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Year : 2022  |  Volume : 22  |  Issue : 2  |  Page : 87-88

Post-COVID-19 death among athletes: Is interleukin-6 screening needed?

1 Department of Public Health, Tuberculosis Program, First Health Cluster, Ministry of Health, Riyadh, Saudi Arabia
2 Department of Physical Therapy for Women's Health, Faculty of Physical Therapy, Cairo University, Giza, Egypt
3 Department of General Medicine, Faculty of Medicine, Zagazig University, Zagazig, Egypt

Date of Submission07-May-2022
Date of Decision30-May-2022
Date of Acceptance03-Jun-2022
Date of Web Publication30-Aug-2022

Correspondence Address:
Dr. Amr Ahmed
Department of Public Health, Tuberculosis Program, First Health Cluster, Ministry of Health, Riyadh
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sjsm.sjsm_10_22

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How to cite this article:
Ahmed A, Refaey N, Brakat AM. Post-COVID-19 death among athletes: Is interleukin-6 screening needed?. Saudi J Sports Med 2022;22:87-8

How to cite this URL:
Ahmed A, Refaey N, Brakat AM. Post-COVID-19 death among athletes: Is interleukin-6 screening needed?. Saudi J Sports Med [serial online] 2022 [cited 2023 Sep 29];22:87-8. Available from: https://www.sjosm.org/text.asp?2022/22/2/87/355189

Dear Editor,

Since COVID-19 or coronavirus disease 2019 (SARS CoV-2) was declared a global pandemic, this pandemic has dramatically impacted the health systems, economy, and lifestyles all around the world. Furthermore, SARS-CoV-2–related illness has a clear impact on physical activity, sport, and athletes of all levels. SARS-CoV-2 can cause medical complications, both short term and long term. The residual effects can complicate medical protocols for returning to play.[1]

Myocarditis is one of the most common causes of sports-related sudden cardiac death in athletes under the age of 35.[2] A common cause of sudden cardiac death in athletes is myocarditis preceded by a viral infection. Concerns about SARS-CoV-2 cardiovascular sequelae in athletes have been accentuated by reports of presumptive myocarditis in several high-profile athletes.[3]

In a cohort study of 1597 university competitive athletes in the United States, 37 athletes (2.3%) developed clinical and subclinical myocarditis after being infected with COVID-19.[4] Furthermore, myocarditis prevalence on cardiovascular magnetic resonance imaging (MRI) in athletes following positive COVID-19 test results is 1%–3%.[5] More than a third of 54 previously healthy college athletes who tested positive for COVID-19 had pericardial inflammation on imaging. Severe cases of myocarditis and pericarditis, in particular, can lead to chronic heart failure or death, posing major public health concerns.[6],[7]

Coronaviruses have the potential to disrupt host immune responses. Several studies have found a “cytokine storm” involving the release of interleukin-1 (IL-1) and IL-6, as well as tumor necrosis factor α and other inflammatory mediators. Myocarditis, arrhythmias, ventricular dysfunction, and sudden death are caused by a “cytokine storm.”[8]

IL-6 is an inflammatory IL that is primarily produced by macrophages and T lymphocytes in response to pathogens. It is crucial to control several viral infections at homeostatic levels, but its increased production significantly contributes to cytokine storms. IL-6 has been considered a critical mediator and a positive predictor of disease severity, radiologic changes, risk for mechanical ventilation, and death.[9]

In a recent study, IL-6 has a direct electrophysiological role of IL-6 in arrhythmogenesis as IL-6 alone was found to be more effective than the combination of azithromycin and hydroxychloroquine in lowering heart rate, increasing PR interval, and increasing QTc. Furthermore, combinations of IL-6, azithromycin, and hydroxychloroquine in vivo or in vitro caused significant bradycardia, conduction problems, QTc prolongation, and asystole.[10]

Skeletal muscles express cytokines through direct autocrine and paracrine effects, so acute and prolonged strenuous exercise raises circulating levels of IL-6, while chronic exercise decreases markers of chronic inflammation.[11] Severe SARS-CoV-2 causes catabolic muscle wasting which raises IL-6 levels.

The resumption of training and competitions without health risks in athletes with cardiovascular complications related to SARS-CoV-2 includes abstinence from competitive sports or aerobic activity for 3–6 months until resolution of myocardial inflammation by cardiac MRI or troponin normalization and monitoring of circulating IL-6 as we consider IL-6 as a relevant tool for prognostic evaluation.[2],[12]

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Conflicts of interest

There are no conflicts of interest.

  References Top

Metzl JD, McElheny K, Robinson JN, Scott DA, Sutton KM, Toresdahl BG. Considerations for return to exercise following mild-to-moderate COVID-19 in the recreational athlete. HSS J 2020;16:102-7.  Back to cited text no. 1
Maron BJ, Udelson JE, Bonow RO, Nishimura RA, Ackerman MJ, Estes NA 3rd, et al. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task force 3: Hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and other cardiomyopathies, and myocarditis: A scientific statement from the American Heart Association and American College of Cardiology. Circulation 2015;132:e273-80.  Back to cited text no. 2
Schellhorn P, Klingel K, Burgstahler C. Return to sports after COVID-19 infection. Eur Heart J 2020;41:4382-4.  Back to cited text no. 3
Daniels CJ, Rajpal S, Greenshields JT, Rosenthal GL, Chung EH, Terrin M, et al. Prevalence of clinical and subclinical myocarditis in competitive athletes with recent SARS-CoV-2 infection: Results from the big ten COVID-19 cardiac registry. JAMA Cardiol 2021;6:1078-87.  Back to cited text no. 4
Udelson JE, Rowin EJ, Maron BJ. Return to play for athletes after COVID-19 infection: The fog begins to clear. JAMA Cardiol 2021;6:997-9.  Back to cited text no. 5
Brito D, Meester S, Yanamala N, Patel HB, Balcik BJ, Casaclang-Verzosa G, et al. High prevalence of pericardial involvement in college student athletes recovering from COVID-19. JACC Cardiovasc Imaging 2021;14:541-55.  Back to cited text no. 6
Husby A, Hansen JV, Fosbøl E, Thiesson EM, Madsen M, Thomsen RW, et al. SARS-CoV-2 vaccination and myocarditis or myopericarditis: Population based cohort study. BMJ 2021;375:e068665.  Back to cited text no. 7
Ye Q, Wang B, Mao J. The pathogenesis and treatment of the 'Cytokine Storm' in COVID-19. J Infect 2020;80:607-13.  Back to cited text no. 8
Liu Z, Li J, Chen D, Gao R, Zeng W, Chen S, et al. Dynamic interleukin-6 level changes as a prognostic indicator in patients with COVID-19. Front Pharmacol 2020;11:1093.  Back to cited text no. 9
Zhu X, Wang Y, Xiao Y, Gao Q, Gao L, Zhang W, et al. Arrhythmogenic mechanisms of interleukin-6 combination with hydroxychloroquine and azithromycin in inflammatory diseases. Sci Rep 2022;12:1075.  Back to cited text no. 10
Lambert CP, Wright NR, Finck BN, Villareal DT. Exercise but not diet-induced weight loss decreases skeletal muscle inflammatory gene expression in frail obese elderly persons. J Appl Physiol (1985) 2008;105:473-8.  Back to cited text no. 11
Hendren NS, Drazner MH, Bozkurt B, Cooper LT Jr. Description and proposed management of the acute COVID-19 cardiovascular syndrome. Circulation 2020;141:1903-14.  Back to cited text no. 12


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