Cardiac Contusion in a Professional Soccer Player
Visualization of Acute and Late Pathological Changes in the Myocardium With Magnetic Resonance Imaging
We report here the case of a 30-year-old professional soccer player who presented to our hospital after sustaining a blunt chest trauma. To the best of our knowledge, this is the first reported case of cardiac contusion when acute myocardial edema and subsequent chronic myocardial injury were visualized with cardiac magnetic resonance (CMR) imaging.
A professional soccer player presented to our hospital with persistent chest pain and fatigue after being hit in the chest by a soccer ball during a national league game. The hospital admission was 10 hours after the accident and onset of symptoms. The patient had no medical history and no recent history of infectious disease. The initial workup revealed elevated cardiac troponin T of 0.576 μg/L (normal range, 0.00 to 0.03 μg/L) and creatine kinase-MB levels of 25.4 U/L (normal range, 0 to 25 U/L); the markers of inflammation proved to be negative (C-reactive protein level, 0.9 mg/L [normal range, 0 to 5.0 mg/L]; white blood cell count, 7.0×103/μL [normal range, 4 to 10×103/μL]). The patient underwent a performance-enhancing drug screening 8 days before the event as part of the regular doping control protocol of professional soccer players, which proved to be negative. Furthermore, the toxicology panel testing for 7 drugs (phencyclidine, barbiturates, cannabinoids, amphetamines, benzodiazepines, opiates, and cocaine metabolites) in spot urine was negative at the time of hospital admission. The 12-lead surface ECG showed ST-elevation in lead V3 and deep T-wave inversions across the precordial leads (Figure 1A). The ischemic ECG pattern in the setting of acute chest pain, elevated cardiac biomarkers, and negative inflammatory markers was concerning for acute coronary syndrome caused by coronary artery injury. The patient underwent urgent cardiac catheterization, which revealed normal epicardial coronary arteries (Movie IA and IB in the online-only Data Supplement). Transthoracic echocardiography showed normal left ventricular systolic function without wall motion abnormalities and no valvular pathology (Movie IIA and IIB in the online-only Data Supplement). CMR study was subsequently ordered to assess for the cause of the myocardial necrosis and was performed with a 1.5-T scanner (Achieva MR, Philips Medical Systems, Best, the Netherlands). Images were evaluated with QMASS 7.1 (Medis, Leiden, the Netherlands) postprocessing software. The CMR assessment revealed mildly enlarged left and right ventricular volumes and preserved left ventricular ejection fraction (54%). Notably, the CMR cine images showed mild regional hypokinesis in the inferior region of the apical septal segment of the left ventricle (Movie IIIA in the online-only Data Supplement). On T2-weighted fast suppressed short τ inversion recovery turbo spin echo sequence, there was increased enhancement of the myocardium corresponding to the hypokinetic myocardial region, signifying the presence of edema and short-term injury (Figures 2A and 3⇓A). At the same anatomic location, a small focal region of hyperenhancement was observed (quantified as 6% of the whole left ventricular mass) in the late gadolinium-enhanced images, which is consistent with myocardial necrosis. The inversion recovery images were acquired 10 minutes after the contrast injection (0.2 mmol/kg gadopentate dimeglumine contrast) (Figures 4A and 5⇓A). The delayed hyperenhancement followed a semicircular pattern and extended from the subendocardium to the midmyocardium, which is not characteristic for acute coronary syndrome or myocarditis. Later, results of the viral (coxsackie virus, parvovirus, cytomegalovirus, Epstein-Barr virus, human herpesvirus 6, hepatitis C virus, and HIV) titers showed no evidence of acute viral infection. Considering the clinical presentation of the patient, the normal coronary angiography, and the findings of the CMR examination, we made the diagnosis of contusio cordis. The patient was advised to refrain from strenuous physical activity for a month. At the 6-week follow-up, the patient was symptom free, and his ECG changes normalized with complete resolution of the ST- and T-wave abnormalities (Figure 1B). On the follow-up CMR examination, both the regional wall motion abnormality and edema were no longer present (Movie IIIB in the online-only Data Supplement and Figures 2B and 3⇓B). On the late gadolinium-enhancement images, the focal region with hyperenhancement persisted, still involving 6% of the left ventricular myocardial mass, reflecting permanent myocardial structural damage (Figures 4B and 5⇓B).
Establishing the correct diagnosis in patients with clinical signs of acute myocardial infarction with angiographically normal coronary arteries is challenging. CMR imaging can be a useful tool to visualize the underlying pathological process because several cardiac disorders that cause myocardial damage have a characteristic pattern of late gadolinium enhancement. The most common patterns of delayed enhancement in the CMR images are subendocardial/transmural in myocardial infarction and subepicardial/midmyocardial in acute myocarditis. Although case reports describing sustained myocardial damage after blunt chest trauma or reports describing immediate myocardial injury after heart contusion have been published previously,1,2 we describe here the first case, to the best of our knowledge, of cardiac contusion when the acute and late pathological changes in the myocardium were visualized with CMR.
Source of Funding
We are grateful to the National Development Agency of Hungary (TÁMOP-4.2.2-08/01/KMR-2008-0004) for providing support to the Heart Center of Semmelweis University, enabling excellent patient care.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/121/22/2456/DC1.