Marathons and half-marathons are associated with a low overall risk of cardiac arrest and sudden death. Cardiac arrest, most commonly attributable to hypertrophic cardiomyopathy or atherosclerotic coronary disease, occurs primarily among male marathon participants; the incidence rate in this group increased during the past decade.

IMPORTANCE The major North American professional sports leagues were among the first to return to full-scale sport activity during the coronavirus disease 2019 (COVID-19) pandemic. Given the unknown incidence of adverse cardiac sequelae after COVID-19 infection in athletes, these leagues implemented a conservative return-to-play (RTP) cardiac testing program aligned with American College of Cardiology recommendations for all athletes testing positive for COVID-19. OBJECTIVE To assess the prevalence of detectable inflammatory heart disease in professional athletes with prior COVID-19 infection, using current RTP screening recommendations. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study reviewed RTP cardiac testing performed between May and October 2020 on professional athletes who had tested positive for COVID-19. The professional sports leagues (Major League Soccer, Major League Baseball, National Hockey League, National Football League, and the men's and women's National Basketball Association) implemented mandatory cardiac screening requirements for all players who had tested positive for COVID-19 prior to resumption of team-organized sports activities. EXPOSURES Troponin testing, electrocardiography (ECG), and resting echocardiography were performed after a positive COVID-19 test result. Interleague, deidentified cardiac data were pooled for collective analysis. Those with abnormal screening test results were referred for additional testing, including cardiac magnetic resonance imaging and/or stress echocardiography. MAIN OUTCOMES AND MEASURES The prevalence of abnormal RTP test results potentially representing COVID-19-associated cardiac injury, and results and outcomes of additional testing generated by the initial screening process. RESULTS The study included 789 professional athletes (mean [SD] age, 25 [3] years; 777 men [98.5%]). A total of 460 athletes (58.3%) had prior symptomatic COVID-19 illness, and 329 (41.7%) were asymptomatic or paucisymptomatic (minimally symptomatic). Testing was performed a mean (SD) of 19 (17) days (range, 3-156 days) after a positive test result. Abnormal screening results were identified in 30 athletes (3.8%; troponin, 6 athletes [0.8%]; ECG, 10 athletes [1.3%]; echocardiography, 20 athletes [2.5%]), necessitating additional testing; 5 athletes (0.6%) ultimately had cardiac magnetic resonance imaging findings suggesting inflammatory heart disease (myocarditis, 3; pericarditis, 2) that resulted in restriction from play. No adverse cardiac events occurred in athletes who underwent cardiac screening and resumed professional sport participation. CONCLUSIONS AND RELEVANCE This study provides large-scale data assessing the prevalence of relevant COVID-19-associated cardiac pathology with implementation of current RTP screening recommendations. While long-term follow-up is ongoing, few cases of inflammatory heart disease have been detected, and a safe return to professional sports activity has thus far been achieved.

A ubiquitous cell adhesion receptor, CD44, preferentially binds hyaluronan, a polysaccharide macromolecule that is present in most extracellular matrices. Hyaluronan molecules have large hydrodynamic volumes that entrap substantial amounts of water and can therefore control tissue hydration (swelling). CD44 is overexpressed by synovial cells and leukocytes, and hyaluronan is overproduced in the rheumatoid synovium and in other inflammatory sites. Nevertheless, the role of the CD44-hyaluronan interaction during inflammation is unclear. Our evidence shows that the CD44 receptor plays a critical role in governing the migration of inflammatory leukocytes into the extravascular compartment of the synovium in murine arthritis. An anti-CD44 antibody induces a rapid loss of CD44 from both leukocytes and synovial cells and displays an inhibitory effect on cell-extracellular matrix interactions in the synovium. As a result, the administration of such an antibody abrogates tissue swelling and leukocyte infiltration, two major components of inflammation.

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Coronavirus disease 2019 (COVID-19) is associated with significant mortality and morbidity, including adverse cardiovascular sequelae. 1 As public health policy begins to guide the resumption of recreational and competitive sport, clinicians are charged with determining when competitive athletes and highly active individuals who have been infected with COVID-19 and recovered are medically appropriate to return to play. There are limited data establishing the epidemiologic and clinical metrics required to facilitate this process. Specifically, the prevalence of asymptomatic COVID-19 cases in the community, the prevalence of cardiac injury among nonhospitalized individuals with COVID-19, and longterm outcomes attributable to COVID-19 cardiac injury remain unknown. Recognizing these limitations, members of the American College of Cardiology's Sports & Exercise Cardiology Council, with input from national leaders in sports cardiology, provide a consensus expert opinion clinical framework on return to play in the era of COVID-19.Significant cardiac morbidity has been observed among hospitalized patients with COVID-19. Acute cardiac injury, defined as troponin levels more than the 99th percentile, electrocardiographic and/or echocardiographic abnormalities, occur in up to 22% of hospitalized patients with COVID-19, 2 which is significantly higher compared with the approximately 1% prevalence in non-COVID-19 acute viral infections. Myocarditis from myocyte invasion by the virus could result in cardiac dysfunction, arrhythmias, and death. In the acute phase, exercise could result in accelerated viral replication, increased inflammation and cellular necrosis, and a proarrhythmic myocardial substrate. Return to play after myocarditis is predicated on normalization of ventricular function, absence of biomarker evidence of inflammation, and absence of inducible arrhythmias. Risk stratification may occur after 3 to 6 months of exercise restrictions 3 and is based on extensive testing including echocardiography, stress testing, and rhythm monitoring.Evidenced-based recommendations for return-toplay guidelines are currently limited and clearly subject to change as further data are obtained in concert with improved COVID-19 case identification. Acknowledging these imperfections, our recommendations are exclusive to cardiovascular considerations and concomitant pulmonary limitations also require consideration. The duration of illness has proved critical in the clinical course of patients infected with COVID-19, with increased risk of clinical deterioration after the first week of symptoms. As such, we recommend an emphasis on the temporal progression of confirmed infection and have incorporated time-based benchmarks in our recommendations (Figure).

