Cover Story

Cardiovascular Considerations for the Athlete With COVID-19

Max Weiss, MD, and Eugene H. Chung, MD

University of Michigan Medicine, Ann Arbor, Michigan

Max Weiss, MD, and Eugene H. Chung, MD

University of Michigan Medicine, Ann Arbor, Michigan

The cardiovascular effects of COVID-19 infection on athletes and the population at large is a topic of ongoing research and debate. Atrial or ventricular arrhythmias, acute coronary syndrome, thrombosis, cardiogenic shock, myocarditis, and stress-induced cardiomyopathy are some of the known manifestations of COVID-19-related cardiac injury.1 Myocarditis, historically attributed to 3% to 12% of sudden cardiac deaths in athletic populations,2 is one of the most concerning consequences of this novel virus in athletes. In the early stages of the pandemic, sporting activities at every level were cancelled. However, more recently, some professional sports — with intensive testing and isolation protocols — have resumed play, while collegiate, high school, and recreational sports have resumed to varying degrees. In this article, we summarize the current body of literature on the cardiovascular effects of COVID-19 on athletes, as well as expert recommendations on the management of affected patients in this population.

Cardiovascular Effects of COVID-19 on Athletes

While unique cardiovascular effects of COVID-19 have been observed,3-5 myocarditis is one of the most concerning for the athlete. Occurring more frequently compared to non-COVID-19 viral illnesses,6 myocarditis can incite acute myocardial injury, impaired systolic function, myocardial scarring, arrhythmia, and death. Acute myocardial injury, including elevated troponin levels >99th percentile, and electrocardiographic or echocardiographic abnormalities, have been described in up to 22% of patients hospitalized with COVID-19.7 Those with pre-existing cardiovascular disease seem to have a significantly adverse prognosis if infected by COVID-19.8 Of particular concern to athletes is a risk of increased inflammation, viral replication, and arrhythmia due to exercise during the acute viral phase.9 

To understand the scope of this problem, study of the prevalence of myocarditis in this population is essential, and so far, we have seen a small number of observational studies. Rajpal et al10 recently published a study of 26 NCAA athletes recovering from mild, or asymptomatic, non-hospitalized COVID-19 infections; while no abnormalities on ECG, echocardiography, or serum troponin were identified, 4 athletes (15%) had cardiac MRI findings consistent with myocarditis. One of the 4 had symptoms. An additional 8 (30.8%) had LGE without T2 elevation. The clinical significance of these cardiac MRI findings is limited by the absence of both baseline cardiac MRI prior to infection as well as a control population; it is difficult to establish causation or whether these are preexisting and/or training-related changes.10 Brito et al11 further published a cross-sectional, observational study of imaging findings among 54 NCAA athletes with primarily asymptomatic or mild COVID-19 cases. On transthoracic echocardiography, 1 athlete had an ejection fraction <50% with global hypokinesis, 6 had reduced global longitudinal strain, and 3 had small pericardial effusions. On CMR, native T2 values were normal and no myocardial edema was present in all studies. However, 19 athletes (40%) had late pericardial enhancement, and pockets of pericardial effusion (≥5 mm) were observed in 28 (58%) patients. Nine athletes (19%) demonstrated increased T1, with 1 symptomatic patient showing late myocardial enhancement. There were no significant differences in imaging findings between asymptomatic and symptomatic cases. The median time from diagnosis to imaging was 27 days.11 In a non-athlete population, Puntmann et al12 studied 100 patients (median age 53 years, 33% requiring hospitalization) recently recovered from COVID-19. Any cardiac involvement on cardiac MRI was reported in 78% of patients, and ongoing inflammation in 60% by abnormal native T1 and T2, at a median interval of 71 days after COVID-19 diagnosis. Seventy-six percent had detectable high-sensitivity troponin.12 This study was limited by several factors, including an older population with comorbidities, lack of outcome data, and selection bias. Despite their limitations, these 3 cardiac MRI studies have raised concern about cardiac involvement in relatively asymptomatic COVID-19 infected patients. More research is sorely needed, and multi-institutional registries are quickly being established to try and provide answers. Specifically, the Big Ten Conference is establishing a cardiac registry for all student athletes recovering from COVID-19 infection.13 Data will be collected and analyzed by specific core labs in the areas of CMR, echocardiography, ECG/arrhythmia, clinical/biomarker, and epidemiology. Testing will be obtained once out of isolation within a 10 to 14 day window after a positive test or after resolution of symptoms, while CMR will be obtained after day 14.13

