Clinical Implications of COVID-19 Cardiac Involvement in Athletes: Management, Cardiac Testing, and Return to Play

Myocarditis is a known cause of sudden cardiac death in athletes.¹ Significant cardiac injury was observed in those hospitalized with SARS-CoV-2,^2-4 which led to concern regarding the safety of competitive sports for athletes after a COVID-19 infection. Significant cardiac involvement associated with poor outcomes among hospitalized patients^5,6 affected initial decision-making as well. Initial return to play (RTP) recommendations for athletes with COVID-19 were limited by an uncertain prevalence of cardiac injury and unknown rates of adverse outcomes with exercise. In this summary, we aim to provide an evidence-based update on RTP guidance for those with COVID-19.

COVID-19 Data and Athletes

Recently published data has improved our ability to provide guidance to readdress resumption of athletics and intense exercise training after COVID-19. Several consensus screening recommendations have been put forth,^7,8 including 2 by the American College of Cardiology’s (ACC) Sports and Exercise Cardiology Council,^9,10 all endorsing a conservative RTP screening approach early on. This consisted of the so-called “triad testing”¹¹ with 12-lead electrocardiogram (ECG), cardiac biomarker assessment [high-sensitivity troponin (hs-cTn)], and transthoracic echocardiography to exclude cardiac injury. Multiple large registries were created to track US professional and collegiate athletes who had recovered from COVID-19. Both the US professional cohort (N=789)¹² and multicenter collegiate athlete cohort (Outcomes Registry for Cardiac Conditions in Athletes [ORCCA], N=3018)¹¹ documented a low prevalence of cardiac injury (0.6%-0.7%) among previously infected athletes, most of whom underwent cardiac triad testing. Within these registries, cardiovascular magnetic resonance (CMR) was generally obtained if any initial triad testing was abnormal or if symptoms were suggestive of myocarditis (excluding 198 athletes in ORCCA with mandated CMR).^11,12 No adverse cardiac outcomes were reported as a direct consequence of COVID-19.^11,12

The Big Ten Conference published data on 1597 athletes who all underwent triad screening as well as screening with CMR.¹³ Abnormalities on CMR consistent with myocarditis¹⁴ were reported in 2.3% of athletes.¹³ Single-center studies revealed marked heterogeneity in the prevalence (0-7.6%) and variety of CMR abnormalities identified among the 13 programs that participated.¹³ Importantly, the results were consistent with the ORCCA and the professional athlete registries, with only 9 athletes (0.6%) identified with clinical symptoms and findings consistent with acute myocarditis.¹³ No confirmed cases of cardiac death in the COVID-19 registries of athletes have been identified.^11-13 Altogether, since the majority of athletes involved in the registries return to play without undergoing screening CMR, it is unlikely that there is added value for CMR that will improve clinical outcomes. Furthermore, cardiopulmonary symptoms suggestive of myocarditis are predictive of SARS-CoV-2 cardiac involvement.^11-13  Similar findings have been noted in an unselected, nonathletic cohort of health care workers, in whom mild COVID-19 symptoms were not associated with discernable cardiovascular pathology.¹⁵ As such, cardiopulmonary symptoms that persist are likely to be of greater relevance than age and athlete competition level when assessing the probability of underlying cardiac pathology.^5,11

As a result of this data, updated ACC Sports and Exercise Cardiology Council recommendations include cardiac testing only in those with moderate, severe, and/or worsening symptoms related to COVID-19, with particular attention to chest pain and exertional dyspnea as important findings suggesting cardiac involvement.¹⁰ These evidence-based changes in consensus recommendations reflect increased experience and an effort to balance identification of cardiac injury with COVID-19,¹⁰ and the time-sensitive need for guidance in this evolving sports medicine community.

Although there have been reports of acute myopericarditis temporally associated with COVID-19 vaccinations, cases are rare in prevalence.^16-18 They are predominantly after the second dose in the 2-shot series, male adolescents, and in those >16 years old. It is not recommended to routinely screen athletes for myocarditis in the absence of clinical pretest probability, including cardiopulmonary symptoms after vaccination.

RTP Assessment Guidance

In athletes recovering from COVID-19 with ongoing cardiopulmonary symptoms concerning for myocardial inflammation (eg, chest pain/tightness, dyspnea, palpitations, lightheadedness/syncope) and/or those requiring hospitalization, further clinical evaluation and cardiac testing should be performed to exclude the presence of myocardial injury prior to resuming exercise (Figure 1).¹⁹ For all others who are asymptomatic or with symptoms less suggestive of a cardiopulmonary etiology (eg, fever [temperature ≥100.4^°F], chills, lethargy, myalgias), additional cardiac testing is not recommended any longer. In addition, in those with prior infection, regardless of the amount of time that has passed since infection, athletes who have remained asymptomatic or who have had noncardiopulmonary symptoms and are exercising without limitation require no further cardiac testing. In contrast, for athletes with prior COVID-19 and a history of cardiopulmonary symptoms, the approach taken should be dictated by the duration of time since symptom resolution and the athlete’s current clinical status. If <1 month has elapsed since resolution of cardiopulmonary symptoms, triad testing should be performed. If >1 month has elapsed since cardiopulmonary symptom resolution and they are training without exercise limitation, it may be reasonable to allow continued exercise without further cardiac evaluation. This decision should be based on clinical judgement guided by the severity of prior symptoms. Of course, symptoms of syncope, sustained exertional palpitations, and/or exertional chest tightness or dyspnea warrant additional testing is most instances.

