key: cord-1004709-w752kfvj
authors: Moulson, Nathaniel; Petek, Bradley J.; Drezner, Jonathan A.; Harmon, Kimberly G.; Kliethermes, Stephanie A.; Patel, Manesh R.; Baggish, Aaron L.
title: SARS-CoV-2 Cardiac Involvement in Young Competitive Athletes
date: 2021-04-17
journal: Circulation
DOI: 10.1161/circulationaha.121.054824
sha: 2d468ef80134ede7d49852bef83ba40c7146a29c
doc_id: 1004709
cord_uid: w752kfvj

Cardiac involvement among hospitalized patients with severe coronavirus disease 2019 (COVID-19) is common and associated with adverse outcomes. This study aimed to determine the prevalence and clinical implications of COVID-19 cardiac involvement in young competitive athletes. METHODS: In this prospective, multicenter, observational cohort study with data from 42 colleges and universities, we assessed the prevalence, clinical characteristics, and outcomes of COVID-19 cardiac involvement among collegiate athletes in the United States. Data were collected from September 1, 2020, to December 31, 2020. The primary outcome was the prevalence of definite, probable, or possible COVID-19 cardiac involvement based on imaging definitions adapted from the Updated Lake Louise Imaging Criteria. Secondary outcomes included the diagnostic yield of cardiac testing, predictors for cardiac involvement, and adverse cardiovascular events or hospitalizations. RESULTS: Among 19 378 athletes tested for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, 3018 (mean age, 20 years [SD, 1 year]; 32% female) tested positive and underwent cardiac evaluation. A total of 2820 athletes underwent at least 1 element of cardiac triad testing (12-lead ECG, troponin, transthoracic echocardiography) followed by cardiac magnetic resonance imaging (CMR) if clinically indicated. In contrast, primary screening CMR was performed in 198 athletes. Abnormal findings suggestive of SARS-CoV-2 cardiac involvement were detected by ECG (21 of 2999 [0.7%]), cardiac troponin (24 of 2719 [0.9%]), and transthoracic echocardiography (24 of 2556 [0.9%]). Definite, probable, or possible SARS-CoV-2 cardiac involvement was identified in 21 of 3018 (0.7%) athletes, including 15 of 2820 (0.5%) who underwent clinically indicated CMR (n=119) and 6 of 198 (3.0%) who underwent primary screening CMR. Accordingly, the diagnostic yield of CMR for SARS-CoV-2 cardiac involvement was 4.2 times higher for a clinically indicated CMR (15 of 119 [12.6%]) versus a primary screening CMR (6 of 198 [3.0%]). After adjustment for race and sex, predictors of SARS-CoV-2 cardiac involvement included cardiopulmonary symptoms (odds ratio, 3.1 [95% CI, 1.2, 7.7]) or at least 1 abnormal triad test result (odds ratio, 37.4 [95% CI, 13.3, 105.3]). Five (0.2%) athletes required hospitalization for noncardiac complications of COVID-19. During clinical surveillance (median follow-up, 113 days [interquartile range=90 146]), there was 1 (0.03%) adverse cardiac event, likely unrelated to SARS-CoV-2 infection. CONCLUSIONS: SARS-CoV-2 infection among young competitive athletes is associated with a low prevalence of cardiac involvement and a low risk of clinical events in short-term follow-up.

competitive athletes. Postviral myocarditis is a welldocumented cause of sudden cardiac death during exercise. [2] [3] [4] Concern for COVID-19 myocarditis contributed to the cancellation of organized sports and led to the development of expert consensus recommendations for the cardiac evaluation of athletes after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. [5] [6] [7] [8] Observational data among middle-aged people recovering from SARS-CoV-2 infection document high rates of potential cardiac involvement (78%) as evidenced by elevated cardiac biomarkers and cardiac magnetic resonance imaging (CMR) abnormalities. 9 Single-center observational cohort studies of collegiate athletes undergoing return-to-play (RTP) cardiac testing inclusive of CMR report highly variable rates of SARS-CoV-2 cardiac involvement (1.4% to 56%) using heterogeneous, nonstandardized definitions of disease. [10] [11] [12] [13] A subsequent study in professional athletes undergoing RTP cardiac testing reported a lower prevalence of cardiac involvement (0.6%) when using a testing strategy of 12-lead ECG, blood cardiac troponin assay, and transthoracic echocardiography (TTE), followed by CMR when clinically indicated. 14 The prevalence, clinical correlates, and outcomes of SARS-CoV-2 cardiac involvement in competitive athletes are unclear.

