Myocarditis, myocardial fibrosis and eligibility for competitive sports

Abstract

Myocarditis is a major and well-known cause of sudden cardiac death (SCD) in competitive athletes [1], and many athletes ask their cardiologists for signs of acute or chronic myocarditis during preparticipation screening. However, the overall diagnostic sensitivity is low, and evidence on treatment strategies is scarce [2]. In addition, once acute myocarditis has been diagnosed, the return-to-field decision after recovery is hampered by limited clinical experience on long-term outcomes. Cardiac Magnetic Resonance Imaging (CMR) is now an established “gold-standard” in the detection of acute myocarditis. In contrast, the predictive value of residual findings such as myocardial fibrosis regarding eligibility for competitive sports is unknown. An 18-year old professional soccer player presented to our outpatient clinic of sports medicine for return-to-field evaluation after severe acute myocarditis one year earlier. At that time, acute chest pain had occurred during a soccer match. External medical evaluation had revealed elevated troponin (181 ng/ml) and ST-segments in inferior ECG leads. Echocardiography had shown a dilated and hypertrophic left ventricle. Subsequently, CMR had been performed, revealing a large edema (Fig. 1; Supplementary file: video), extensive midand epimyocardial Late Gadolinium Enhancement (LGE) and mild hypokinesia in the LV lateral wall, consistent with acute myocarditis. Extensive serologic testing for causative agents was negative, and no endomyocardial biopsy had been performed. The patient had been advised to strictly refrain from any exercise. During follow-up, he had completely recovered clinically, but several further CMR studies had shown a persistent epimyocardial LGE in the lateral and parts of the apical and posterior walls (Fig. 2). In our clinic, physical examination, ECG, cardiac enzymes, inflammatorymarkers, echocardiography and exercise testing showed completely normal findings. However, as a consequence of the CMR findings of myocardial fibrosis, we considered the athlete ineligible for competitive sports at our evaluation. One year later, the athlete again presented to our outpatient clinic. Despite our recommendations he had continued his professional career and was still free of complaints. ECG and echocardiography showed normal findings, but exercise testing now revealed frequent ventricular premature beats originating from the left ventricular apical region, which were confirmed by 72-hour-Holter ECG, in particular during exercise. Again, competitive sport was discouraged. An18-year old professional soccer playerpresented to ouroutpatient clinic of sportsmedicine for return-to-field evaluation after severe acute myocarditis one year earlier. At that time, acute chest pain had occurred during a soccer match. External medical evaluation had revealed elevated troponin (181 ng/ml) and ST-segments in inferior ECG leads. Echocardiography had shown a dilated and hypertrophic left ventricle. Subsequently, CMRhad beenperformed, revealing a large edema (Fig.1; Supplementary file: video), extensive midand epimyocardial Late Gadolinium Enhancement (LGE) and mild hypokinesia in the LV lateral wall, consistent with acute myocarditis. Extensive serologic testing for causative agents was negative, and no endomyocardial biopsy had been performed. The patient had been advised to strictly refrain from any exercise. During follow-up, he had completely recovered clinically, but several further CMR studies had shown a persistent epimyocardial LGE in the lateral and parts of the apical and posterior walls (Fig. 2). In our clinic, physical examination, ECG, cardiac enzymes, inflammatory markers, echocardiography and exercise testing showed completely