Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Commotio Cordis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2003

[Sudden cardiac death by commotio cordis].

Commotio cordis due to blunt trauma to the precordium is a rare cause of death in young athletes, occurring less frequently than all of the other athletics-related deaths. Commotio cordis is a term used to describe cases of blunt thoracic impact causing fatality without structural damage of the heart and internal organs. Death is attributed to ventricular fibrillation, which is often resistant to resuscitative therapy. In this article we discussed this catastrophic event, its historical development, epidemiology and clinical presentation, mechanisms for sudden death in commotio cordis, limitations of evidence using animal models, autopsy findings, resuscitation and preventive measures.

Adolescent↗
PubMed2005

Evolution of our knowledge of sudden death due to commotio cordis.

Commotio cordis refers to circulatory arrest due to a nonpenetrating blow to the chest. First discovered in 1932 in a study using large rabbits, it came to the attention of clinicians who encountered children dying suddenly from a chest blow while engaging in sports activities. This review traces the history of commotio cordis, establishes the conditions necessary for sudden death from a nonpenetrating chest blow, and presents the first ECG record showing that a chest blow landing in the ventricular vulnerable period can produce ventricular fibrillation. The conditions necessary for sustaining ventricular fibrillation and numerous examples of sudden death by commotio cordis are presented.

Adolescent↗
PubMed2004

Commotio cordis.

Commotio cordis is ventricular fibrillation that results from blunt chest trauma and is a life threatening condition; early resuscitation and defibrillation are critical. This may occur during sporting events or from child abuse and most patients are boys who are younger than 16 years. Commotio cordis' prognosis depends on the availability of cardiac defibrillation. Automatic defibrillators at convenient locations near sporting events, combined with improved cardiopulmonary resuscitation education, may improve chances of survival after this rare phenomenon. Transient cardiac conduction abnormalities and arrhythmias have been observed in survivors; therefore, cardiac clearance before resumption of sports is indicated.

Arrhythmias, Cardiac↗
PubMed1999

Biomechanical predictor of commotio cordis in high-speed chest impact.

BACKGROUND: Commotio cordis is a term used to describe cases of blunt thoracic impact causing fatality without gross structural damage of the heart and internal organs. Death is attributed to ventricular fibrillation or cardiac arrhythmia aggravated by traumatic apnea. The biomechanical response related to the risk of commotio cordis has not been determined. METHODS: Reanalysis of previously published experimental data was performed to determine which biomechanical parameter predicts the occurrence of commotio cordis. Logistic regression was used to determine the risk for commotio cordis with the level of chest compression, rate of chest deformation, and viscous criterion. RESULTS: By using only cases without serious tissue injury (Abbreviated Injury Scale score < 4), viscous criterion was the best predictor of commotio cordis or ventricular fibrillation (chi2 = 7.69, p = 0.006). It was also the best predictor of heart rupture (chi2 = 13.19,p = 0.0003) and severe cardiac injury with Abbreviated Injury Scale score > or = 4 (chi2 = 25.03, p = 0.0001). CONCLUSION: Based on this in-depth analysis, the viscous criterion is the relevant biomechanical response to assess the risk of commotio cordis and more severe thoracic injury in high-speed blunt impact.

Abbreviated Injury Scale↗
PubMed2002

Clinical profile and spectrum of commotio cordis.