The Outcomes Registry for Cardiac Conditions in Athletes was designed to address these issues. This registry collected data documenting cardiac diagnoses, noncardiac diagnoses, and attendant clinical outcomes among competitive collegiate athletes returning to organized athletics during the SARS-CoV-2 pandemic.

The data that support the findings of this study are available from the corresponding author on reasonable request. This was a prospective observational cohort study. The primary aim was to determine the prevalence of cardiac involvement in collegiate athletes diagnosed with SARS-CoV-2 infection. Secondary aims were to assess the diagnostic yield of cardiac testing, identify risk factors for cardiac involvement, and determine the prevalence of adverse cardiac events or hospitalizations after SARS-CoV-2 infection in collegiate athletes. Deidentified data were collected from participating institutions from September 1, 2020, to December 31, 2020, inclusive of all athletes with previous SARS-CoV-2 infection. All aspects of this study were approved by the Massachusetts General Brigham Institutional Review Board (protocol 2020P002667).

All National Collegiate Athletic Association institutions that implemented SARS-CoV-2 infection testing and performed cardiac preparticipation evaluations for athletes infected with SARS-CoV-2 were eligible. Athletes with confirmed SARS-CoV-2 infection by laboratory testing (polymerase chain reaction, antigen, or antibody) and who underwent local cardiovascular evaluation were included. Athletes were often tested for SARS-CoV-2 infection multiple times by participating institutions, and were included in this study if they had any positive SARS-CoV-2 test. Each athlete is only represented once in the registry based on the initial positive SARS-CoV-2 test. Evaluations included a clinical assessment and a range of cardiac testing as determined by the institution including 1 or more of the following: 12 The Massachusetts General Hospital served as the central data collection center. Each participating institution submitted data using a standardized data capture tool and deidentified original clinical reports of the cardiovascular testing performed. Raw imaging data for both TTE and CMR were not available to the study investigators and diagnoses were therefore adjudicated using original clinical reports. Submitted data collection spreadsheets were reviewed for completeness and accuracy before being transcribed into a central REDCap database. Further details on recruitment and data collection methods are provided in the Methods in the Data Supplement.

Symptom severity was categorized using reported symptoms from the initial infection and the presence of any recurring symptoms with return to exercise as initially proposed for collegiate athletes. 5 Prespecified symptom severity categories included asymptomatic, mild, moderate, and cardiopulmonary. 5 Mild symptoms were defined as cough, fatigue, gastrointestinal symptoms (nausea, vomiting, or diarrhea), headache, anosmia, ageusia, rhinorrhea, sore throat, or nasopharyngeal congestion. Moderate symptoms were defined as the presence of COVID-19 toes or fingers, chills, fever, or myalgias. Cardiopulmonary symptoms were defined as chest pain, shortness of breath, palpitations, or exercise intolerance. If an athlete had symptoms in multiple categories, he or she was assigned the most severe category on the basis of the symptoms. ECGs were deemed normal or abnormal using international criteria for ECG interpretation in athletes. 15 Abnormal ECG, TTE, and CMR reports were adjudicated as related to SARS-CoV-2 infection or unrelated to SARS-CoV-2 infection using prespecified definitions ( Table I in the Data Supplement). A troponin measurement was considered abnormal if it was >99% upper limit of normal per the local laboratory commercial assay standards. Borderline abnormal triad testing was defined as any cardiac test that was considered abnormal by the local institution and led to CMR testing but did not meet prespecified study definitions after adjudication ( Table I in the Data Supplement). These included detectable troponin level but not >99th percentile, nonspecific ECG abnormalities not fulfilling the international criteria, and TTE findings including abnormalities of unclear significance or those at the upper or lower limit of the normal range and considered to potentially represent pathology (ie, left ventricular ejection fraction 50%).

