P282 PAUCISYMPTOMATIC POST–COVID MYOCARDITIS IN A YOUNG ATHLETE DURING THE DIAGNOSTIC INVESTIGATIONS BEFORE RETURNING TO COMPETITIVE PRACTICE, POSSIBLE USEFULNESS OF THE GLS ANALYSIS

Abstract

Abstract It is now known that the Covid19 infection can cause myocardial inflammatory damage. Several studies have shown that the echocardiographic parameter of the global longitudinal strain (GLS) was reduced compared to the general population even in paucisymptomatic patients. A young competitive athlete came to our observation for the diagnostic investigations before returning to competitive practice (return to play protocol) after Sars–Cov2 infection. The electrocardiogram did not show significant abnormalities as well as spirometry examination. Negative inflammation indexes and markers of myocardial damage were observed. The cycloergometer test showed no signs of myocardial distress, rapid chronotropic increase and dyspnea at 100W work load. HolterECG was performed showing 830 isolated ventricular ectopic beats. Echocardiographic examination showed preserved left ventricular systolic function (FEVS 59% – Simpson method) with a moderate reduction of GLS parameter –16,9%. The cardiopulmonary exercise test (CPET) showed an early anaerobic threshold and a normal pVO2max but not in line with the presumed range for a top–level athlete. Putting together the symptoms described, the CPET data and GLS parameter, despite the negative first–level investigations he underwent MRI that documented a myocardial edema in the mid–basal region of inferior and inferolateral walls of the left ventricle. Suitability for competitive practice was blocked, a gradual physical readaptation path was started and therapy with low–dose bisoprolol was set. An important clinical improvement is reported at the 6–month follow–up with evidence of normalization of the GLS parameter –23%. The CPET howed a realignment of the HR/VCO2 curve with a late threshold and increment of pVO2max. The 6–month control MRI examination showed almost no signs of myocardial inflammation and so the patient was made suitable for returning to competitive sport. In our case first–level investigations did not support any hypothesis of myocardial inflammation. The presence of stress symptoms confirmed by CPET data but especially the reduction of GLS parameter led to a deepening investigation with MRI that confirmed the presence of myocardial inflammatory lesion. Our case suggests that within a “return to play” protocol for athletes with recent SarsCov2 infection, the analysis of left ventricular systolic function by GLS may represent an additional useful element to be considered in support of standard investigations.