous depolarization, thereby creating an arrhythmogenic substrate. Treatment involves timely delivery of high-quality cardiopulmonary resuscitation. The outcome of resuscitation in commotio cordis is similar to other forms of sudden cardiac death, with better results seen in early use of a defibrillator (within 3 minutes) after the event. Commercially available chest barriers have not shown to be effective in preventing commotio cordis. A biomechanical surrogate is now available to access the ability of chest wall protectors to lower the risk of commotio cordis.
Abnormalities in heart rhythm continue to cause high rates of illness and death. Better treatment could be provided by solving two main challenges: the early identification of patients who are at risk, and the characterization of molecular pathways that culminate in arrhythmias. By analysing mechanisms that increase susceptibility to arrhythmia in individuals with genetic syndromes, it might be possible to improve current therapies and to develop new ways to treat and prevent common arrhythmias.
Objectives
In an animal model of commotio cordis, sudden death with chest-wall impact, we sought to systematically evaluate the importance of impact velocity in the generation of ventricular fibrillation (VF) with baseball chest-wall impact.Background
Sudden cardiac death can occur with chest-wall blows in recreational and competitive sports (commotio cordis). Analyses of clinical events suggest that the energy of impact is often not of unusual force, although this has been difficult to quantify.Methods
Juvenile swine (8 to 25 kg) were anesthetized, placed prone in a sling to receive chest-wall strikes during the vulnerable time window during repolarization for initiation of VF with a baseball propelled at 20 to 70 mph.ResultsImpacts at 20 mph did not induce VF; incidence of VF increased incrementally from 7% with 25 mph impacts, to 68% with chest impact at 40 mph, and then diminished at ≥50 mph (p < 0.0001). Peak left ventricular pressure generated by the chest blow was related to the incidence of VF in a similar Gaussian relationship (p < 0.0001).Conclusions
The energy of impact is an important variable in the generation of VF with chest-wall impacts. Impacts at 40 mph were more likely to produce VF than impacts with greater or lesser velocities, suggesting that the predilection for commotio cordis is related in a complex manner to the precise velocity of chest-wall impact.
Objectives:
We performed a meta-analysis of prognostic studies of patients with a Brugada ECG to assess predictors of events.
Background:
The Brugada syndrome is an increasingly recognized cause of idiopathic ventricular fibrillation; however, there is wide variation in the prognosis of patients with the Brugada ECG.
Methods and results:
We retrieved 30 prospective studies of patients with the Brugada ECG, accumulating data on 1,545 patients. Summary estimates of the relative risk (RR) of events (sudden cardiac death [SCD], syncope, or internal defibrillator shock) for a variety of potential predictors were made using a random-effects model. The overall event rate at an average of 32 months follow-up was 10.0% (95% CI 8.5%, 11.5%). The RR of an event was increased (P < 0.001) among patients with a history of syncope or SCD (RR 3.24 [95% CI 2.13, 4.93]), men compared with women (RR 3.47 [95% CI 1.58, 7.63]), and patients with a spontaneous compared with sodium-channel blocker induced Type I Brugada ECG (RR 4.65 [95% CI 2.25, 9.58]). The RR of events was not significantly increased in patients with a family history of SCD (P = 0.97) or a mutation of the SCN5A gene (P = 0.18). The RR of events was also not significantly increased in patients inducible compared with noninducible by electrophysiologic study (EPS) (RR 1.88 [95% CI 0.62, 5.73], P = 0.27); however, there was significant heterogeneity of the studies included.
Conclusions:
Our findings suggest that a history of syncope or SCD, the presence of a spontaneous Type I Brugada ECG, and male gender predict a more malignant natural history. Our findings do not support the use of a family history of SCD, the presence of an SCN5A gene mutation, or EPS to guide the management of patients with a Brugada ECG.
The commotio cordis literature has largely focused on events occurring in the United States. However, with enhanced public awareness, commotio cordis has been increasingly recognized internationally as a cause of cardiac arrest and sudden death due to blunt nonpenetrating chest blows.
This study sought to characterize the demographics of commotio cordis globally in comparison to the U.S. experience.
This study used interrogation of the Commotio Cordis Registry (Minneapolis, Minnesota).
