Abstract 12567: Reduced Myocardial Strain is Associated With Myocardial Inflammation and Fibrosis on Cardiovascular Magnetic Resonance Imaging in Collegiate Athletes Recovering From SARS-CoV-2 Infection

Abstract

Introduction: Myocarditis is an important cause of sudden cardiac death in competitive athletes. There have been reports of myocardial inflammation on cardiovascular magnetic resonance (CMR) in athlete and non-athlete populations after SARS-CoV-2 infection; however, their clinical and functional significance is not known. We sought to investigate the relationship between left ventricular (LV) strain and other CMR markers suggestive of myocardial inflammation or fibrosis. Hypothesis: Reduced myocardial strain is associated with the presence of CMR abnormalities suggestive of inflammation, fibrosis, or necrosis in athletes recovering from SARS-CoV-2 infection. Methods: Collegiate athletes (N = 123) underwent a comprehensive CMR exam including strain encoded (SENC) imaging. We analyzed LV global longitudinal strain (GLS) across five groups defined by the presence or absence of late gadolinium enhancement (LGE), and T1 or T2 abnormalities. Myocarditis diagnosis on CMR required both abnormal T1 or LGE, and abnormal T2, in the same LV segment. Results: We enrolled 11 COVID negative control athletes (Group 1). Among COVID positive athletes, 42 had no abnormalities on CMR (Group 2), 31 had isolated right ventricular insertion point (RVIP) LGE (Group 3), 28 had LGE beyond RVIP (Group 4), and 11 athletes had myocarditis (Group 5). GLS was significantly lower in Groups 3, 4, and 5 compared with negative controls (p<0.05, Figure 1). There was a deterioration in GLS as CMR abnormalities progressed from control athletes to those with LGE and myocarditis. There was no significant difference in LV ejection fraction between the 5 groups. Conclusions: In conclusion, SARS-CoV-2 infection in collegiate athletes leads to subtle abnormalities in cardiac function detected by GLS that correlate with abnormal mapping and LGE suggestive of myocardial inflammation and fibrosis. The clinical significance of these abnormalities remains to be determined.