Myocarditis in the Athlete: A Focus on COVID-19 Sequelae

Abstract

Myocarditis is a leading cause of sudden death in athletes. Early data demonstrating increased prevalence of cardiac injury in hospitalized patients with COVID-19 raised concerns for athletes recovered from COVID-19 and the possibility of underlying myocarditis. However, subsequent large registries have provided reassuring data affirming low prevalence of myocarditis in athletes convalesced from COVID-19. Although the clinical significance of subclinical myocarditis detected by cardiac MRI remains uncertain, clinical outcomes have not demonstrated an increase in acute cardiac events in athletes throughout the pandemic. Future directions include defining mechanisms underlying "long-haul" COVID-19 and the potential impact of new viral variants.

Keywords: Athletes; COVID-19; Cardiac magnetic resonance imaging; Myocarditis; SARS-CoV-2.

Fig. 1

Case 1. A 34-year-old former professional rugby player and recreational cyclist, presenting with cardiac arrest. Two week earlier, he suffered a witnessed spell during sleep with erratic breathing, loss of bladder continence, and transient unresponsiveness. He woke shortly before arrival of emergency responders and felt otherwise normal. Initial evaluation including 12-lead ECG (A), head CT and EEG, high sensitivity troponin, transthoracic echocardiography, and coronary CT angiography (not shown) were unremarkable. The patient was discharged with an event monitor and maintained his exercise routine without symptom limitation. Two days after cycling 80 miles, he suffered a ventricular fibrillation arrest captured on the event monitor (B); again, recognized by erratic breathing during sleep. Following successful resuscitation, he experienced transient LV dysfunction requiring circulatory support with V-A ECMO. Ventricular function normalized by hospital day 2 and the patient was weaned from cardiopulmonary support. Serial COVID-19 testing was negative. Cardiac MRI 1 week after admission revealed normal cardiac chamber dimensions, LV wall thickness, and biventricular function (EF 65%). Delayed gadolinium enhancement images (C) revealed a midmyocardial stripe of LGE (arrows) involving the mid- and distal septum and basal and apical lateral walls (quantitative scar burden 8%). Parametric mapping demonstrated diffusely elevated native T1 (D, E) and T2 values. Clinical history and MRI features were most consistent with myocarditis.

Fig. 2

Case 2. A 25-year-old highly active male presented with pharyngitis and an irregular pulse. ECG (A) showed a junctional rhythm with occasional atrial activity and a variable PR interval. He reported no chest discomfort or shortness of breath. High-sensitivity troponin was elevated at 5452 ng/L, and COVID-19 testing was positive. Echocardiography revealed normal left ventricular chamber and wall thickness with low to normal LV systolic function (EF 53%). No regional wall motion abnormalities were evident, and global longitudinal strain was normal at −17.3%. RV size and function were normal, and a trivial posterior pericardial effusion was noted. Troponin levels normalized within 2 weeks. Cardiac MRI performed 3 weeks after presentation revealed a mildly dilated LV chamber with normal wall thickness and an LVEF of 67%. Subepicardial LGE was present in the basal to apical inferior and apical lateral segments (B) with a scar size of 14%. Native T1 values were mildly elevated along the lateral segments (C) and normal in all other regions. T2 values were normal.