We report 60 cases of commotio cordis occurring outside the United States from 19 countries (most commonly the United Kingdom and Canada) on 5 continents and compared these events to 2:3 occuring in the U.S. In the 2 groups, events were largely similar demographically, including frequency of survival (26% in U.S. vs 25%; P = .84), and the striking male predominance evident in both groups (i.e., 95%), although non-U.S. victims were somewhat older (19 ± 13 vs 15 ± 9; P = .002). Not unexpectedly, the groups differed with baseball/softball and football predominant in the United States (55% of events) and soccer, cricket, and hockey most common internationally (47% of events). Notably, the frequency with which soccer participation caused commotio cordis was much more common than expected, particularly in non-U.S. athletes (20% vs 3% U.S.; P < .001).
Commotio cordis demonstrates a global occurrence, very similar demographically in the United States and internationally. However, the frequency with which chest blows from soccer balls caused commotio cordis events (particularly during sports played internationally) seems to contradict the prevailing notion that air-filled projectiles convey less risk for ventricular fibrillation than do those with solid cores (e.g., baseball or lacrosse balls).
Sudden death due to low-energy blunt trauma to the precordium (commotio cordis) has been described with a variety of sporting objects. However, the risk of ventricular fibrillation (VF) relative to the shape of the impact object is not known.
The objective of the current experiment is to test whether the impact object shape is a clinical variable that affects the risk for commotio cordis.
In a juvenile swine model, impacts were given in random order with two different spherical shapes (72 mm diameter, equivalent to a baseball; 42 mm diameter, equivalent to a golf ball) and a flat round object 72 mm in diameter. Objects were equal in weight (150 g), thrown at 30 mph, and gated to the vulnerable portion of the cardiac cycle.
Sixteen swine received 144 impacts. The flat object did not cause VF (P = .01 compared with the two spherical objects), nonsustained VF, ST elevation, or bundle branch block. The smaller diameter sphere caused VF in nine of 48 impacts (19%), and the larger diameter sphere caused VF in five of 48 impacts (10%; P = .25). The smaller diameter sphere was associated with a greater increase in left ventricular pressure (P <.0001 and P = .001 compared with larger sphere only) and a higher likelihood of ST segment elevations (P <.001 and P = .08 compared with larger sphere only) and bundle branch block (Fisher's exact P = .008, and Fisher's exact P = .18 compared with larger sphere only).
The shape of the projectile markedly influences the risk of VF from chest wall impact. This effect is likely mediated via a greater increase in left ventricular pressure with smaller diameter objects. Spreading the impact force over a larger area may decrease the risk of sudden death and has implications for the design of protective athletic equipment.
Precordial blows in sports and daily activities can trigger ventricular fibrillation (VF) (commotio cordis). Whereas chest wall blows are common, commotio cordis is rare. Although factors such as timing, location, orientation, and energy of impact are critically important, we also hypothesize that there is individual susceptibility to commotio cordis. Using our model of commotio cordis, we evaluated individual animal susceptibility to VF induction and assessed animal characteristics that might be involved.
This retrospective analysis included 139 juvenile swine (weight, 8 to 54 kg) that were anesthetized and placed prone in a sling to receive chest wall strikes with a ball propelled at 30 to 40 mph. Each animal received a minimum of 4 impacts directly over the cardiac silhouette, all timed to a narrow vulnerable window during cardiac repolarization. Of 1274 total impacts, 360 impacts (28%) resulted in VF. There was wide variability in individual animal susceptibility to VF. In 38 animals, none of the impacts resulted in VF (range, 4 to 18 impacts per animal). The majority of animals (91; 65%) were induced into VF with <30% of the strikes. In fact, only 19 animals (14%) had >50% occurrence of VF with chest wall impacts, and only 7 (5%) had >80% occurrence of chest impacts that induced VF. In the animal-based analysis, individual correlates of VF included animal weight, mean impact velocity, mean left ventricular pressure generated by the blow, mean QRS duration, mean QTc, and QTc variability. In multivariable analysis, mean left ventricular pressure generated by the blow, mean QRS duration, and QTc variability remained significant correlates of risk, and number of impacts gained statistical significance such that animals with more impacts were less susceptible to VF.
Swine display a wide range of individual vulnerability to VF triggered by chest wall impact, with a distinct minority being uniquely susceptible. Mild abnormalities in cardiac depolarization and repolarization might underlie this susceptibility. Such individual susceptibility may also be present in humans and contribute to the rarity of commotio cordis.