CONTEXT: Although blunt, nonpenetrating chest blows causing sudden cardiac death (commotio cordis) are often associated with competitive sports, dangers implicit in such blows can extend into many other life activities. OBJECTIVE: To describe the comprehensive spectrum of commotio cordis events. DESIGN AND SETTING: Analysis of confirmed cases from the general community assembled in the US Commotio Cordis Registry occurring up to September 1, 2001. MAIN OUTCOME MEASURE: Commotio cordis event. RESULTS: Of 128 confirmed cases, 122 (95%) were in males and the mean (SD) age was 13.6 (8.2) years (median, 14 years; range, 3 months to 45 years); only 28 (22%) cases were aged 18 years or older. Commotio cordis events occurred most commonly during organized sporting events (79 [62%]), such as baseball, but 49 (38%) occurred as part of daily routine and recreational activities. Fatal blows were inflicted with a wide range of velocities but often occurred inadvertently and under circumstances not usually associated with risk for sudden death in informal settings near the home or playground. Twenty-two (28%) participants were wearing commercially available chest barriers, including 7 in whom the projectile made direct contact with protective padding (baseball catchers and lacrosse/hockey goalies), and 2 in whom the projectile was a baseball specifically designed to reduce risk. Only 21 (16%) individuals survived their event, with particularly prompt cardiopulmonary resuscitation/defibrillation (most commonly reversing ventricular fibrillation) the only identifiable factor associated with a favorable outcome. CONCLUSIONS: The expanded spectrum of commotio cordis illustrates the potential dangers implicit in striking the chest, regardless of the intent or force of the blow. These findings also suggest that the safety of young athletes will be enhanced by developing more effective preventive strategies (such as chest wall barriers) to achieve protection from ventricular fibrillation following precordial blows.

Adolescent↗
PubMed2003

Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis).

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. RESULTS: Impacts 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.

Animals↗
PubMed2003

Homicidal commotio cordis: the final blow in a battered infant.

OBJECTIVE: This report describes in detail the occurrence of inflicted commotio cordis (cardiac concussion) in a previously abused 7-week-old. Though inflicted commotio cordis has been reported in three toddlers, this is the first report in a young infant. METHOD: Following documentation of abuse in a living child, the case of a death of a prior sibling--previously regarded as natural--was re-opened for further investigation. Original autopsy materials were reviewed, and the body of the deceased child was exhumed. RESULTS: Exhumation and second autopsy documented more than 50 fractures in the deceased child. When re-interviewed, the children's father admitted to causing the injuries in both children, and gave a textbook description of commotio cordis as the mechanism of death in the fatal case. CONCLUSIONS: Commotio cordis is a rare event in which a fatal dysrhythmia--usually ventricular fibrillation--is precipitated by a blow to the precordial chest. Previous reports have indicated that homicidal commotio cordis can occur in small children. This report demonstrates that commotio cordis can occur even in the very young, previously abused infant.

Autopsy↗
PubMed2006

Importance of the autonomic nervous system in an experimental model of commotio cordis.

BACKGROUND: Young athletes may die suddenly when they are struck in the chest (commotio cordis). Proposed mechanisms of sudden death in commotio cordis include hypervagatonia and activation of the sympathetic nervous system. In an experimental model of commotio cordis, the importance of the sympathetic and parasympathetic nervous system in the initiation of ventricular fibrillation was evaluated. MATERIAL/METHODS: Juvenile swine weighing between 8 and 12 kg were anesthetized with ketamine and isoflurane and placed prone in a sling. Twenty animals were randomized to pretreatment with placebo or sympathetic and parasympathetic blockade. Chest blows were guided by echocardiography to the center of the left ventricle and animals received 1-3 strikes with a regulation baseball propelled at 30 mph and timed to impact 10-30 ms prior to the peak of the T-wave. RESULTS: With 17 impacts in 10 autonomically blocked animals, 6 episodes of ventricular fibrillation were seen; with 15 impacts in 10 control animals, ventricular fibrillation occurred 6 times. There was also no significant difference between the groups in occurrence of nonsustained polymorphic ventricular tachycardia or ST elevation. Transient complete heart block was less commonly seen in animals treated with autonomic blockade, although this did not achieve statistical significance. CONCLUSIONS: In this experimental model of commotio cordis, autonomic blockade did not affect the frequency of sudden cardiac death, polymorphic ventricular tachycardia or ST segment elevation. Thus, vagotonic and sympathetic surges likely do not contribute to the syndrome of sudden death due to chest blows in young people and athletes.

Animals↗
PubMed1999

Commotio cordis: sudden cardiac death in athletes.