Finally, detection of isolated CMR findings may be encountered, such as late gadolinium enhancement (LGE) without concomitant edema.^13,20,21 In those with a suspicion of myocarditis or supportive abnormal findings on triad testing, this may be representative of resolving myocarditis.^22-24 Athletes may have mildly reduced left ventricular (LV) systolic function, isolated mild troponin elevation, or an abnormal ECG. This can be the result of an exercise-induced cardiac remodeling or a pathologic expression of myocarditis.²⁵ Involvement of experts in the field of sports cardiology is recommended, when possible, to help determine pathologic vs physiologic change is present. If pathologic change is less likely, consider maximal-effort exercise testing (including stress echocardiography if there is reduced LV systolic function to assess for appropriate exercise augmentation)²⁶ and ambulatory rhythm monitoring.

Return to Exercise

Prior consensus guidance related to return to exercise has been conservative and recommended individuals should abstain from exercise throughout this period, in part, because of the potential for clinical cardiac deterioration.^9,10 As a result of the aforementioned studies demonstrating a lack of  cardiac injury among athletes with mild COVID-19,^11-13 activity restriction is no longer necessary during self-isolation. For asymptomatic athletes with COVID-19, 3 days of abstinence from training has been the consensus recommendation to ensure that symptoms do not develop.

For individuals with mild noncardiopulmonary symptoms, exercise training should generally be withheld until symptom resolution (except isolated anosmia/ageusia). For athletes with cardiopulmonary symptoms, intense exercise training should be limited until symptoms resolve, self-isolation is complete, and further cardiac testing can be obtained. Lastly, a graded RTP exercise plan should be employed for all individuals with prior COVID-19 to ensure close monitoring for development of new cardiopulmonary symptoms. An individualized graded exercise program should be implemented with guidance provided by athletic trainers and primary care sports medicine clinicians when available. For most individuals participating in high-level recreational athletics, a graded return to exercise program equates to more qualitative gradual increases in effort.

For those retuning to sport with cardiopulmonary symptoms, the initial evaluation should ideally be with an ECG, cardiac biomarkers (hs-cTnI are preferred, if available), and transthoracic echocardiogram (Figure 1). Abnormal findings with triad testing or persistence of cardiopulmonary symptoms (specifically chest pain/tightness, palpitations, or syncope) would include more sensitive testing with CMR. Symptom-limited max effort exercise testing may also be a useful adjunct in cases of persistent cardiopulmonary symptoms, only after myocardial injury has been excluded with cardiac biomarkers and CMR.

Further research is needed to better understand the significance of cardiac injury detected by CMR,^13,20 particularly in the absence of symptoms. Therefore, use of CMR to screen athletes who are asymptomatic or with noncardiopulmonary symptoms has limited utility and is not recommended. However, such testing may be considered in those with abnormal triad testing and increased concern of cardiac involvement, or in those with either persistent or new cardiopulmonary symptoms.

In those with documented clinical myocarditis, existing guidance regarding sports eligibility recommends 3-6 months of complete exercise abstinence.²⁷ There is no clear recommendation for how to determine the exact RTP strategy, but should be based on resolution of cardiopulmonary symptoms and laboratory evidence of cardiac inflammation, normalization of LV systolic function, and absence of inducible cardiac arrhythmias. Whether this 3-month minimum of exercise abstinence independently reduces the risk of acute cardiac events is uncertain. In the Big Ten COVID-19 Cardiac Registry, 27 athletes (27/37, 73%) with clinical or subclinical myocarditis completed repeat CMR within 4-14 weeks after initially testing positive for COVID-19.¹³ In 11 of these athletes (41%), LGE and T2 mapping abnormalities had completely resolved after a median of 8 weeks.¹³ Whether this resolution equates complete inflammation without underlying subclinical findings is unknown. These data suggest that it is reasonable to reassess for resolution of myocardial inflammation in those with clinical myocarditis <3 months since testing positive for COVID-19, especially if they have had rapid resolution of symptoms and prior demonstration of normal LV systolic function, or in those with subclinical myocarditis identified with CMR screening. The best time for this reassessment likely should be individualized, but no sooner than previously recognized. For asymptomatic athletes with complete resolution of myocardial inflammation and no spontaneous arrhythmias, a RTP approach using conservative, graded exercise should be pursued. Further research is required to define the temporal pattern of myocardial inflammation, along with predictors of clinical myocarditis progression among all viral pathogens with affinity for the heart. 

Disclosures: Dr Martinez has completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. He has no conflicts of interest to report regarding the content herein.   

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