Athletes are thought the healthiest segment of the population. Yet, there is a general appearance that athletes are more prone to sudden cardiac death and arrhythmias than nonathletes. Bradycardias in athletes are nearly universal, but advanced heart block is usually pathologic. Athletes may be more prone to atrial fibrillation, but not likely to other types of supraventricular tachycardias. Sudden cardiac death in athletes is rare in the absence of heart disease, with the exception of commotio cordis. Treatment strategies for athletes are focused for the return to athletics. Guidelines for treatment will be derived from the 36th Bethesda Guidelines for athletes, and the European Society of Cardiology (ESC) guidelines for athletes.
In the past decade, the general public and the medical community have become more aware of commotio cordis as an important cause of sudden death. Commotio cordis occurs in otherwise healthy and active young people, typically during recreational and competitive sports but in some cases even during normal daily activities. A variety of experimental models indicate that if delivered at a particular moment in the cardiac cycle, even innocent-appearing precordial blows can trigger ventricular fibrillation and result in fatal commotio cordis events. Further efforts are needed to prevent these largely avoidable deaths by providing more education, better-designed athletic equipment (e.g., effective chest-wall protectors), and wider access to AEDs at organized athletic events. These strategies should result in a safer sports environment for our youth.
Athletic field risks associated with blunt, nonpenetrating chest blows (commotio cordis) are receiving increasing attention, but the epidemiology of these events is incomplete.
We assessed our Sudden Death in Young Athletes Registry, 1980-2008, to formulate a clinical profile of those sudden deaths attributed to commotio cordis (and other causes) occurring in competitive lacrosse, the most rapidly growing youth sport in the United States.
Twenty-three sudden deaths or cardiac arrests were identified in high school and college lacrosse participants. Ages were 18 +/- 2 years; each athlete was male. Ten died after blunt precordial blows, including 4 goalies wearing commercially available chest protectors. Twelve others collapsed because of presumed or documented cardiovascular disease, including hypertrophic cardiomyopathy, long QT syndrome, mitral valve prolapse, or ruptured cerebral aneurysm. The mortality rate associated with lacrosse was 1.46 deaths per 100,000 person-years and was similar to that of other sports including baseball, basketball, football, and hockey. However, deaths attributed to commotio cordis were more frequent in lacrosse (0.63 deaths per 100,000 person-years) than in other sports (P < .02), with the exception of hockey.
Sudden deaths in competitive lacrosse participants are rare and no more common than in most other sports. These catastrophic events were caused disproportionately by commotio cordis and included athletes wearing chest barriers, thereby underscoring the importance of developing effective chest protection to create a safer athletic environment for our youth.
Sudden death from cardiac arrest in a young person may occur during sports play after a blunt blow to the chest in the absence of structural cardiovascular disease or traumatic injury (cardiac concussion or commotio cordis). We studied the clinical features of this apparently uncommon but important phenomenon.
We identified cases from the registries of relevant agencies and organizations, as well as newsmedia accounts, and developed a clinical profile of 25 children and young adults, 3 to 19 years of age.
Each victim collapsed with cardiac arrest immediately after an unexpected blow to the chest, which was usually inflicted by a projectile (such as a baseball or hockey puck). Incidents took place during organized competitive sports in 16 cases and in recreational settings at home, at school, or on the playground in 9. In each instance, the impact to the chest was not judged to be extraordinary for the sport involved and did not appear to have sufficient force to cause death. Twelve victims collapsed virtually instantaneously on impact, whereas 13 remained conscious and physically active for a brief time before cardiac arrest. Cardiopulmonary resuscitation was administered within about three minutes to 19 victims, but normal cardiac rhythm could be restored in only 2 (both incurred irreversible brain damage and died shortly thereafter). Seven victims (28 percent) were wearing some form of protective chest padding.
We speculate that most sudden deaths related to impact to the chest (not associated with traumatic injury) are due to ventricular dysrhythmia induced by an abrupt, blunt precordial blow, presumably delivered at an electrically vulnerable phase of ventricular excitability. This profile of blunt chest impact leading to cardiac arrest adds to our understanding of the range of causes of sudden death on the athletic field and may help in the development of preventive measures.
