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Cardiovascular changes in athletes post-COVID-19 infectionJulia Sysło1, Monika Bobek1, Andrew Rożek1 Introduction Coronavirus (COVID-19) caused by the SARS-CoV-2 virus is a multisystem disorder that can result in cardiovascular changes in patients. Several mechanisms have been identified to explain how COVID-19 infection can lead to cardiovascular changes. Firstly, the virus can directly attack myocardial cells which results in tissue damage. COVID-19 infection can also cause indirect damage to the cardiovascular system since SARS-CoV-2 proteins have the ability to bind to angiotensin-converting-enzyme 2 (ACE-2) receptors in the host cell. ACE-2 receptors are located throughout the cardiovascular system including in the heart, endothelial cells, smooth muscle cells and pericytes. ACE-2 is a regulator of the angiotensin-aldosterone system, which plays a vital role in many cardiovascular processes. When SARS-CoV-2 binds to the ACE-2 receptor, it is able to gain entry into cardiovascular cells and promote fibrosis, inflammation and cardiovascular disease. Additionally, the infiltration of SARS-CoV-2 into endothelial cells promotes a hypercoagulable state within the vasculature that is associated with viral-vasculitis. Finally, COVID-19 -infection can result in immune dysregulation via activation of dendritic cells in response to viral infection. This can result in inflammatory cardiovascular disease [1]. Although cardiovascular changes may occur during acute COVID-19 infection, they have also been reported in patients experiencing Post-Acute COVID-19 Syndrome (PACS). PACS refers to persistent symptoms of COVID-19 infection more than 4 weeks after acute COVID-19 infection. Many of the symptoms of PACS are non-specific, but cardiovascular symptoms have been reported to persist after acute infection. Cardiovascular changes seen in PACS include chest pain, palpitations and arrhythmias, dizziness, increased resting heart rate, myocarditis and pericarditis. The pathophysiology of PACS is not well understood, but is believed to be a consequence of pathological inflammation. Another theory suggests that SARS-CoV-2 could potentially linger in reserves within the body, making it difficult to eliminate [2]. Cardiovascular changes in PACS have been reported in both hospitalized and non-hospitalized patients. Additionally, there appears to be no correlation between developing cardiovascular changes during PACS and having a pre-existing cardiovascular disorder. Many factors increase the risk of developing cardiovascular changes during or after COVID-19 infection. Some factors include pre-existing conditions, patient age and lifestyle factors (e.g. smoking, obesity). However, certain lifestyle factors can have a positive impact on the outcome of COVID-19 infection. Both aerobic and resistance exercise reduce inflammation and improve immune function. Acute infections can result in hyperactivation of the immune system and cytokine storm, which may result in cardiac depression. Evidence suggests that in patients diagnosed with COVID-19, hospitalization was inversely related to aerobic exercise. This concludes that increased exercise capacity can reduce the severity of COVID-19 infection, a phenomenon which can commonly be noticed in athletes [3]. Though athletes may have a less severe course of COVID-19 infection, they are not immune to being left with PACS symptoms after infection. The COVID-19 pandemic has had a massive impact on day-to-day life in several aspects; including sport. In order to minimize the spread of the virus, many sporting events and training sessions were suspended. Additionally, medical clearance was required in athletes following COVID-19 infection due to risk of cardio-respiratory complications. This has resulted in the development of treatment strategies and recovery plans for athletes so that they may return to physical exercise and sport. Cardiovascular outcomes As stated earlier, the types of cardiovascular changes that can occur, not only in the general population, but also in athletes, include myocarditis (including fulminant type), myocardial oedema, pericarditis, pericardial effusion, arrhythmias, both acute and chronic heart failure, and myocardial infarction [4, 5, 6]. Out of these possible outcomes, myocarditis has been found to be one of the most common ones in athletes post-COVID-19 infection in numerous studies. Alosaimi