Study definitions were derived for both myocardial and pericardial involvement with imaging components adapted from the Updated Lake Louise Imaging Criteria ( Table I in the Data Supplement). 16 Definite myocardial involvement was defined as CMR T1 abnormality or presence of late gadolinium enhancement + T2 abnormality or CMR T2 abnormality + 1 or more supportive findings (left ventricular ejection fraction <45%, small or greater pericardial effusion, pericardial enhancement, or troponin >99% upper limit of normal). Probable myocardial involvement was defined as CMR T1 abnormality or presence of late gadolinium enhancement + 1 or more supportive findings (same as definite myocardial involvement). Possible myocardial involvement was defined as isolated CMR T1 abnormality or presence of late gadolinium enhancement. SARS-CoV-2 pericardial involvement was defined as a small or greater pericardial effusion or pericardial enhancement on CMR. Any athlete meeting criteria for myocardial involvement of SARS-CoV-2 infection who also had pericardial involvement was labeled as definite, probable, or possible myopericardial involvement based on the definitions for myocardial involvement.

Outcomes for this study included adverse cardiovascular events (new clinically significant arrhythmias, clinical heart failure, or sudden cardiac arrest or death) or hospitalizations related to SARS-CoV-2. Follow-up time was defined as the date of symptom onset or date of positive SARS-CoV-2 test if asymptomatic (or if symptoms were not reported) to the date of last cardiovascular outcomes update from each institution.

Patient characteristics, SARS-CoV-2 symptoms, and cardiac testing results were described using basic descriptive methods including frequency distributions, means and SDs, and medians and interquartile ranges; 95% CIs for all prevalence estimates were calculated by exact binomial distribution. Because of the small number of observed SARS-CoV-2 cardiac cases and the known small sample bias with maximum likelihood estimation, the Firth penalized logistic regression method was used to assess unadjusted associations with definite, probable, and possible SARS-CoV-2-related cardiac involvement. A multivariable Firth logistic regression model using backwards variable selection was built to identify independent predictors of SARS-CoV-2 myocardial/pericardial involvement. The final model was determined on the basis of goodness of fit using Akaike information criteria. Odds ratios (ORs) and 95% CIs are reported. Secondary analyses modeling only definite and probable SARS-CoV-2-related cardiac involvement were also conducted using the same approach. Statistical analyses were performed using SAS (version 9.4; SAS Institutes) and R: A Language and Environment for Statistical Computing (R Core Team; https://www.R-project.org/).

Among 19 378 athletes enrolled during the study period, 3384 (17.5%) tested positive for SARS-CoV-2 infection and 3018 (15.6%) met study inclusion criteria ( Figure  I in the Data Supplement). Baseline characteristics for the cohort and for the subgroup with SARS-CoV-2 cardiac involvement are presented in Table 1 . The cohort, comprising athletes from 42 colleges or universities, includes representation from 26 distinct sporting disciplines including American-style football (36%), baseball (9%), cross country/track and field (8%), lacrosse (6%), and basketball (6%) ( Table II in the Data Supplement). The majority of athletes were asymptomatic (33%) or had mild symptom burden (29%), most commonly accounted for by loss of taste or smell (40%), headache (39%), and sore throat (31%) during the acute phase of SARS-CoV-2 infection ( Figure 1 ). Cardiopulmonary symptoms (chest pain, shortness of breath, palpitations, had cardiac abnormalities unrelated to SARS-CoV-2 infection (a combination of known and new cardiac findings). Among athletes with 1 or more abnormal triad test results potentially related to SARS-CoV-2 (n=67), 37 underwent CMR, whereas the remaining 30 were ultimately deemed to have isolated testing abnormalities unrelated to SARS-CoV-2 (Table IV in the Data Supplement). Of the 37 athletes who underwent CMR for an abnormal triad test, only 2 (5.4%) had multiple abnormal tests ( Figure 4) . Fourteen athletes had normal triad testing but were found to have CMR abnormalities potentially related to SARS-CoV-2. 

