Commotio Cordis in a Professional Soccer Player
Value of MRI in Unraveling Myocardial Damage
A 35-year-old male premier league soccer player was admitted to the intensive coronary care unit after aborted cardiac sudden death. A routine echocardiogram performed 2 years earlier was entirely normal.
The player was struck along the left anterior chest wall by a direct blow from a soccer ball during a practice game. He reported a prodrome of dizziness for several minutes before collapsing on the field. An emergency medical team documented monomorphic ventricular tachycardia, which rapidly deteriorated to ventricular fibrillation. Four electric shocks were delivered with the restoration of sinus rhythm and immediate full neurological recovery.
Initial workup revealed elevated high-sensitivity cardiac troponin T of 283 ng/L (normal range, 0–14 ng/L) and creatine kinase levels of 12 480 U/L (normal range, 20–200 U/L). The 12-lead ECG showed biphasic T waves in the precordial leads, with a normal QTc interval. Transthoracic echocardiography revealed mild biventricular dysfunction (Movie I in the Data Supplement). Coronary angiography showed normal coronary arteries (Movie II in the Data Supplement). Cardiac magnetic resonance (CMR) study with a 3T scanner (Ingenia, Philips Medical Systems, Best, The Netherlands) was performed on day 4 after admission. Images were evaluated with Intelispace Portal 6.0 software. CMR cine images revealed mild biventricular dilatation, normal left ventricular wall thickness with mild systolic dysfunction (ejection fraction, 49%) and inferolateral wall hypokinesis (Movie III in the Data Supplement). The right ventricle was mildly hypokinetic, without evidence of dyskinesia or aneurysm; hence, CMR criteria for arrhythmogenic right ventricular dysplasia were not fulfilled. A small pericardial effusion was noted. On T2-weighted short-tau inversion recovery turbo spin echo sequence, there was no increase in myocardial enhancement, indicating the absence of myocardial edema (Figure 1). However, confluent subepicardial late gadolinium enhancement was noted in the inferior and lateral walls of the left ventricle, corresponding with the wall motion abnormality and indicating myocardial fibrosis (Figures 2 and 3). These findings were compatible with remote myocarditis.
During hospitalization, the player remained asymptomatic without further arrhythmias. Subsequent CMR 2 months later revealed no change in biventricular dimensions, ejection fraction and late gadolinium enhancement extent and pattern (Figures 2 and 3). The player was instructed to strictly avoid intense exercise and refrain from competitive sports and has begun a cardiac rehabilitation program.
Definition and Cause
Commotio cordis is a rare cardiac phenomenon in which sustained ventricular arrhythmia is induced by a blunt impact to the anterior chest wall. It reflects an external, nonpenetrative force that generates stretch-sensitive changes in cardiac myocytes, severely disrupting normal tissue electrophysiology. In vivo studies demonstrate that commotio cordis is contingent on impact hitting the precordial region at the precise window of early ventricular repolarization. This phenomenon occurs in the absence of any insult to the cardiac substructure. Because of its unique cause, commotio cordis is most often seen in sports involving a high-speed projectile object, including soccer, baseball, and hockey. These projectiles strike athletes on the precordium at high velocity at a perpendicular vector. Should the strike occur within the vulnerable period of the cardiac cycle, the patient may sustain ventricular arrhythmia; sudden death may follow unless prompt medical intervention and defibrillation are offered. Observers usually report the blow as unremarkable, with the athlete subsequently collapsing because of pulseless electrical activity.
Commotio cordis is considered to be a diagnosis of exclusion. Postmortem analysis of suspected commotio cordis cases are unrevealing of myocarditis, ischemic damage, congenital anomalies, or other cardiovascular trauma.
CMR imaging has rarely been used in commotio cordis survivors. Reports show evidence of myocardial edema and focal delayed hyperenhancement that essentially represent cardiac contusion.1
The case presented herein illustrates the lack of acute myocardial changes, therefore, compatible with commotio cordis rather than a cardiac contusion. CMR excluded other cardiac pathologies that are associated with sudden cardiac death in athletes, such as arrhythmogenic right ventricular dysplasia and hypertrophic cardiomyopathy, by accurately defining right and left ventricular volumes and wall thickness. The presence of significant subepicardial scar probably representing remote myocarditis might have served as the underlying substrate for fatal arrhythmia in this case of commotio cordis. The combination of prior myocardial scar and a strike to the precordium by a high-speed projectile could be a plausible cause in other cases of commotio cordis as well. Thus, CMR imaging may serve as a valuable tool to elucidate the underlying mechanisms which predispose to commotio cordis and differentiate between various cardiac pathologies based on the absence of edema, cardiac morphology, and the presence and pattern of late gadolinium enhancement.
All authors of this article participated in the conception and interpretation of the case study. All authors have contributed to the drafting and revision of the article for intellectual content and have given final approval for its submission. The article is not being considered for publication elsewhere, and none of the article’s contents have been previously published. None of the authors have any financial relationships with any company or any other bias or conflict of interest.
The Data Supplement is available at http://circimaging.ahajournals.org/lookup/suppl/doi:10.1161/CIRCIMAGING.118.007848/-/DC1.
- © 2018 American Heart Association, Inc.
- Vago H,
- Toth A,
- Apor A,
- Maurovich-Horvat P,
- Toth M,
- Merkely B