et al. published a systematic review about these various types of cardiovascular outcomes, which pulled together findings from 15 studies and a total of 6,229 athletes [6]. In their review, the researchers found that myocarditis is prevalent from 0.4-15% of the athletic population. On the contrary, a result of just 0-2% cases of myocarditis was reached after van Hattum et al. pulled together the analysis of 12 studies involving 3,131 athletes. Another large scale study done by researchers in Italy, Casasco et al., found that in a pool of 4,143 athletes, only 1.4% of them were observed to have myocarditis. In yet another screening of 789 professional athletes, this time in the United States, 0.4% had diagnosed myocarditis [7]. Finally, Modica et al. came to the conclusion that myocarditis, though one of the more commonly seen complications after COVID-19 in athletes, is actually quite rare when after looking at 15 different studies, they reached the final calculation of only 1-4% of athletes with the disease [8]. These 15 studies had a total of 7,988 athletes involved. Based on all of these results, it can be concluded that myocarditis, in fact, is not a very common consequence of COVID-19 infection in sportspeople. It should be kept in mind however, that like with all other viral-related causes of myocardial inflammation, it can be a very dangerous and serious consequence, especially in athletes. This is related to the well-known fact that exercising whilst having myocarditis can increase virus replication within the heart, in turn also causing an increase of inflammation and worsening the myocarditis. This can result in permanent severe damage to the heart or sudden death [9, 6]. In fact, myocarditis is a known cause of sudden cardiac death in athletes, frequently being found only during autopsy, which is supported by the presence of myocardial infiltration with mononuclear inflammatory cells, and even in athletes with a normal left ventricular function [5, 6, 10, 11]. Before COVID-19, it was said that myocarditis accounted for 7-20% of all sudden cardiac deaths in young athletes [12]. Therefore, caution should be taken when a physician decides whether or not a sportsman is allowed to return to training, and in depth cardiac screenings should be performed. Besides myocardial inflammation, one of the next most common effects of SARS-CoV-2 found to occur in sportspeople are arrhythmias, mainly ventricular arrhythmias. Arrhythmias can be a result of both direct SARS-CoV-2 infection, as well as related to acute or chronic myocardial infection resulting from SARS-CoV-2. Myocarditis can serve as a trigger for ventricular arrhythmias, especially following physical exertion, as mentioned previously [13]. Modica et al. states that "in acute myocarditis, myocardial inflammation represents an arrhythmogenic substrate that predisposes patients to ventricular arrhythmias (VAs); in chronic myocarditis, on the other hand, myocardial fibrosis promotes VAs through the creation of re-entry circuits around the myocardial scar." Based on the analysis from van Hattum et al., who cited the findings from Gervasi et al., one athlete, or 5.6% had ventricular premature beats (VPBs) and one (5.6%), had supraventricular premature beats (SVPBs) during exercise, which, when compared to previous exercise tests, were not present prior to COVID-19 infection. Cavigli et al. also found in their study of 90 participants that 53.3% of athletes presented with VPBs, and 52.5% with SVPBs on 24-hour Holter monitoring electrocardiograms (ECGs). However, no malignant arrhythmias were found. Dores and Cardim measured in 41 cases, 17% had acute arrhythmias, and 239 out of 4143 sportsmen (5.8%), had arrhythmic events found by Casasco et al.[12] Out of these 239 people, ventricular arrhythmias were observed in 101 of them (2.4%), consisting mainly of individual events or couplets of premature ventricular beats. When compared with previous ECGs of the participants, of those 239 observed with arrhythmias, 27 (12%) had a history of arrhythmias due to cardiac damage known before COVID-19 infection, and 15 (6.7%) had a history of pre ventricular beats (PVBs), whereas the remaining 197 (82%) had new onset arrhythmias [12]. A more detailed description of the results made by Casasco et al. can be found in the attached Table 1.
Table 1. Cardiovascular outcomes in athletes post-COVID-19 based on data by Casasco et al. [12], adapted by Julia Sysło.