Commotio cordis due to blunt trauma to the precordium is a rare cause of death in young athletes, occurring less frequently than all of the other athletics-related deaths. Several measures, such as the use of safety baseballs and the use of chest protectors, can help protect young athletes from commotio cordis. In general, sudden cardiac death in athletes is receiving increasing attention from the public as a result of recent deaths of high-profile athletes. Sudden cardiac death, however, is rare, with an estimated 1 out of 200,000 high school athletes at risk each year. However, the personal, physiological, and cardiovascular benefits of athletics far outweigh the risks. Therefore, the message to parents is to allow their children to participate in athletics because the benefits far outweigh the risks.

Adolescent↗
PubMed2000

Dangerous impact--commotio cordis.

Sudden death following blunt chest trauma is a frightening occurrence known as 'commotio cordis' or 'concussion of the heart'. It is speculated that commotio cordis could be caused by ventricular fibrillation secondary to an impact-induced energy that was transmitted via the chest wall to the myocardium during its vulnerable repolarization period. We describe a survivor of commotio cordis caused by a baseball. In this patient, an initial ventricular fibrillation was documented and converted by direct current defibrillation. Serial electrocardiographic changes (bifascicular conduction block and T wave inversion in precordial leads) were noticed in this patient. Our case suggested that coronary vasospasm might also play a role in commotio cordis.

Baseball↗
PubMed2004

Commotio cordis--a report of three cases.

Commotio cordis is a recognised cause of sudden death in which an apparently minor blow to the chest causes ventricular fibrillation and cardiac arrest. It is best known for causing death during games of youth baseball in the United States, but individual cases have been recorded as a result of a wide range of activities, principally sporting. The underlying biochemical and mechano-electric causes have been well documented. However, there are few reported cases where commotio cordis is implicated as the cause of death in homicide cases. We present three cases from the north-east of England where an assault caused death by this mechanism.

Adult↗
PubMed2006

Ventricular fibrillation induced by stretch pulse: implications for sudden death due to commotio cordis.

INTRODUCTION: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Action Potentials↗
PubMed2003

Automated external defibrillator arrhythmia detection in a model of cardiac arrest due to commotio cordis.

INTRODUCTION: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.

Animals↗
PubMed1999

Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio cordis).

BACKGROUND: 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. METHODS AND RESULTS: 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). CONCLUSIONS: 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.

Adenosine Triphosphate↗
PubMed1998

An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis)

BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Animals↗
PubMed2005

Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis).

INTRODUCTION: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.

Animals↗
PubMed2002

Reduced risk of sudden death from chest wall blows (commotio cordis) with safety baseballs.

OBJECTIVES: 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. BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Animals↗
PubMedDate not supplied

Mechanically induced sudden death in chest wall impact (commotio cordis).

Sudden death due to nonpenetrating chest wall impact in the absence of injury to the ribs, sternum and heart is known as commotio cordis. Although once thought rare, an increasing number of these events have been reported. Indeed, a significant percentage of deaths on the athletic field are due to chest wall impact. Commotio cordis is most frequently observed in young individuals (age 4-18 years), but may also occur in adults. Sudden death is instantaneous or preceded by several seconds of lightheadedness after the chest wall blow. Victims are most often found in ventricular fibrillation, and successful resuscitation is more difficult than expected given the young age, excellent health of the victims, and the absence of structural heart disease. Autopsy examination is notable for the lack of any significant cardiac or thoracic abnormalities. In an experimental model of commotio cordis utilizing anesthetized juvenile swine, ventricular fibrillation can be produced by a 30 mph baseball strike if the strike occurred during the vulnerable period of repolarization, on the upslope of the T-wave. Energy of the impact object was also found to be a critical variable with 40 mph baseballs more likely to cause ventricular fibrillation than velocities less or greater than 40 mph. In addition, more rigid impact objects and blows directly over the center of the chest were more likely to cause ventricular fibrillation. Peak left ventricular pressure generated by the chest wall blow correlated with the risk of ventricular fibrillation. Activation of the K(+)(ATP) channel is a likely cause of the ventricular fibrillation produced by chest wall blows. Successful resuscitation is attainable with early defibrillation.

Adolescent↗