ABSTRACT
Background/Introduction: SARS-CoV-2 (subclinical) myocarditis has been demonstrated in up to 5% in athletes, and is currently a topic being intensively investigated. However, more subtle changes in function and volumetric parameters have been less well documented, especially in elite athletes, who perform at the highest levels of sports, with potentially the most outspoken adaptation. Purpose: To determine differences in cardiac function and volumetric parameters using cardiac magnetic resonance imaging (CMR) in elite athletes recovered from a SARS-CoV-2 infection as compared to non-infected elite athletes (controls). Methods: We included elite athletes from the ELITE (Evaluation of Lifetime Intensive Top-level sports and Exercise) cohort, who voluntary undergo cardiovascular pre-participation screenings, which includes cardiac magnetic resonance imaging (CMR). SARS-CoV-2 infection was diagnosed with a positive-PCR or antibody test (if unvaccinated). The primary outcome was the incidence of structural cardiac changes on CMR, defined as LV/RV BSA indexed-EDV (EDVi), LV/RV BSA indexed-ESV (ESVi), LV/RV EF, presence of pathological late gadolinium enhancement (LGE) (excluding hinge point fibrosis), and T1 times. Results: We included 234 elite athletes, mean age 27 (±7), 39% female, with main athletic disciplines (≥10 hours/week) of cycling (24%), field hockey (13%), and water polo (12%). In total 69 elite athletes had documented SARS-CoV-2 infection, and 165 were documented as not exposed to SARS-CoV-2. The majority reported mild symptoms 61/69 (88%), 1/69 (1%) severe symptoms, and 7/69 (11%) no symptoms. Mean time between infection and CMR was 2.8 (±2) months. CMR showed no significant difference between elite athletes with SARS-CoV-2 and without (Table) in mean LVEDVi (117±19 vs 120±19 ml/m2, p=0.29), LVESVi (50.6±11 vs 53.2±11 ml/m2, p=0.12), LVEF (56.9% ±5 vs 55.8% ±5, p=0.14), RVEDVi (120±20 vs 122±19 ml/m2, p=0.56), RVESVi (54.5±11 vs 56.2±11 ml/m2, p=0.29), and RVEF (54.6% ±4 vs 53.9% ±5, p=0.23). In 4/69 (4.7%) vs 1/165 (1.3%) pathological non-ischemic pattern of myocardial LGE was present (≤20% of total LV mass), of which one athlete (1.2%) showed increased T1 time, all with no deterioration in right and left ventricle function and volumetric parameters (Figure) after SARS-CoV-2 infection. All athletes made a full recovery and returned to elite competitive sports. Conclusion(s): This cross-sectional study of elite athletes demonstrates that infection with SARS-CoV-2 is not associated with deterioration in cardiac function and volumetric parameters on CMR compared with non-infected athletes, also in the small subset of athletes with pathological LGE patterns after SARS-CoV-2 infection. Prospective studies with long-term follow-up are needed to establish whether intensive sports is associated with long-term cardiac deleterious effects in elite athletes exposed to SARS-CoV-2. Funding Acknowledgement: Type of funding sources: Foundation. Main funding source(s): Dutch Heart FoundationDutch National Olympic Committee & National Sports Federation (NOC*NSF)
ABSTRACT
Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Dutch National Olympic Committee & National Sports Federation (NOC*NSF) Dutch Heart Foundation Background/Introduction Active myocarditis is regarded as an absolute contra-indication to competitive sports. Subclinical SARS-CoV-2 myocarditis/myocardial damage has been demonstrated 2-5% in athletes. However, the prognosis in elite athletes after SARS-CoV-2 cardiac involvement, with potentially detrimental effects on recovery, is currently unknown. Purpose We aimed to investigate the prevalence and clinical course of cardiac abnormalities in elite athletes after SARS-CoV-2 infection. Methods We retrospectively and prospectively included elite athletes in the COMMIT (COvid-19 Myocardial Manifestations in Intensive Top-level sports) cohort. Outcomes of interest were 1) incidence and clinical course of cardiac abnormalities on CMR, defined as reduced EF, increased EDV, presence of late gadolinium enhancement (LGE) (excluding hinge point fibrosis), increased T1 and/or T2 time);2) clinically important arrhythmias defined as premature ventricular complex, (non-)sustained ventricular tachycardia on exercise ECG or 4-8 days Holter monitoring;3) cardiac- symptoms/ events. SARS-CoV-2 infection was diagnosed with a positive- PCR or antibody test if unvaccinated. Results We included 85 elite SARS-CoV-2 recovered athletes (34% women), mean age 26.5 (±7) years, with main athletic disciplines (≥10 hours/week) football (27%), cycling (12%), water polo (9%), field hockey (9%), and rowing (8%). Mean time between infection and CMR was 2.6 months (±3). Mean CMR LVEDV/BSA was 120.6 ml/m2 (±21), LVEF 57.3% (±5), RVEDV/BSA 126.2 ml/m2 (±22), RVEF 54% (±4), and 1/85 (1.2%) showed increased T1 time after infection. In 4/85 (4.7%) myocardial LGE was present (Figure 1 and 2). In cases with LGE, after 11 (±2) months of follow-up, one demonstrated complete resolution (i.e. no LGE present) after 3 months. One case showed persistent inflammation on three sequential CMRs (1, 3, 6 months post-COVID-19);at 9 months CMR demonstrated no inflammation, but persistent LGE. Two elite athletes had unchanged LGE, one at 3 months, and one at 5 and 9 months. No clinically important arrhythmias were found in athletes with LGE. At a mean follow-up of 7.8 (±3.3) months, no symptoms/events were reported, and all had returned to sports. Pre-/post-SARS-CoV-2 infection CMR was available in 13/85 athletes;in this subgroup, no pathologic LGE or clinically important changes in ventricular volumes/function were found. Conclusion This longitudinal cohort of elite athletes demonstrates that infection with SARS-CoV-2 is associated with 4.7% of myocardial abnormalities, with varying clinical courses. There were no important arrhythmias, and we found no evidence of deleterious effects of sports after COVID-19. Prospective studies with comprehensive arrhythmia monitoring and long-term follow-up are needed to establish whether intensive sports is associated with long-term deleterious cardiac effects. Figure 1. Figure 2.