 [please click on the image to enlarge] Based on these findings, it can be concluded that though myocarditis is a dangerous finding and should be monitored for closely, it is actually more common to find isolated cases of arrhythmias in athletes post-COVID-19 as it is to find myocarditis. However, caution should be taken when analyzing various studies and their results, as it is important to note that some studies may have used a smaller number of test subjects, in turn increasing the percentage that a certain finding, like myocarditis, is represented with. This is particularly the case when noting the up to 15% prevalence of myocarditis cited from one of the analyses done by Alosaimi et al. [6] On the same note, when analyzing the presence of arrhythmias on ECGs and 24-hour Holter monitoring systems, it is important that previous results of these tests prior to COVID-19 be compared, as it is common for athletes, who exert much strenuous activity, especially on the heart, to have arrhythmias with no other cause but the exercise they perform. The other mentioned cardiovascular outcomes seen post-COVID-19 are less commonly observed, and thus far, a number of studies have not focused on them very much, with only a few studies mentioning the number of cases they have found. When it comes to the pericardium, only 2 athletes out of the cohort of 789, or 0.3%, were found to have pericarditis by Martinez et al. [7] Out of 90 athletes in the study done by Cavigli et al., 3 participants (3.3%) had pericardial effusion, 2 (2.2%) had pericarditis, and 1 (1.1%) had myopericarditis [14]. In the 15 study analysis, performed by Alosaimi et al., 5 studies resulted with pericarditis ranging from 0.06-2.2%, and 9 studies with pericardial effusion within the ranges of 0.27-58%. It should also be noted here, that just as with Alosaimi et al. analysis of myocarditis, caution should be taken with the larger percentages reported, as they may come from studies done on a small amount of athletes, and may not reflect the true prevalence of these diseases within the athletic population. Looking for the prevalence rate of acute or chronic myocardial injury, only one study reported 7% of a cohort of 41 patients (3 persons) having acute myocardial injury [5]. More studies need to be done in order to monitor the exact outcomes of COVID-19 infection in athletes, especially when considering chronic myocardial injury, as it takes more time to see this outcome. Therefore, with the passage of time and more knowledge about the virus, it should be easier to recognize the end-products that it leaves. Types of arrhythmias Numerous data conclude that arrhythmias are the most prevalent phenomenon seen in athletes after COVID-19 infection. Similar to the various types of cardiovascular outcomes that can occur, there is not just one arrhythmia that can be obtained, but a multitude of types. These types can be classified based on a range of criteria. In the first place, arrhythmias can be broken down into two categories:
Tachyarrhythmias can also be classified based on the duration of the QRS complex, in other words, whether it is a narrow QRS complex tachycardia, or a wide QRS complex tachycardia. A narrow QRS complex is a QRS complex that is <120 milliseconds (ms) in duration or <3 millimeters (mm) on an ECG, whereas a wide QRS complex is a QRS complex which is >120 ms or >3 mm. SVTs, for example, are usually narrow QRS complex tachycardias, which encompass atrioventricular reciprocating tachycardia (AVRT), atrioventricular nodal reentrant tachycardia (AVNRT), atrial tachycardia, and atrial flutter and fibrillation. Wide complex tachycardias can also be further classified into monomorphic ventricular tachycardias, polymorphic ventricular tachycardias, and ventricular fibrillation. The most common ways of classifying tachyarrhythmias however, are based on heart rate and location. Bradyarrhythmias, on the other hand, are assorted into heart blocks, such as type I, II, and III degree AV blocks, and sinus node disorders, such as sinus pause, sinus arrest, and sinoatrial (SA) nodal exit block. No matter which class of arrhythmia is procured, each one can have its consequences, some greater than others. The most frequent arrhythmia seen is atrial fibrillation, which is considered an SVT [15]. Atrial fibrillation can lead to such complications like hypotension, increased risk of thromboembolic events, such as a stroke or pulmonary thromboembolism, and heart failure [15, 16]. Though these events can be dangerous and even life-threatening, atrial fibrillation is not the arrhythmia with the leading cause of death. Generally, other SVTs including atrial flutter, atrial premature complex (PAC) and atrial tachycardia, also do not lead to high mortality rates. VTs, on the other hand, come with a very high risk of death and should be treated immediately. In fact, VTs are the major cause of sudden cardiac death. Sustained or non-sustained ventricular tachycardias, ventricular premature beats (PVCs), and ventricular fibrillation are all considered VTs, with ventricular fibrillation being the leading source of sudden cardiac deaths. The above-mentioned tachyarrhythmias are regarded as the most dangerous arrhythmias; however, bradyarrhythmias similarly can lead to life-threatening outcomes. Out of all of the bradyarrhythmias mentioned, III degree heart block, also called a complete heart block, has the largest probability of serious adverse events, as it can result in asystole (the most severe form of cardiac arrest), and ultimately death [15]. |