We report data characterizing collegiate athletes undergoing cardiovascular evaluation after SARS-CoV-2 Values are presented as n (%) or mean (SD). BMI indicates body mass index; CMR, cardiac magnetic resonance imaging; PCR, polymerase chain reaction; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; and TTE, transthoracic echocardiography.

*Partial data are available for the following characteristics: age, n=3006 (total cohort); sex, n=3017 (total cohort); BMI, n=2621 (total cohort) and n=20 (myocardial/pericardial SARS-CoV-2 involvement); race, n=2980 (total cohort); preexisting conditions, n=2800 (total cohort); and symptom categories, n=2676 (total cohort).

†The "Other" category includes Asian, American Indian, Native Hawaiian, Pacific Islander, and self-selected other.

‡Includes other combinations not listed. The mean age was 21±0.4 years (range, 17 to 24), with athletes from sporting disciplines including baseball, basketball, cheerleading, cross-country/track and field, football, lacrosse, soccer, softball, tennis, and volleyball. ADHD indicates attention-deficit/hyperactivity disorder; c/w, consistent with; CMR, cardiac magnetic resonance imaging; CP, chest pain; DOE, dyspnea on exertion; ECV, extracellular volume fraction; FIESTA, fast imaging employing steady-state acquisition; HLD, hyperlipidemia; hs, high sensitivity; HTN, hypertension; LAE, left atrial enlargement; LGE, late gadolinium enhancement; LV, left ventricular; LVEF, left ventricular ejection fraction; NA, not applicable; PCR, polymerase chain reaction; RAE, right atrial enlargement; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; SOB, shortness of breath; T1D, type 1 diabetes; TTE, transthoracic echocardiography; TWI, T-wave inversion; and WMA, wall motion abnormality.

*If the patient was asymptomatic, time is listed as the time from positive SARS-CoV-2 testing to CMR. infection with the following key findings. First, cardiac evaluation conducted in accordance with current recommendations, 5, 7 which suggest risk stratification based on SARS-CoV-2 symptom burden to determine the role of triad testing and CMR, had a diagnostic yield for definite, probable, or possible cardiac involvement of 0.5% (95% CI, 0.3-0.9). Second, the prevalence of definite, probable, or possible SARS-CoV-2 cardiac involvement, derived from the first multicenter cohort of competitive athletes undergoing screening CMR, was 3.0% (95% CI, 1.1-6.5). Our data suggest these represent the lower and upper estimates (0.5% to 3.0%) of cardiac involvement after SARS-CoV-2 infection in young otherwise healthy individuals. Third, clinical predictors of SARS-CoV-2 cardiac involvement include cardiopulmonary symptoms during acute infection or on return to exercise and any abnormality on triad testing suggestive of SARS-CoV-2 cardiac involvement. In this cohort, a stepwise approach that used the presence of moderate severity or cardiopulmonary symptoms or any abnormal triad test to trigger a diagnostic CMR would have identified 9 of 11 (81.8%) athletes diagnosed with definite or probable myocardial or myopericardial involvement. Last, no athlete diagnosed with definite, probable, or possible cardiac involvement had an adverse cardiac event through the follow-up period.

The prevalence and clinical implications of cardiac sequalae after SARS-CoV-2 infection among people not requiring hospitalization have yet to be determined. Defining disease prevalence is of paramount importance to understand diagnostic testing performance and inform recommendations for population-based screening. Among a German cohort recovering from SARS-CoV-2 infection (mean age, 49 years; 33% hospitalized for symptoms of SARS-CoV-2 infection), 78% were reported to have cardiac involvement as defined by abnormalities on CMR. 9 Recent singlecenter cross-sectional studies of collegiate athletes undergoing screening CMR after SARS-CoV-2 infection have documented highly variable prevalence estimates of cardiac involvement, ranging from 1.4% to 56%. [10] [11] [12] [13] The basis for this heterogeneity is multifactorial with contributions from variable study designs, limited sample sizes, and inconsistent definitions of cardiac involvement. Findings from the present study, leveraging multicenter CMR data, and the use of strict and conservative definitions that adhere to contemporary clinical imaging criteria suggest that SARS-CoV-2 cardiac involvement among collegiate athletes is less common than previously reported. This finding is similar to the prevalence rate of cardiac involvement recently A, Athletes undergoing primary CMR screening protocol. B, Athletes undergoing clinically indicated CMR screening protocol. *Borderline triad testing as indication for CMR included detectable troponin level but not >99th percentile, nonspecific ECG abnormalities not fulfilling international criteria, and transthoracic echocardiogram (TTE) findings including abnormalities of unclear significance or those at the upper or lower limit of the normal range and considered to potentially represent pathology (ie, left ventricular ejection fraction 50%). CMR indicates cardiac magnetic resonance imaging; cTn, cardiac troponin; and SARS-CoV-2, severe acute respiratory syndrome coronavirus 2.