ATP-sensitive K+ channels are activated when the myocardium becomes ischemic. However, the role of the ATP-sensitive K+ current in the emergence of ECG ST changes during ischemia remained unclarified.
The left anterior descending coronary artery (LAD) was cannulated and perfused with arterial blood from the carotid artery through a bypass tube in 8 anesthetized, open-chest dogs. An array of 60 unipolar electrodes mounted on a sock was used to record epicardial electrograms of the whole heart. Pinacidil (10 micrograms.kg-1 x min-1), an ATP-sensitive K+ channel opener, was infused into the bypass tube for 2 minutes, and the electrograms were recorded before and after the infusion. The elevation of the ST segment and the increase of QRST area were observed spatially over the LAD-perfused region. At the electrode showing the largest ST segment elevation, the activation recovery interval, an index of action potential duration, was shortened from 202 +/- 9 to 111 +/- 18 milliseconds (P < .001). These electrographic changes were similar to those noted in 2-minute coronary occlusion (n = 8). The extent of ST segment elevation during coronary occlusion was attenuated after the intravenous pretreatment with glibenclamide (0.3 mg/kg), a blocker of the KATP channel (n = 5).
The findings of this study suggest that the activation of ATP-sensitive K+ channels during a bout of acute myocardial ischemia plays an important role in the emergence of ECG ST elevation.
Cell-attached and inside-out excised-patch recording techniques were used to search for mechanosensitive ion channels in neonatal and adult rat atrial myocytes. A channel activated by negative pressure applied to the patch, with a single-channel conductance of 52 pS in symmetric potassium solutions, was frequently observed. This channel has been identified as the atrial ATP-sensitive potassium (KATP) channel on the basis of its potassium selectivity, as well as its inhibition by ATP or tolbutamide in the inside-out excised patch. Mechanosensitive modulation of the KATP channel has not previously been reported. In the presence of 1 mM ATP, 10-50 microM pinacidil (a specific KATP channel agonist) does not significantly increase basal KATP channel activity; however, these concentrations of pinacidil potentiated the mechanosensitive modulation of the KATP channel. A hypotonic swelling protocol (a mechanical stimulus) was used in an effort to determine whether mechanosensitive modulation of this channel can generate significant whole-cell currents. Under perforated-patch whole-cell recording conditions, superfusion of atrial myocytes with a 240 mosm/kg solution (control solution, 290 mosm/kg) stimulated whole-cell currents with a magnitude similar to those activated by 10 microM pinacidil. These results demonstrate that the gating of the atrial KATP channel is mechanosensitive and suggest that mechanosensitive modulation may be an additional and significant mechanism, modulating channel activity under both physiological and pathological conditions.
ECG peaked T wave appears during the early phase of myocardial ischemia, but the underlying mechanisms remain unknown. The purpose of this study was to elucidate the role of ATP-sensitive K+ channel (KATP) in this ECG change.
In 12 anesthetized, open-chest dogs, the sinus node was crushed and the right atrium was paced at a cycle length of 400 ms. The left anterior descending coronary artery was abruptly occluded for 60 s before (control) and 15 min after an intravenous infusion of vehicle (n = 6) or glibenclamide (1 mg/kg, n = 6), a blocker of KATP. Forty-eight epicardial electrograms were simultaneously recorded from the anterior surface of the left ventricle. The potentials at 40, 80 and 120 ms from the J point were measured, and these points corresponded to the early, middle and late phases of the T wave, respectively.
During the control occlusion, T wave increased time-dependently and the maximal T-wave change was noted at the end of 60 s of coronary occlusion. The extents of T-wave elevation at the early, mid and late T phases were 5.5 +/- 0.5, 7.3 +/- 0.8 and 11.7 +/- 1.8 mV, respectively, and these T-wave elevations were significantly reduced by 33 +/- 21%, 59 +/- 12% and 63 +/- 13%, respectively, after the pretreatment with glibenclamide but not with its vehicle. The % reductions of mid and late T by glibenclamide were significantly larger than that of early T wave (P < 0.05).
An abrupt coronary occlusion accompanied peaked T wave as an early ECG wave change. As the extent of this T-wave elevation was attenuated by glibenclamide, the ischemia-induced alteration of ventricular repolarization can partly (60%) be explained by the modification of KATP activation.