 Generate PDF/or right-click and save as.../  Figure 1. Challenges with ECG screening in athletes post–COVID-19 (based on the image from Phelan et al. [13] (recreated and modified by Julia Sysło): A. Normal healthy athlete with diffuse ST-segment elevation because of early repolarization (blue arrows). B. 23-year-old athlete with positional pleuritic chest pain, elevated high-sensitivity troponin (>5,000 ng/l) and confirmed myopericarditis on cardiac magnetic resonance; the ECG also shows diffuse ST-segment elevation (blue arrows) and also subtle PR depression (red arrow). [please click on the image to enlarge] Imaging Imaging of the heart is deemed the most important tool in helping physicians recognize the short and long-term effects that SARS-CoV-2 has on the athletic heart. These vary from the most basic biological markers assessment, namely cardiac troponin (cTn) or highly sensitive cardiac troponin (hs-cTn), to the most complex cardiac magnetic resonance imaging (cMRI). The most important tools, however, are electrocardiograms (ECGs) and echocardiograms (echos). No matter which screening tool is used, it is always important to first differentiate whether a change is seen due to true myocardial injury post-COVID-19 infection, or related to physiological changes attributable to the amount of arduous work athletes put on their hearts. Myocardial damage due to COVID infection, as based on cTn in the blood, is defined as a "level greater than the 99th percentile upper reference limit" [13]. This number is frequently seen especially in hospitalized patients. Cardiac troponin levels, though they can show that there is some myocardial strain, have many limitations to their use. First off, they are not specific as to what is the exact cause of the strain on the heart. This fact is extremely important when considering athletes. The athletic heart has a number of damaging changes, such as enlargement of the ventricles. This damage is reflected by an increase in cardiac troponin, therefore, it is key to differentiate whether a noticed increase is due to an infection, or due to prolonged exercise. One major change to keep in mind is the fact that after a session of formidable exercise and an increase in cardiac troponins, there is a subsequent drop observed within 24-48 hours, which will not be observed in infection-related myocardial injury. In order to account for this and try to isolate for infection-related injury, an athlete’s cTn levels should be checked after rest for 48 hours. Another limitation to the use of cardiac troponins is that there are no reference ranges for them as of yet in the athletic population. Lastly, cTn levels may decrease once a patient recovers from COVID-19 infection, and may not reflect the post-COVID-19 damage that could have occurred [3, 13]. This last quality is a significant one, leading to the need to have more specific imaging done to help check for any sequelae of the infection. ECG assessment (including 24-hour ECG Holter monitoring) is the imaging modality which is always used to check for any cardiac abnormalities, and is frequently done in par with checking cTn levels. ECGs are similar to cTns in the sense that they also are not specific to the cause of the changes seen, they only show that there is a change in the functioning of the heart, for example that there is the presence of an arrhythmia or block, which can be seen in both athletic heart or infections. Myocarditis, which was stated earlier to be one of the main problems after COVID-19, can cause such ECG changes as disclosed by Phelan et al. (2020, p. 2637): "...frequent or multiform premature ventricular beats or arrhythmias, ST- and T- wave changes, left bundle branch block, and atrioventricular block. However, the sensitivity for detecting myopericarditis with these changes is as low as 47%. Furthermore, over 70% of athletes have repolarization anomalies characterized by J-point elevation, ascending concave ST segments in the inferior or lateral leads, and tall T waves that may be confused with myopericarditis." This direct quote provides evidence that ECG changes in athletes, when found, need to be properly differentiated, since the changes may imitate one another, and can further be supported when looking at the ECGs done on 2 athletes, which are also taken from the original paper published by Phelan et al. [13] These ECGs can be seen below in Figure 1. Though ECGs are helpful in seeing functional abnormalities, just as was seen in cTns, these alterations may disappear after the patient has recovered from an infection, making it impossible to note if there are any post-infectious abnormalities present [13]. Regardless of these limitations, ECG remains one of the mainstays of checking for any aberrations. After checking ECGs, common practice is to check the echo of the heart, as this can show more in depth changes seen on the anatomy of the heart, not just the function as was seen with cTn and ECGs. In fact, echocardiograms