key: cord-0821446-ynwc739g
authors: Ibarrola, Martin; Dávolos, Ignacio
title: Myocarditis in athletes after COVID-19 infection: The heart is not the only place to screen
date: 2020-09-22
journal: Sports medicine and health science
DOI: 10.1016/j.smhs.2020.09.002
sha: b8524a653f3b33e51d6054f4e6fdf3be9faeb9e0
doc_id: 821446
cord_uid: ynwc739g

COVID-19 patients are susceptible to hypercoagulability. For the safe return to sports after COVID-19, athletes or individuals wanting to resume physical activity should complete screening for myocardial injury and myocarditis. In addition, patients with COVID-19 are reported at prevalence of 27% to 31% for venous thromboembolic events. The probability of deep vein thrombosis and pulmonary embolism prior to intensive exercise after COVID-19 infection should be considered. The prevalence of cardiac injury is reported at 19%, and the prevalence of deep vein thrombosis and pulmonary embolism is higher than that for myocarditis. Thus, the heart is not the only system needing screened. Examination for myocardial injury and myocarditis are mandatory. Also, deep vein thrombosis, and pulmonary thromboembolism must be considered, and when possible, blood troponin values, D-dimer prothrombin time, and activated partial thromboplastin time levels are determined for COVID-19 infection athletes or any individual before returning to sporting practice or intense physical activity or exercise.

by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The overall virus's course and outcome still remain uncertain. The first human cases of COVID-19, the disease caused by the novel coronavirus causing COVID-19, subsequently named SARS-CoV-2, were first reported by officials in Wuhan City, China, in December 2019. 1 The pathophysiology of COVID-19 is complex, but some unrecognized complications of the illness include coagulation disorders and cardiovascular system complications follow this illness. COVID-19 has the potential to negatively impact the safe resumption of competitive sports, increasing risk for sudden cardiac death. Coagulation cascades with thrombin generation are activated by proinflammatory cytokines is a process known as immune-thrombosis or thromboinflammation and is known as a complication in COVID-19 infection patients. 2 The cell entry of SARS-CoV-2 depends on the angiotensin-converting-enzyme 2 (ACE2) receptor, which is widely expressed in the heart, endothelial cells and is linked to inflammatory activation. Autopsy data from three COVID-19 patients showed infection of the endothelial cells in the heart and diffuse endothelial inflammation, but no sign of lymphocytic myocarditis. 3 Because the heart abundantly expresses ACE2, the heart is However, this report does not consider the possibility of venous or pulmonary thromboembolic complications due to COVID-19 which must be evaluated prior to the return of athletes to sporting activities. 7 The highest mortality rates are observed in patients with underlying cardiovascular disease and elevated cardiac troponin levels. Observed cardiac injuries are 19% of patients hospitalized with COVID-19 and is associated with a higher risk of in-hospital mortality. 2, 5 Is the heart the only place to screen prior to safe returning to sports or physical activity? This question is most important. When an evaluation is correctly completed, the answer is no. Consideration only given to the heart is not enough. Increased D-dimer level, a fibrin degradation product, is used in the initial screening for determining the stage of hypercoagulopathy in COVID-19 infection patients. In most patients suffering mild COVID-19 disease, hypercoagulopathy, a common condition associated with DVT, a high risk of hypercoagulopathy exist, and is a likely COVID-19 complication. 8, 9 Thromboembolic complications that lead to pulmonary embolism are reported in the composite incidence of thrombotic events, which is 31%. Venous thromboembolic events are the most common (27%), and the majority of these events are pulmonary embolisms. Predictors of thrombotic events are increased age, evidence of coagulopathy on screening blood tests, higher D-dimer levels, prothrombin time above the upper limit of normal, and an activated partial thromboplastin time above the upper limit of normal. 2, 9 A large Chinese study that included 1,099 COVID-19 positive patients from 552 hospitals revealed that D-dimer concentrations above the threshold of 0.5 mg/L in 46.4% of the patients; 60% of these patients developed severe COVID-19 manifestations. In these patients, D-dimer levels (2.12 µg/mL, 0.77-5.27) were four times higher than non-severely COVID-19 infected patients (0.61 µg/mL, 0.35-1.29). The use of a D-dimer cut-off value >1.5 µg/mL to predict DVT demonstrated a sensitivity of 85% and specificity of 88.5%. 10 The heart is not the only place to screen. At discharge, determining myocardial injury and myocarditis are mandatory. Also, DVT and pulmonary thromboembolism should 

Updated understanding of the outbreak of 2019 novel coronavirus (2019-nCoV) in Wuhan

Pulmonary Embolism in Patients With COVID-19: Awareness of an Increased Prevalence

Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation

SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS

Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)

A Game Plan for the Resumption of Sport and Exercise After Coronavirus Disease 2019 (COVID-19) Infection

Return to sports after COVID-19: a position paper from the Dutch Sports Cardiology Section of the Netherlands Society of Cardiology

Coagulopathy of Coronavirus Disease

COVID-19 and its implications for thrombosis and anticoagulation

COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation

The manuscript has not been published and is not under consideration for publication elsewhere.

The authors have no conflict of interest to report.

All authors contributed equally to the publication.

To Jonathan A. Drezner and Jackie. For your advice.J o u r n a l P r e -p r o o f