COVID-19: EFFECTS ON THE HEART AND IMPLICATIONS FOR RETURN TO SPORT
Blog post written by John Durkin. Podiatrist and Chiropodist at The Putney Clinic
The UK Government’s recent announcement that we can – and should – all take more outside exercise, and for the possible return of Premiership Football (behind closed doors) is very exciting. Interestingly, during lockdown the increase in indoor exercise has far outweighed any reduction in outdoor exercise for most European countries according to data revealed by Garmin.com. However, it must be stressed that there are perils for an early and over vigorous return to sport following coronavirus. In this article we will look at COVID-19 and the effects on the heart and implications for returning to sport.
HISTORY OF CORONAVIRUSES
In 2002 medical science was aware of just a few coronaviruses that could infect human beings. These viruses did not cause serious illness. Then, in 2002 a virus now called SARS-cov surfaced in the Chinese province of Guangdong. The accepted story is that the virus spread from bats to civets at markets. The subsequent outbreak of severe acute respiratory syndrome (SARS) killed 774 people in 29 countries. This equates to approximately 19% of those infected.
Although studies were small and often anecdotal, it appears that some transient diastolic dysfunction occurred in patients who had no previous heart conditions. However, in patients with pre-existing cardiovascular conditions, tachycardia was the most common finding (72%), and other complications included hypotension (50%). Men were most affected.
In 2012 another new illness, Middle Eastern respiratory syndrome (MERS), caused by MERS-cov virus. This virus was confined to the Middle East and South Korea. It has not yet been eliminated and has killed 858 people to date, the most recent in February. In the case of MERS-cov, the virus spread from bats into camels. It can pass easily from camels to humans, which makes it hard to control but only spreads between people who are in close proximity, making it manageable.
The third time, it is SARS-Cov-2, (Coronavirus). At the time of writing there are over 4 million COVID-19 cases and 279,489 deaths worldwide.
[Goldfinger, villain of the novel which bears his name, says to James Bond: “Once is happenstance, twice is coincidence, the third time it’s enemy action.]
The clinical risk factors for mortality are older age, male sex, and underlying medical conditions including diabetes mellitus, cardiac diseases, chronic kidney disease, respiratory disease, hypertension, and cancer. A systematic analysis of MERS patients showed that 30% of cases had underlying cardiac diseases, 50% had hypertension, 50% had diabetes, and 16% had obesity.
The (Coronavirus) infection causes a severe respiratory illness with clinical and laboratory risk factor findings similar to SARS infection in 2003. Transmission of Coronavirus seems to be primarily from person to person via close contact, through respiratory droplets, with an incubation period of 2-14 days. There is concern about a possible faecal-oral route of transmission for SARS-Corona – as was found with SARS and MERS.
The 3 main symptoms of COVID-19 are fever, cough, and shortness of breath (dyspnea). Other symptoms may include muscle pain, anorexia, malaise, sore throat, nasal congestion, headache, and loss of taste and smell.
An incubation period of 2 to 14 days is when symptoms may appear after exposure. The detected viral load is similar in the asymptomatic and symptomatic patients with COVID-19, which suggests potential transmission of the virus from asymptomatic or minimally symptomatic patients to other persons.Viral loads are higher in the nose compared with the throat.
Myocarditis in COVID-19
Myocarditis is a non-ischaemic inflammatory heart muscle disease that can result in cardiac dysfunction and arrhythmias. The aetiology of myocarditis is diverse. Infections, toxic or autoimmune conditions are the most common causes. Viral myocarditis being most prevalent.
SARS CoV-2 appears to affect the myocardium and cause myocarditis. After COVID-19 infections cases of severe myocarditis with reduced systolic function have been reported. Studies suggest a high prevalence of cardiac injury in those patients that have been hospitalised. Infection-related myocarditis and/or ischaemia is an important prognostic factor in C-19.
Influenza research had shown that causes of death from was due to myocardial infarction and chronic ischaemic heart disease. This was observed in both genders at all age groups. In cases of influenza cardiac mortality is associated with respiratory disease.
The importance of medication that might be taken to reduce the symptoms and knock-on effects of C-19, such as antibiotics, antimalaria drugs, immunosuppressant drugs and anti-inflammatory drugs: steroids and NSAIDs will affect the heart and must be taken into account.
Myocarditis and Sudden Cardiac Death in Athletes
Myocarditis is not as prevalent as other cardiac diseases, accounting for 5-22% of sudden cardiac deaths in younger populations. Acute and subacute myocarditis and perimyocarditis are the cause of sudden cardiac death in 5% –25% of athletes.
This process is thought to begin with a period of immune suppression as a result of excessive physical exertion. This suppresses the T lymphocytes, interleukin and the natural killer cell system can predispose the patient to upper respiratory infections or allow an already infected patient a period of time where the virus can replicate at rapid rates. This phase is then followed by a surge of inflammation due to the rapidly replicating virus. This leads to more necrosis, fibrosis, and subsequently a pro-arrhythmic myocardium. Exercise was associated with a pronounced inflammatory response that led to structural changes in the heart. Furthermore, this inflammation means degradation of myocardium and of skeletal muscle due to a higher demand for energy sources. This will delay recovery and hinder athletic performance.
US guidelines state that athletes with a probable or definite diagnosis of recent myocarditis should not participate in competitive sports while active inflammation is present regardless of age, gender, or left ventricular function.
The duration of inflammation is variable and can take many months to resolve and there are currently no tests for this (inflammation). Athletes should undergo clinical testing with an exercise ECG monitoring and 24 Holter monitoring between 3 and 6 months after the initial illness.
The length of exclusion, being 3-6 months is based on the individual and the severity of the initial illness. European guidelines are similar.
Stopping training and exercise during and after and inflammatory heart disease is strongly advised because it is known that viral persistence or autoimmune processes could last for several months after the illness. The correlation between acute respiratory infections and inflammatory heart disease is robust.
Numerous studies have stressed the disadvantages of physical exercise during acute myocarditis with a risk of permanent damage to the heart or even the risk of death, albeit small. The cause of death in many patients was secondary to scar related arrhythmia, which also may occur long after the initial illness.
Put simply listen to your body: if – during and after training – you experience breathlessness and are unusually fatigued, stop and rest. A delay in returning to sport or for an event will be far safer in the short and in the long term. In all cases seek advice from your GP or sports physician.
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