are considered first-line screening for athletes after COVID-19 infection. Here it is also very important to know the many norms of the athletic dimension changes that can be observed in both male and female athletes, for example left ventricular hypertrophy or volume changes, as these changes can mimic the changes seen in myocarditis post-infection. In myocarditis, it will be possible to see reduced wall motion or increased wall thickness, although many times myocarditis can actually present with completely normal left ventricular ejection fraction (LVEF), therefore, a good measurement to use to check for subclinical injury is GLS, or global longitudinal strain in the left ventricle. The normal GLS is >17%, therefore, any number lower than that should raise concern for myocardial injury. Unfortunately, there are no set norms for GLS in athletes, with many values between the scope of 16-22%, thus alternative measurements should be taken to help check for pathology and differentiate it from a typical athlete’s heart. One of these alternatives is checking the atrial function. Normally, athletes will have an increased atrial reservoir due to an increase in preload from heavy exercise. Consequently, if a decreased reservoir is noted on ECHO, this can raise concern that the athlete may have an underlying myocardial pathology [13]. If no clinical changes can be seen on either ECG or ECHO, but myocarditis is still suspected, the most specific imaging that can be resorted to is cardiac magnetic resonance imaging or cMRI. The most common anomalies on cMRI included elevated T1 and T2 signals, such as those for myocardial oedema, as well as late gadolinium enhancement (LGE). cMRI is considered gold-standard for checking both regional and global abnormalities resulting from myocarditis, including change in ventricular function, inflammation, oedema, and scarring. Furthermore, LGE is deemed a strong marker for prognosis of adverse effects, such as arrhythmias, heart failure, or mortality, also stemming from myocarditis, with any LGE uptake being attributed to a worse prognosis. These screening modalities are so well-liked because they provide the most detailed myocardial tissue characterization, facilitating finding all of the above-mentioned changes, as well as providing the most information about the seen changes. The ideal time to obtain a cMRI for an athlete is >10 days after the initial diagnosis of COVID-19, and should only be done in the beginning stages of the illness if there is an emergent decision needing to be made in the hospital. Myocarditis on cMRI can be confirmed if on T1 or T2 sequencing there is a >2 standard deviation above normal reference ranges, extracellular volume fraction (ECF) >30%, or any LGE [4, 13]. What is interesting to note, although cMRI is the most detailed imaging modality, GLS measurements can help in finding myocarditis which is not found on cMRI [17]. Return to training The imaging techniques mentioned previously are all used to help a physician decide whether or not to allow an athlete to return to training after their diagnosis of COVID-19. Though every country has its own suggested scheme to follow, many of the return-to-play strategies overlap. These schemes are assembled based on findings from current research, meaning that with new discoveries made by ongoing and future research, the recommendations may change. Thus far, athletes have had to go through pre-participation examinations, or PPEs, before they start their seasons. These PPEs were traditionally used to screen for cardiovascular diseases that can predispose to sudden death, just as genetic or congenital abnormalities. With the coronavirus pandemic, these PPE screenings have needed to be broadened to include post-infection heart problems [18]. The current recommendations for return to play (RTP) after COVID-19 are based on the type of illness the player has gone through, such as whether their infection was asymptomatic, mildly symptomatic, or severe, and the amount of time that has passed since their original diagnosis of COVID-19. It has been accepted that if a sportsperson has had an asymptomatic course of the disease, or a very mild course, they can return to training after their self-isolation period is over, although some physicians may opt to do a physical examination with medical history. Many experts deem the best time to consider this is 7-10 days after the initial diagnosis. If mild symptoms are still present after this 10 day period, or if there are moderate symptoms, a 12-lead ECG and echo should be performed. Along with the screenings done for less severe courses of infection, more specialized screenings, such as cMRI, are recommended to be done in patients who have symptoms greater than 14-21 days, have had a severe course of COVID-19, or have had ECG and echo monitoring come out with abnormal results [9, 14]. Wilson et al. also suggests performing a 24-hour Holter ECG and cardiopulmonary exercise testing if cMRI comes out normal. This is to ensure that the athlete is thoroughly screened before exercising again in order to counteract serious complications from occurring. Generally speaking, the more severe the infection, the more tests need to be done before a physician can allow an athlete to go back to training. Alosaimi et al. created a timeline in order to easily show experts’ current recommendations for RTP. Their timeline can be seen under Figure 2 below [6].  