Mechanically Induced Ectopy via Stretch-Activated Cation-Nonselective Channels Is Caused by Local Tissue Deformation and Results in Ventricular Fibrillation if Triggered on the Repolarization Wave Edge (Commotio Cordis).

BACKGROUND: External chest impacts (commotio cordis) can cause mechanically induced premature ventricular excitation (PVEM) and, rarely, ventricular fibrillation (VF). Because block of stretch-sensitive ATP-inactivated potassium channels curtailed VF occurrence in a porcine model of commotio cordis, VF has been suggested to arise from abnormal repolarization caused by stretch activation of potassium channels. Alternatively, VF could result from abnormal excitation by PVEM, overlapping with normal repolarization-related electric heterogeneity. Here, we investigate mechanisms and determinants of PVEM induction and its potential role in commotio cordis-induced VF. METHODS AND RESULTS: Subcontusional mechanical stimuli were applied to isolated rabbit hearts during optical voltage mapping, combined with pharmacological block of ATP-inactivated potassium or stretch-activated cation-nonselective channels. We demonstrate that local mechanical stimulation reliably triggers PVEM at the contact site, with inducibility predicted by local tissue indentation. PVEM induction is diminished by pharmacological block of stretch-activated cation-nonselective channels. In hearts where electrocardiogram T waves involve a well-defined repolarization edge traversing the epicardium, PVEM can reliably provoke VF if, and only if, the mechanical stimulation site overlaps the repolarization wave edge. In contrast, application of short-lived intraventricular pressure surges neither triggers PVEM nor changes repolarization. ATP-inactivated potassium channel block has no effect on PVEM inducibility per se, but shifts it to later time points by delaying repolarization and prolonging refractoriness. CONCLUSIONS: Local mechanical tissue deformation determines PVEM induction via stretch-activation of cation-nonselective channels, with VF induction requiring PVEM overlap with the trailing edge of a normal repolarization wave. This defines a narrow, subject-specific vulnerable window for commotio cordis-induced VF that exists both in time and in space.

Pathophysiology, prevention, and treatment of commotio cordis.

Commotio cordis is increasing described and it is now clear that this phenomenon is an important cause of sudden cardiac death on the playing field. Victims are predominantly young, male, and struck in the left chest with a ball. An animal model has been developed and utilized to explore the important variables and mechanism of commotio cordis. Impact during a narrow window of repolarization causes ventricular fibrillation. Other important variables include location, velocity, shape, and hardness of the impact object. Biological characteristics such as gender, pliability of the chest wall, and genetic susceptibility also play a role in commotio cordis. The mechanism of ventricular fibrillation appears to be an increase in heterogeneity of repolarization caused by induced abnormalities of ion channels activated by abrupt increases in left ventricular pressure. In the setting of altered repolarization a trigger of ventricular depolarization (premature ventricular depolarization caused directly by the chest blow) initiates a spiral wave that quickly breaks down into ventricular fibrillation. Prevention of commotio cordis is possible. Improved recognition and resuscitation have led to an improvement in outcome.

Emergency management of blunt chest trauma in children: an evidence-based approach.

Pediatric trauma is commonly encountered in the emergency department, and trauma to the head, chest, and abdomen may be a source of significant morbidity and mortality. As children have unique thoracic anatomical and physiological properties, they may present with diagnostic challenges that the emergency clinician must be aware of. This review examines the effects of blunt trauma to the pediatric chest, as well as its relevant etiologies and associated mortality. Diagnostic and treatment options for commonly encountered injuries such as pulmonary contusions, rib fractures, and pneumothoraces are examined. Additionally, this review discusses rarely encountered--yet highly lethal--chest wall injuries such as blunt cardiac injuries, commotio cordis, nonaccidental trauma, and aortic injuries.

Muerte súbita / Sudden death

La muerte súbita probablemente sea el desafío más importante de la cardiología moderna. En este artículo, después de realizar una revisión histórica de la muerte súbita, se comentan la epidemiología y las enfermedades asociadas a ella y se hace énfasis en los aspectos fisiopatológicos, especialmente los factores desencadenantes que actuando sobre un miocardio vulnerable precipitan la arritmia final, que en general lleva a la fibrilación ventricular y en menor medida a bradiarritmia y muerte súbita. Se comentan especialmente la importancia de la isquemia aguda y la disfunción ventricular y el papel de la genética, no sólo en las cardiopatías de origen genético, sino también su posible efecto desencadenante en la cardiopatía isquémica aguda y crónica. Por último, se describe cuál es la mejor forma de identificar a los pacientes en riesgo, cómo prevenir la muerte súbita y qué conducta seguir ante un paciente resucitado de una parada cardiaca (AU)

Sudden death is probably the greatest challenge in modern cardiology. After reviewing its history, we describe the epidemiology of sudden death and its associated diseases. We highlight its physiopathologic aspects, including the factors that act on vulnerable myocardium triggering the final arrhythmia, mainly ventricular fibrillation and, to a lesser extent, bradycardia and sudden death. We emphasize the relevance of acute ischemia, ventricular dysfunction and genetic factors, not only in genetic heart disease, but also as triggers of sudden death in acute and chronic ischemic heart disease. Finally, we describe the best way to identify candidates at risk, discuss how to prevent sudden death, and outline the best approach to managing a patient resuscitated from cardiac arrest (AU)

[Commotio cordis]. / Commotio cordis.

Blunt, non-penetrating trauma of the chest (commotio cordis) can cause sudden death in individuals without known cardiac disease. Sudden death in commotio cordis is due to ventricular fibrillation. The timing of the blow must be during the electric vulnerable period of the ECG cyclus, 10-40 milliseconds before the peak of the T-wave. The risk of arrhythmia increases progressively, until a velocity of 64 km/h, and at higher velocities the risk of ventricular fibrillation begins to diminish. The location of the impact must be directly over the cardiac silhouette.

Reduced diameter spheres increases the risk of chest blow-induced ventricular fibrillation (commotio cordis).

BACKGROUND: 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. OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.

Marked variability in susceptibility to ventricular fibrillation in an experimental commotio cordis model.

BACKGROUND: 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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.

[Sudden cardiac death in young athletes--causes, prevention and treatment].

The sudden death of a young athlete is a tragic event which affects teammates, the local community and the medical community. In this review the authors present the main causes of sudden cardiac death and compare between pre-participation medical evaluation recommendations in the United States, Europe and Israel. Finally, the authors present the new approaches of promoting the use of Automated External Defibrillators (AEDs).