Moulson et al SARS-CoV-2 Cardiac Involvement in Athletes reported among professional athletes (0.6%) who were assessed using triad testing followed by clinically indicated CMR. 14 CMR has emerged as the noninvasive reference standard for confirming myocarditis among patients with disease-specific symptoms or other cardiac testing suggestive of this diagnosis. Numerous factors including the paucity of normative CMR data in athletes, interreader interpretation variability, financial cost, and access to testing underlie uncertainties about the use of CMR as a primary screening tool. Our data highlight important tradeoffs pertaining to use of CMR as a screening modality versus its use to confirm cardiac involvement. Among athletes undergoing clinically indicated CMR based on symptom burden or an abnormal triad test (n=119), 12.6% (95% CI, 7.2-17.9) were diagnosed with definite, probable, or possible cardiac involvement. This diagnostic yield was 4-fold higher than that observed when CMR was used as part of a primary screening protocol (6 of 198 [3.0%; 95% CI, 1.1-6.5]). However, 3 of 6 of athletes with definite, probable, or possible cardiac involvement undergoing screening CMR were asymptomatic or had mild symptoms and normal triad testing. CMR detected isolated late gadolinium enhancement or abnormal T1 data, age indeterminant markers of myo-cardial fibrosis, or abnormal tissue architecture in a small number of athletes with no other features suggestive of acute SARS-CoV-2 cardiac involvement. Although we strongly suspect that these findings were unrelated to recent SARS-CoV-2 infection, we categorized these findings as "possible cardiac involvement, " underscoring the need to better understand their prevalence and clinical significance among young competitive athletes. In aggregate, these issues illustrate the inherent tradeoff between a CMR-inclusive screening protocol that may enhance sensitivity and a clinically driven approach that maximizes specificity.

Autopsy series have established myocarditis as an important cause of sudden death during exercise. [2] [3] [4] Before the SARS-CoV-2 pandemic, myocarditis was routinely diagnosed among patients presenting with postviral cardiovascular symptoms, malignant arrhythmias, or myocardial dysfunction. Diagnostic CMR criteria and sport eligibility recommendations were developed on the basis of considerable experience with this clinical presentation. [16] [17] [18] It remains unclear whether isolated cardiac abnormalities detected through CMR-based screening harbor a risk similar to typical clinically diagnosed myocarditis and how often these findings occur in other viral infections. Our SARS-CoV-2 cardiac involve- *Borderline triad testing as indication for CMR included detectable troponin level but not >99th percentile, nonspecific ECG abnormalities not fulfilling international criteria, and TTE findings including abnormalities of unclear significance or those at the upper or lower limit of the normal range and considered to potentially represent pathology (ie, left ventricular ejection fraction 50%). †New and known diagnoses. ASA indicates atrial septal aneurysm; ASD, atrial septal defect; CMR, cardiac magnetic resonance imaging; cTn, cardiac troponin; HCM, hypertrophic cardiomyopathy; LV, left ventricular; NCAA, National Collegiate Athletic Association; PFO, patent foramen ovale; RV, right ventricular; SARS-COV-2, severe acute respiratory syndrome coronavirus 2; and TTE, transthoracic echocardiogram.

Moulson et al SARS-CoV-2 Cardiac Involvement in Athletes ment prevalence estimate is similar to documented prevalence rates of myocarditis after influenza infection. 19 Although many collegiate athletes in this cohort did not undergo CMR as part of their RTP screening algorithm, we observed no adverse cardiac events in this group. Whereas longer follow-up is of critical importance, our data suggest that the potential for subclinical cardiac involvement characterized by isolated CMR abnormalities is of low short-term clinical risk.