The syndrome of sudden death due to low-energy trauma to the chest wall (commotio cordis) has been described in young sports participants, but the mechanism is unknown.
We developed a swine model of commotio cordis in which a low-energy impact to the chest wall was produced by a wooden object the size and weight of a regulation baseball. This projectile was thrust at a velocity of 30 miles per hour and was timed to the cardiac cycle.
We first studied 18 young pigs, 6 subjected to multiple chest impacts and 12 to single impacts. Of the 10 impacts occurring within the window from 30 to 15 msec before the peak of the T wave on the electrocardiogram, 9 produced ventricular fibrillation. Ventricular fibrillation was not produced by impacts at any other time during the cardiac cycle. Of the 10 impacts sustained during the QRS complex, 4 resulted in transient complete heart block. We also studied whether the use of safety baseballs, which are softer than standard ones, would reduce the risk of arrhythmia. A total of 48 additional animals sustained up to three impacts during the T-wave window of vulnerability to ventricular fibrillation with a regulation baseball and safety baseballs of three degrees of hardness. We found that the likelihood of ventricular fibrillation was proportional to the hardness of the ball, with the softest balls associated with the lowest risk (two instances of ventricular fibrillation after 26 impacts, as compared with eight instances after 23 impacts with regulation baseballs).
This experimental model of commotio cordis closely resembles the clinical profile of this catastrophic event. Whether ventricular fibrillation occurred depended on the precise timing of the impact. Safety baseballs, as compared with regulation balls, may reduce the risk of commotio cordis.
Sudden death due to relatively innocent chest-wall impact has been described in young individuals (commotio cordis). In our previously reported swine model of commotio cordis, ventricular fibrillation (with T-wave strikes) and ST-segment elevation (with QRS strikes) were produced by 30-mph baseball impacts to the precordium. Because activation of the K(+)(ATP) channel has been implicated in the pathogenesis of ST elevation and ventricular fibrillation in myocardial ischemia, we hypothesized that this channel could be responsible for the electrophysiologic findings in our experimental model and in victims of commotio cordis.
In the initial experiment, 6 juvenile swine were given 0.5 mg/kg IV glibenclamide, a selective inhibitor of the K(+)(ATP) channel, and chest impact was given on the QRS. The results of these strikes were compared with animals in which no glibenclamide was given. In the second phase, 20 swine were randomized to receive glibenclamide or a control vehicle (in a double-blind fashion), with chest impact delivered just before the T-wave peak. With QRS impacts, the maximal ST elevation was significantly less in those animals given glibenclamide (0.16+/-0.10 mV) than in controls (0.35+/-0.20 mV; P=0.004). With T-wave impacts, the animals that received glibenclamide had significantly fewer occurrences of ventricular fibrillation (1 episode in 27 impacts; 4%) than controls (6 episodes in 18 impacts; 33%; P=0.01).
In this experimental model of commotio cordis, blockade of the K(+)(ATP) channel reduced the incidence of ventricular fibrillation and the magnitude of ST-segment elevation. Therefore, selective K(+)(ATP) channel activation may be a pivotal mechanism in sudden death resulting from low-energy chest-wall trauma in young people during sporting activities.
In an experimental model of sudden death from chest wall impact (commotio cordis), we sought to define the chest wall areas important in the initiation of ventricular fibrillation (VF).
Sudden death can result from an innocent chest blow by a baseball or other projectile. Observations in humans suggest that these lethal blows occur over the precordium. However, the precise location of impact relative to the risk of sudden death is unknown.
Fifteen swine received 178 chest impacts with a regulation baseball delivered at 30 mph at three sites over the cardiac silhouette (i.e., directly over the center, base or apex of the left ventricle [LV]) and four noncardiac sites on the left and right chest wall. Chest blows were gated to the vulnerable portion of the cardiac cycle for the induction of VF.
Only chest impacts directly over the heart triggered VF (12 of 78: 15% vs. 0 of 100 for noncardiac sites: p < 0.0001). Blows over the center of the heart (7 of 23; 30%) were more likely to initiate VF than impacts at other precordial sites (5 of 55; 9%, p = 0.02). Peak LV pressures generated instantaneously by the chest impact were directly related to the risk of VF (p < 0.0006).
