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Interest in the condition known as commotio cordis recently resurfaced after American football player Damar Hamlin collapsed in his game after experiencing a severe blow to his chest. The impact Hamlin received triggered a series of events that resulted in ventricular fibrillation, a rapid irregular beating of the heart; Hamlin was later diagnosed as having commotio cordis (Snipe). This extremely rare occurrence is triggered when blunt force trauma is delivered to the chest during the precise timing of repolarization, which is the peak of the T wave on an electrocardiogram (ECG) (Maron et al.). With no evident underlying cardiac damage or contusion, this condition affects the electrical stimulus that is transferred throughout the heart during ventricular repolarization, a crucial and vulnerable time in the systematic beating of the heart (Maron et al., Nesbitt et al.). This results in insufficient blood flow throughout the body, which can cause organ damage or death. This article will discuss the series of unfortunate events that result from commotio cordis.
In a regular cardiac cycle, there are two events that occur – diastole and systole. Diastole represents the filling of the heart chambers and is the phase where the cardiac muscles are relaxed which allows blood to enter the heart. Following this event, the heart goes into systole, wherein the muscles of the heart contract to force the blood out from the chambers and into the rest of the body. The rhythm of this filling-to-beating system is crucial for adequate blood flow throughout the body. If the heart were to go into a rapid irregular rhythm, such as what happens during ventricular fibrillation, then the blood supply to the rest of the organs of the body would decrease, resulting in organ failure and possibly death. Controlled by the impulses and action potential relayed throughout the heart, the methodical contraction and relaxation supply the body with sufficient blood flow. Looking further into the mechanics of the action potential and the contraction of each cell, it is important to understand that cardiac cells, when at rest, are polarized; this means that there is a separation between two opposing groups. In this case, the two groups are sodium and potassium ions. During this state of rest, sodium is unable to enter the cell, as the membrane is not permeable to the ion and is highly selective of which molecules and atoms can diffuse. However, when an electrical impulse is generated, the membrane becomes permeable, and the sodium-potassium pump, an active transport channel, is activated, allowing for an inflow of sodium. This opening of the channel and the inflow of sodium is called depolarization, as there is no longer a separation between the opposing ions, and this results in the contraction of the heart. To maintain homeostasis in the cell, potassium is released in exchange, which leads to the cell returning to its relaxed state in preparation for the next impulse. In most people, this complete cycle occurs uniformly in the whole heart.
A rare asymptomatic population possesses a latent electrical abnormality that can predispose them to this sudden arrhythmic event. The condition may either be acquired through genetic mutations or as a result of former cardiac events that have altered the electrophysiology, such as a myocardial infarction. This electrical abnormality originates from the heterogeneity of the cells' repolarization, making it vulnerable to the succeeding electrical impulse, resulting in an uncoordinated repolarization of the tissue. If a person, who possesses this substrate, the genetic or acquired predisposition– having cells with heterogenic repolarization periods, receives such a blow to the chest at the exact vulnerable stage of the cardiac cycle – where repolarization is at its peak, this heterogeneity during the refractory period of the cardiac cycle can result in a redirected path of the unidirectional impulse, giving rise to a situation called reentry which may result in ventricular fibrillation (Link). This heterogeneous electrical substrate often goes undetected as it is subcellular and affects the electrical physiology of the repolarization rather than the anatomical structure. It is not diagnosed through scans and imaging, making it difficult to identify a candidate for the condition. Currently, the only approach to detecting the predisposition is through invasive intracardiac electrophysiologic studies, wherein doctors surgically implant an electrical impulse, similar to that of the impulse generated by the heart itself, to test whether or not a patient will go under ventricular fibrillation when stimulated.
Commotio cordis is increasingly becoming one of the leading cardiac conditions in young athletes. According to a research article by the New England Journal of Medicine entitled “Commotio Cordis,” written by Maron and Estes, the epidemiology shows a disproportion between cases in male athletes as compared to female athletes, with 95% of the victims being male. An additional factor that contributes to the susceptibility of this cardiac event is the thickness of the chest wall, which explains why many young athletes, the majority of whom are below the age of ten years old, are more susceptible (Link). Due to the absence of exhibited symptoms, there is a lack of appropriate immediate action, which can lead to higher chances of death caused by uncontrolled ventricular fibrillation. Despite the ongoing research on innovations and techniques for detecting the possession of the unfortunate substrate, commotio cordis, which is generated by a blunt force trauma to the chest, is highly unpredictable, especially in sports. Only through proper reaction to the event, such as cardiopulmonary resuscitation (CPR) and a defibrillator can a victim of this life-threatening condition be saved.
Commotio Cordis truly is a disease brought about by a series of unfortunate events.
References
Link, M. S. Commotio Cordis. Circulation: Arrhythmia and Electrophysiology, vol. 5, issue 2, pp. 425–432. Ovid Technologies (Wolters Kluwer Health). https://doi.org/10.1161/circep.111.962712.
Maron, B. J., & Estes, N. A. M., III. “Commotio Cordis.” New England Journal of Medicine, vol. 362, issue 10, pp. 917–927. Massachusetts Medical Society. https://doi.org/10.1056/nejmra0910111.
Maron, B. J., Poliac, L. C., Kaplan, J. A., & Mueller, F. O. Blunt Impact to the Chest Leading to Sudden Death from Cardiac Arrest during Sports Activities. New England Journal of Medicine, vol. 333, issue 6, pp. 337–342. Massachusetts Medical Society. https://doi.org/10.1056/nejm199508103330602.
Nesbitt, A. D., Cooper, P. J., & Kohl, P. Rediscovering commotio cordis. The Lancet, vol. 357, issue 9263, pp. 1195–1197. Elsevier BV. https://doi.org/10.1016/s0140-6736(00)04338-5
Snipe, M. “Damar Hamlin’s Collapse Shows the Elevated Risk for Heart Failure Among Black Athletes.” Morehouse School of Medicine. https://www.msm.edu/RSSFeedArticles/2023/January/DamarHamlin.php.
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