Current Expert Recommendations

Several sets of recommendations from experienced sports cardiologists have been published to provide guidance for the management of athletes during the COVID-19 pandemic. While asymptomatic athletes without COVID-19 are encouraged to follow social distancing guidelines and continue physical activity, subtle differences exist in the evaluation and management of COVID-19-positive athletes. In a statement sponsored by the American College of Cardiology’s (ACC) Sports and Exercise Cardiology Leadership Council, Phelan et al initially suggested 2 weeks of rest/no exercise in COVID-19 positive athletes from either 1) the time of positive test in an asymptomatic athlete, or 2) the time of symptom resolution in symptomatic athletes.6 This recommendation was updated by a writing group convened by the same council, shortening this period to 10 days, while further emphasizing cardiac testing in the asymptomatic or mildly symptomatic patient only if new symptoms develop. Many universities have chosen to evaluate all COVID-19-positive athletes with high-sensitivity troponin, 12-lead ECG, and 2-dimensional echocardiography to assess for signs of myocarditis prior to returning to play. Athletes with abnormalities in any of the above testing should be managed with cardiac consultation as appropriate and within the ACC/American Heart Association (AHA) athlete myocarditis guidelines. Troponin testing in non-hospitalized athletes should ideally be performed at least 24 to 48 hours after exercise.14 Further testing with cardiac MRI, exercise testing, or ambulatory rhythm monitoring can be considered as needed depending on the results of initial testing and clinical context.6,14 Athletes with moderate-to-severe cases of COVID-19 should be evaluated with ECG, high-sensitivity cardiac troponin, and an echocardiogram, with abnormal test results warranting consideration for serial high-sensitivity cardiac troponin and/or CMR testing. Of note, the Big Ten Conference has published its own document and requires a cardiac MRI in addition to the above in the context of a conference-wide cardiac registry, for all COVID-19-positive athletes.13 

Around the same time as the ACC Council’s first paper, Baggish et al15 proposed utilizing a 12-lead ECG as the initial evaluation in COVID-19-positive athletes with asymptomatic or mild clinical courses; those with abnormal ECGs would subsequently undergo exercise testing and 2-dimensional echocardiography. Pathologic ECG patterns include ST segment depression, (new) diffuse ST segment elevation, T-wave inversion, and pathologic Q waves. Athletes requiring hospitalization due to COVID-19 should be re-evaluated prior to returning to play with consideration given to performing testing for high-sensitivity troponin and natriuretic peptide, 12-lead ECG, 2-dimensional echocardiography, exercise testing, and ambulatory rhythm monitoring. Cardiac MRI should be considered in athletes with evidence of myocardial involvement on prior testing or strong clinical suspicion. Return to training in athletes with myocarditis should be done gradually under the supervision of a cardiologist, with serial cardiac imaging in those with abnormal cardiac function.15

Wilson et al recommended an ECG and echocardiogram for all athletes with symptomatic COVID-19 independent of severity, with abnormal results warranting CMR, ambulatory rhythm monitoring, high-sensitivity cardiac troponin T, and cardiopulmonary exercise testing.16 These follow-up tests can be considered part of the initial evaluation in those with persistent symptoms (>14 days from symptom onset) or severe symptoms requiring hospitalization. Noting the difficulty in determining the cause of persistent cardiopulmonary symptoms in athletes, pulmonary testing including follow-up chest imaging, pulmonary function testing, D-dimer, and CRP are suggested in those hospitalized or with persistent symptoms.16

Schellhorn et al suggest a 2-week restriction from intense exercise in asymptomatic COVID-19-positive athletes and a 2- to 4-week restriction for symptomatic athletes without evidence of myocarditis, with a normal ECG after these periods needed prior to resuming activity.17

Future Considerations

Baseline testing and the use of an appropriate control group are critical for defining the prevalence and severity of cardiac involvement, particularly with respect to emerging data with cardiac MRI. Though professional sports leagues have been largely successful in resuming play by implementing strict isolation and testing protocols, additional research is needed to determine the risks to all athletes and sports leagues with fewer financial and medical resources. Large-scale, longitudinal data for abnormal non-invasive cardiovascular testing and clinical outcomes in athletes with COVID-19 infection is essential for safely returning to sports. 

Disclosures: The authors have no conflicts of interest to report regarding the content herein.

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