There are several limitations of this study. First, screening protocol heterogeneity across participating institutions may have affected our estimates of prevalence and diagnostic yield. Nonetheless, this study examines the largest number of athletes who have undergone some form of cardiac testing after SARS-CoV-2 infection (n=3018) and the largest multicenter CMR-inclusive screening cohort (n=198) of competitive athletes to date. Second, diagnostic testing results reported for both TTE and CMR were extracted from the primary clinical reports provided by participating institutions. Whereas this approach captures the actual clinical experience of our cohort, the unblinded clinical interpretation of the testing may have resulted in a degree of observer bias on the part of the interpreting physician. Unbiased imaging adjudication by a centralized core facility represents an important area of future work. Third, there is no uniformly accepted definition of cardiac involvement attributable to SARS-CoV-2 infection. We therefore used fundamental components of the Updated Lake Louise Imaging Criteria 16 to generate de novo definitions of possible, probable, and definite cardiac involvement and presented full clinical profiles of athletes meeting these criteria. Future work is warranted to validate this approach. Last, we acknowledge the relatively short duration of our clinical follow-up and underscore the need for ongoing clinical surveillance of this cohort. However, the median of 113 days (interquartile range, 90-146) follow-up captured coincides with the period of highest risk of adverse events during exercise after acute myocardial injury.

Findings from this study provide an opportunity to assess and refine consensus recommendations for preparticipation cardiac screening of athletes after SARS-CoV-2 infection. 5, 7 Given the low prevalence of cardiac involvement and the absence of adverse events during shortterm clinical surveillance related to SARS-CoV-2 infection among both collegiate and professional athletes, 14 we propose the following considerations regarding future RTP cardiac testing after SARS-CoV-2 infection. First, our data support that athletes with asymptomatic or mild symptom burden from acute SARS-CoV-2 infection do not require additional cardiac testing before resumption of organized athletics. Second, triad test-ing in the form of a 12-lead ECG, cardiac troponin, and TTE should be considered among athletes after acute SARS-CoV-2 infection who experience moderate systemic or cardiopulmonary symptoms, with the presence of cardiopulmonary symptoms representing a particularly important marker of risk. Last, our data suggest that the diagnostic yield of CMR will be optimized by confining its use to athletes presenting with increased clinical pretest probability of acquired myocardial pathology as defined by the presence of SARS-CoV-2-related cardiopulmonary symptoms or abnormalities on triad testing. These recommendations are generally consistent with the most recent RTP cardiac testing guidelines.

In a large prospective registry of collegiate athletes, SARS-CoV-2 infection occurred in 17.5% of athletes. Clinical evaluation revealed a low prevalence (0.5% to 3.0%) of definite, probable, or possible SARS-CoV-2 cardiac involvement and a low risk of adverse cardiac events during short-term follow-up. The clinical relevance of cardiac testing abnormalities after SARS-CoV-2 infection among athletes without other clinical features of myocardial involvement requires additional study. Future studies with extended clinical follow-up and appropriate control populations including athletes without SARS-CoV-2 infection are needed to better inform risk and the refinement of evidence-based screening strategies. 

Moulson et al SARS-CoV-2 Cardiac Involvement in Athletes US Rowing, the New England Patriots, the Boston Bruins

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The authors thank the collaborators for the Outcomes Registry for Cardiac Conditions in Athletes registry. 

Dr Patel reports advisory board participation from Amgen, Bayer, Janssen, Heartflow, and Medscape; grant funding from National Heart, Lung, and Blood Institute, Bayer, Janssen, Heartflow, and Idorsia; and support from the Joel Cournette Foundation for research on athlete's hearts. Dr. Baggish has received funding from the National Institute of Health/National Heart, Lung, and Blood Institute, the National Football Players Association, and the American Heart Association and receives compensation for his role as team cardiologist from the US Olympic Committee/US Olympic Training Centers, US Soccer,

 Tables I-VI