For nonpenetrating, low-energy chest blows to cause sudden death, impact must occur directly over the heart. Initiation of VF may be mediated by an abrupt and substantial increase in intracardiac pressure. Prevention of sudden death from chest blows during sports requires that protective equipment be designed to cover all portions of the chest wall that overlie the heart, even during body movements and positional changes that may occur with athletic activities.
In an experimental model of sudden death from baseball chest wall impact (commotio cordis), we sought to determine if sudden death by baseball impact could be reduced with safety baseballs.
Sudden cardiac death can occur after chest wall impact with a baseball (commotio cordis). Whether softer-than-standard (safety) baseballs reduce the risk of sudden death is unresolved from the available human data. In a juvenile swine model, ventricular fibrillation (VF) has been shown to be induced reproducibly by precordial impact with a 30-mph baseball 10 to 30 ms before the T-wave peak, and this likelihood was reduced with the softest safety baseballs (T-balls). To further test whether safety baseballs would reduce the risk of sudden death at velocities more relevant to youth sports competition, we used our swine model of commotio cordis to test baseballs propelled at the 40-mph velocity commonly attained in that sport.
Forty animals received up to 3 chest wall impacts at 40 mph during the vulnerable period of repolarization for VF with 1 of 3 different safety baseballs of varying hardness, and also by a standard baseball.
Safety baseballs propelled at 40 mph significantly reduced the risk for VF. The softest safety baseballs triggered VF in only 11% of impacts, compared with 19% and 22% with safety baseballs of intermediate hardness, and 69% with standard baseballs.
In this experimental model of low-energy chest wall impact, safety baseballs reduced (but did not abolish) the risk of sudden cardiac death. More universal use of these safety baseballs may decrease the risk of sudden death on the playing field for young athletes.
Cardiac arrest due to chest wall blows (commotio cordis) has been reported with increasing frequency in children, and only about 15% of victims survive. Automated external defibrillators (AEDs) have been shown to be life saving in adults with cardiac arrest, but data on their use in children are limited. In a swine model of commotio cordis designed to be most relevant to young children, we assessed the efficacy of a commercially available AED for recognition and termination of ventricular fibrillation.
Ventricular fibrillation was produced in anesthetized juvenile swine by precordial impact from a baseball under controlled conditions. Animals were randomized to defibrillation after 1, 2, 4, or 6 minutes of ventricular fibrillation. Twenty-six swine underwent 50 ventricular fibrillation inductions. Sensitivity of the AED for recognition of ventricular fibrillation was 98%, and specificity for nonshockable episodes was 100%. All episodes of ventricular fibrillation were successfully terminated by the AED.
In this experimental model of commotio cordis, the AED proved to be highly sensitive and specific for recognition of ventricular fibrillation and effective in terminating the arrhythmia and restoring sinus rhythm. These findings suggest that early defibrillation with the AED could save young lives on the athletic field.
We aimed to determine whether long QT syndrome (LQTS) genotype has a differential effect on clinical course of disease in male and female children and adults after adjustment for QTc duration.
Genotype influences clinical course of the LQTS; however, data on the effect of age and gender on this association are limited.
The LQTS genotype, QTc duration, and follow-up were determined in 243 cases of LQTS caused by the KCNQ1 potassium channel gene mutations (LQT1), 209 cases of LQTS caused by the HERG potassium channel gene mutations (LQT2), and 81 cases of LQTS caused by the SCN5A sodium channel gene mutation (LQT3) gene carriers. The probability of cardiac events (syncope, aborted cardiac arrest, or sudden death) was analyzed by genotype, gender, and age (children < or = 15 years and adults 16 to 40 years). In addition, the risk of sudden death and lethality of cardiac events were evaluated in 1,075 LQT1, 976 LQT2, and 324 LQT3 family members from families with known genotype.
During childhood, the risk of cardiac events was significantly higher in LQT1 males than in LQT1 females (hazard ratio [HR] = 1.72), whereas there was no significant gender-related difference in the risk of cardiac events among LQT2 and LQT3 carriers. During adulthood, LQT2 females (HR = 3.71) and LQT1 females (HR = 3.35) had a significantly higher risk of cardiac events than respective males. The lethality of cardiac events was highest in LQT3 males and females (19% and 18%), and higher in LQT1 and LQT2 males (5% and 6%) than in LQT1 and LQT2 females (2% for both). CONCLUSIONS; Age and gender have different, genotype-specific modulating effects on the probability of cardiac events and electrocardiographic presentation in LQT1 and LQT2 patients.