Figure 2. Recommended Timeline for a safe return to sport following COVID-19 infection in athletes. Taken from Open Access article by Alosaimi et al. [6] [please click on the image to enlarge] Though each expert suggestion varies slightly from one to the other, the main points of the types of tests to do and in which circumstances remain similar. Each individual situation is different and these guidelines should also be flexible based on the changes or symptoms that a particular athlete is showing. Those sportsmen who have been diagnosed with myocardial injury need to go through more extensive RTP procedures, and are told to withhold from any physical activity for 3-6 months. These patients should also have a cardiac complication monitoring plan and a rehabilitation program for a safe return to sport [6]. After this period, all heart functions, arrhythmias, and serum biomarker increases resulting from the myocardial injury must be re-evaluated and disappear before allowing any intensive exercise to be performed [5]. Those athletes who have had severe illness or note reduced performance when beginning sports again, must immediately stop all physical activity and have a cardiac re-evaluation 4 weeks after initial COVID-19 infection [6]. It will be important to see what changes in the guidelines will be made with more research and knowledge of the cardiovascular effects of COVID-19. Conclusion COVID-19 is an infection that can affect the cardiovascular system and create complications in the long-term lives of patients and athletes. Some of these complications include cardiac sequelae or PACS. Although possible and a serious consequence, myocarditis is not necessarily the most common post-infection finding in athletes. Ventricular arrhythmias, ventricular premature beats, as well as supraventricular beats have been seen to occur on a larger scale in these populations compared with myocarditis. This could be from varying/smaller sizes in test subject groups. Imaging is essential in ascertaining the status of cardiac function and any associated pathologies. Biochemical markers and ECG’s can be helpful, albeit non-specific. These tests can return to normal after recovery, concealing any changes that are present in the heart. Echocardiograms are considered the gold standard in diagnosing post-infection myocardial injury in athletes and give a clear understanding of the patient's status. GLS and atrial reservoir volume can be calculated during this time for further investigation and confirmation. Another imaging modality like cMRI is best for determining global changes as well as focal changes from myocarditis. During cMRI it is useful to check for LGE which can indicate a worse prognosis. In a PPE, these modalities inform a physician of possible risks and status of athletes so that they may follow an RTP algorithm to correctly rehabilitate and recover. More large scale research should be conducted in juxtaposing the incidence of pathologies, especially cardiological, before and after a COVID-19 infection. This will truly help with understanding the chronic effects perpetuated by PACS or even the course of the infection itself. 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DOI: 10.1016/j.jcmg.2020.10.005 [14] Cavigli L, Frascaro F, Turchini F, Mochi N, Sarto P, Bianchi S, Parri A, Carraro N, Valente S, Focardi M, Cameli M, Bonifazi M, D'Ascenzi F. A prospective study on the consequences of SARS-CoV-2 infection on the heart of young adult competitive athletes: Implications for a safe return-to-play. Int J Cardiol 2021; 336:130-6. DOI: 10.1016/j.ijcard.2021.05.042 [15] Desai DS, Hajouli S. Arrhythmias. In Statpearls [Internet]. Arrhythmias - StatPearls - NCBI Bookshelf 2022. Access valid on 16 February 2023: https://www.ncbi.nlm.nih.gov/books/NBK558923/ [16] Carlisle MA, Fudim M, DeVore AD, Piccini JP. Heart Failure and Atrial Fibrillation, Like Fire and Fury. JACC Heart Fail 2019; 7:447-56. DOI: 10.1016/j.jchf.2019.03.005 [17] van Hattum JC, Spies JL, Verwijs SM, Verwoert GC, Planken RN, Boekholdt SM, Groenink M, Malekzadeh A, Pinto YM, Wilde A, Jorstad HT. Cardiac abnormalities in athletes after SARS-CoV-2 infection: a systematic review. BMJ Open Sport Excer Med 2021; 7:e001164. DOI: 10.1136/bmjsem-2021-001164 [18] Baggish A, Drezner JA, Kim J, Martinez M, Prutkin JM. Resurgence of sport in the wake of COVID-19: cardiac considerations in competitive athletes. Br J Sports Med 2020, 54:1130-1. DOI: 10.1136/bjsports-2020-102516 Conflict of interest: none declared. Authors’ affiliations: 1 Jagiellonian University Medical College, School of Medicine in English, Cracow, Poland. Corresponding author: Julia Sysło 10985 S. 84th Ave. Apt. 3A Palos Hills, Il, 60465 USA Telephone no.: +48 600 186 277 e-mail: juvima63@gmail.com To cite this article: Sysło J, Bobek M, Rożek A. Cardiovascular changes in athletes post-COVID-19 infection. World J Med Images Videos Cases 2023; 9:e4-16. Submitted for publication: 16 November 2022 Accepted for publication: 16 February 2023 Published on: 24 February 2023 |
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