and Exercise Cardiology Section generated recommendations to promote safe return to play (RTP) for athletes involved with competitive sports after severe acute respiratory syndrome coronavirus 2 infection. 1 Motivated by observations of cardiac injury in patients hospitalized with coronavirus disease 2019 (COVID-19), 2 that document 1 and others 3-5 proposed algorithms for preparticipation screening, geared toward the detection of COVID-19-associated cardiac complications. At present, the prevalence and clinical implications of COVID-19 cardiac pathology in athletes are unknown. However, publicized media reports of athletes with suspected COVID-19-induced myocarditis, 6,7 coupled with emerging data documenting cardiac injury among community-based cohorts, 8,9 have fueled concerns about the safety of athletics. The definition of an athlete can also be arbitrary. From enthusiasts of youth sports to masters-level exercise (in those aged >35 years), athletes are generally considered individuals who place a high premium on training, competition, and sports achievement. 10 As such, targeted RTP risk stratification for all athletes deserves careful consideration. Relaxation of stay-at-home orders across the US enabled many athletes to return to training and competition. In collaboration with the sports medicine community and despite the current lack of supportive data, we have since accrued considerable experience overseeing RTP testing among athletes with prior COVID-19 infection at all levels of sport. This document was written to address the most common questions posed by the media and in clinics, athletic training rooms, and ongoing discussions among cardiologists who participate in the care of athletes. The authors were selected by the Leadership Council of the Sports and Exercise Cardiology Section of the American College of Cardiology to provide this narrative reassessment of the previous consensus statement. IMPORTANCE Cardiac injury with attendant negative prognostic implications is common among patients hospitalized with coronavirus disease 2019 (COVID-19) infection. Whether cardiac injury, including myocarditis, also occurs with asymptomatic or mild-severity COVID-19 infection is uncertain. There is an ongoing concern about COVID-19-associated cardiac pathology among athletes because myocarditis is an important cause of sudden cardiac death during exercise. OBSERVATIONS Prior to relaxation of stay-at-home orders in the US, the American College of Cardiology's Sports and Exercise Cardiology Section endorsed empirical consensus recommendations advising a conservative return-to-play approach, including cardiac risk stratification, for athletes in competitive sports who have recovered from COVID-19. Emerging observational data coupled with widely publicized reports of athletes in competitive sports with reported COVID-19-associated cardiac pathology suggest that myocardial injury may occur in cases of COVID-19 that are asymptomatic and of mild severity. In the absence of definitive data, there is ongoing uncertai...

As our understanding of the complications of coronavirus disease–2019 (COVID-19) evolve, sub-clinical cardiac pathology such as myocarditis, pericarditis and right ventricular dysfunction in the absence of significant clinical symptoms represents a concern. The potential implications of these findings in athletes are significant given the concern that exercise, during the acute phase of viral myocarditis, may exacerbate myocardial injury and precipitate malignant ventricular arrhythmias. Such concerns have led to the development and publication of expert consensus documents aimed at providing guidance for the evaluation of athletes after contracting COVID-19 in order to permit safe return-to-play. Cardiac imaging is at the center of these evaluations. This review seeks to evaluate the current evidence regarding COVID-19associated cardiovascular disease and how multi-modality imaging may be useful in the screening and clinical evaluation of athletes with suspected cardiovascular complications of infection. Guidance is provided with diagnostic “red flags” that raise the suspicion of pathology. Specific emphasis is placed on the unique challenges posed in distinguishing athletic cardiac remodeling from sub-clinical cardiac disease. The strengths and limitations of different imaging modalities are discussed and an approach to return-to-play decision making for athletes’ post COVID-19, as informed by multi-modality imaging, is provided.

Background-Hypertension, a strong determinant of cardiovascular disease risk, has been documented among elite, professional American-style football (ASF) players. The risk of increased blood pressure (BP) and early adulthood hypertension among the substantially larger population of collegiate ASF athletes is not known. Methods and Results-We conducted a prospective, longitudinal study to examine BP, the incidence of hypertension, and left ventricular remodeling among collegiate ASF athletes. Resting BP and left ventricular structure were assessed before and after a single season of competitive ASF participation in 6 consecutive groups of first-year university athletes (n=113