The single most common cause of the withdrawal or restriction of the use of marketed drugs has been QT-interval prolongation associated with polymorphic ventricular tachycardia, or torsade de pointes, a condition that can be fatal. This review summarizes the current knowledge about molecular and clinical predictors of drug-induced QT-interval prolongation and torsade de pointes and discusses how new molecular predictors of drug action might be incorporated into drug-development programs and clinical practice. A general approach to drugs suspected of causing this problem is presented.
Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur.
In a randomized and blinded experiment, 12 swine (mean 17.1 +/- 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 +/- 18 muM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph.
There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53%) compared to those control animals receiving only sterile water (10 of 31: 32%) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 +/- 19 mV) versus controls (61 +/- 46 mV) (P = 0.015).
Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.
Sudden cardiac death that results from chest wall blows (commotio cordis) the second leading cause of death in young athletes. Most events are caused by blows from projectiles, such as baseballs or lacrosse balls, with a substantial proportion occurring despite the use of a chest protector. In the present experiment, we tested the effectiveness of commercially available chest protectors in preventing ventricular fibrillation (VF) that results from chest wall strikes with baseballs and lacrosse balls.
Twelve different baseball or lacrosse chest protectors were evaluated in juvenile swines that were subjected to 40-mph baseball or lacrosse ball blows to the precordium during the vulnerable period of repolarization for VF and were compared with control impacts without chest protectors. Seven baseball chest protectors were hit by regulation baseballs, and 5 lacrosse chest protectors were tested by blows with standard lacrosse balls. Each animal received 2 chest blows for each protector and 2 control impacts without a chest protector, with the sequence of impacts assigned randomly.
VF was elicited by 12 (32%) of 37 strikes in control animals without baseball chest protectors. None of the baseball chest wall protectors tested were shown to decrease significantly the occurrence of VF when compared with controls. VF was elicited by 11 (46%) of 24 strikes in control animals without lacrosse chest protectors. None of the lacrosse chest wall protectors tested decreased significantly the occurrence of VF when compared with controls.
In our experimental animal model of commotio cordis, commercially available baseball and lacrosse chest wall protectors were ineffective in protecting against VF that was triggered by chest blows and, by inference, sudden cardiac death. Improvements in materials and design of chest wall barriers are necessary to reduce the occurrence of these tragic events and make the athletic field safer for youths.
Nonpenetrating chest wall impact (commotio cordis) may lead to sudden cardiac death due to the acute initiation of ventricular fibrillation (VF). VF may result from sudden stretch during a vulnerable window, which is determined by repolarization inhomogeneity.
We examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). In six Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains.
Sudden balloon inflation induced VF when pressure pulses of 208-289 mmHg were applied within a window of 35-88 msec after MAP upstroke, a period of intrinsic increase in repolarization dispersion. During the pressure pulse, MAPs revealed an additional increase in repolarization dispersion (time domain) by 9 +/- 6 msec (P < 0.01). The maximal difference in repolarization levels (voltage domain) between sites increased from 19 +/- 3% to 26 +/- 3% (P < 0.05). Earliest stretch-induced activation was observed near a site with early repolarization, while sites with late repolarization showed delayed activation.
Sudden myocardial stretch can elicit VF when it occurs during a vulnerable window that is based on repolarization inhomogeneity. Stretch pulses applied during this vulnerable window can lead to nonuniform activation. Repolarization dispersion might play a crucial role in the occurrence of fatal tachyarrhythmias during commotio cordis.
Commotio cordis (CC), sudden death as a result of a blunt, often innocent-appearing chest wall blow, is being reported with increasing frequency. The clinical spectrum is diverse; however, a substantial number of cases occur in youth athletics. In events that occur during sport, victims are struck by projectiles regarded as standard implements of the game. Sudden death is instantaneous and victims are most often found in ventricular fibrillation (VF). Overall survival is poor; however, successful resuscitation can be achieved with early defibrillation. Autopsy is notable for the absence of any significant cardiac or thoracic injury. Development of an experimental model has allowed for substantial insights into the underlying mechanisms of sudden death. In anesthetized juvenile swine, induction of VF is instantaneous following chest wall blows occurring during a vulnerable window before the T wave peak. Crucial variables including the velocity of impact, impact location, and hardness of the impact object have been identified. Rapid left ventricular (LV) pressure rise following chest impact likely results in activation of ion channels via mechano-electric coupling. The generation of inward current via mechano-sensitive ion channels likely results in augmentation of repolarization and nonuniform myocardial activation, and is the cause of premature ventricular depolarizations that are triggers of VF in CC. While softer-than-standard safety baseballs reduce the risk of CC, commercially available chest protectors are ineffective in preventing CC. The development of more effective chest protectors and more widespread use of automated external defibrillators at youth sporting events are needed.
Blunt precordial blows triggering ventricular fibrillation (commotio cordis) represent a leading cause of sudden death in young athletes. Attention has focused on the primary prevention of these tragedies with chest barriers. The U.S. Commotio Cordis Registry was accessed to determine the likelihood of sudden death in athletes exposed to precordial blows while wearing chest protectors. Of 182 cases of commotio cordis, 85 (47%) occurred during practice or competition in organized sports. In 32 of these 85 competitive athletes (38%), fatal chest blows occurred despite the presence of potentially protective equipment. Athletes wore standard, commercially available chest barriers made of polymer foam covered by fabric or hard shells, generally perceived as protective from arrhythmic consequences of the blows. These events occurred in 4 sports: hockey (n = 13; 1 goalie), football (n = 10), lacrosse (n = 6; 3 goalies), and baseball (n = 3; all catchers). Scenarios included the failure of the padding to cover the precordium so that blows circumvented the protective barrier (n = 25) or projectiles that struck the chest barrier directly (n = 7). In conclusion, a significant proportion (about 40%) of sudden deaths reported in young competitive athletes due to blunt chest blows (commotio cordis) occur despite the presence of commercially available sports equipment generally perceived as protective.
Previous studies that assessed the risk of life-threatening cardiac events in patients with congenital long-QT syndrome (LQTS) have focused mainly on the first 4 decades of life, whereas the clinical course of this inherited cardiac disorder in the older population has not been studied.
The risk of aborted cardiac arrest or death from age 41 though 75 years was assessed in 2759 subjects from the International LQTS Registry, categorized into electrocardiographically affected (corrected QT interval [QTc] > or = 470 ms), borderline (QTc 440 to 469 ms), and unaffected (QTc < 440 ms) subgroups. The affected versus unaffected adjusted hazard ratio for aborted cardiac arrest or death was 2.65 (P<0.001) in the age range of 41 to 60 years and 1.23 (P=0.31) in the age range of 61 to 75 years. The clinical course of study subjects displayed gender differences: Affected LQTS women experienced a significantly higher cumulative event rate (26%) than borderline (16%) and unaffected (12%) women (P=0.001), whereas event rates were similar among the 3 respective subgroups of men (29%, 26%, and 27%; P=0.16). Recent syncope (< 2 years in the past) was the predominant risk factor in affected subjects (hazard ratio 9.92, P<0.001), and the LQT3 genotype was identified as the most powerful predictor of outcome in a subset of 871 study subjects who were genetically tested for a known LQTS mutation (hazard ratio 4.76, P=0.02).
LQTS subjects maintain a high risk for life-threatening cardiac events after age 40 years. The phenotypic expression of affected subjects is influenced by age-specific factors related to gender, clinical history, and the LQTS genotype.
Recent new information on the dynamics and molecular mechanisms of electrical rotors and spiral waves has increased our understanding of both atrial fibrillation and ventricular fibrillation. In this brief review, we evaluate the available evidence for the separate roles played by individual sarcolemmal ion channels in atrial fibrillation and ventricular fibrillation, assessing the clinical relevance of such findings. Importantly, although human data support the idea that rotors are a crucial mechanism for fibrillation maintenance in both atria and ventricles, there are clear inherent differences between the 2 chamber types, particularly in regard to the role of specific ion channels in fibrillation. But there also are similarities. This knowledge, together with new information on the changes that take place during disease evolution and between structurally normal and diseased hearts, may enhance our understanding of fibrillatory processes pointing to new approaches to improve disease outcomes.
Injuries and deaths related to baseball
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