Dr Helen Dixon MbChB, anaesthetic trainee at East Lancashire Hospitals NHS Trust, reviews the presentation, diagnosis and management of myocarditis in COVID-19 .
On the 31st December 2019, Wuhan Municipal Health Commission reported a cluster of unusual Pneumonias in Hubei Province. By the 7th January 2020 they had identified the causative organism as a novel Coronavirus [1, 2]. Since then more than 9 million people worldwide have been infected with what we now know as ‘SARS-CoV-2’referred to as COVID-19. With death rates fast exceeding 500,000 globally, mortality has far surpassed that of the biologically similar MERS and SARS viruses [1].
While many features of SARS-CoV-2 are generic to other respiratory viruses, there are ever growing concerns over patients developing a clinical picture similar to that of myocarditis [2-6].
This article reviews the presentation, diagnosis and management of myocarditis, comparing this to current SARS CoV-2 research and its potential for causing myocarditis.
What is myocarditis?
Myocarditis is inflammation of cardiac myocytes. In Western Europe and Northern America the most common causative agent is a virus [7]. Myocarditis can present in many ways from mild chest pain to ventricular arrhythmias and cardiogenic shock [8]. ECG analysis demonstrates a wide range of non-specific changes with low sensitivity including sinus tachycardia, ventricular conduction delays, ST segment elevation or depression and ventricular arrhythmias [7].
The pathogenesis of myocarditis has been linked to the overexpression of T helper 1 cells (Th1) with Tumour Necrosis Factor (TNF) alpha and Interleukin 1 (IL-1) beta commonly found within cardiac myocytes during the acute stage [7]. Studies have shown that approximately 30 per cent of people with acute myocarditis will go on to develop dilated cardiomyopathy [8], with animal studies suggesting that genetic susceptibility, and the male sex hormone testosterone, further predisposes to this clinical progression [7].
How is it Diagnosed?
A combination of clinical suspicion, serial biomarkers, ECG changes otherwise proven not to be caused by an ischaemic event, Echocardiography and more specialist diagnostic tests are required to adequately diagnose myocarditis.
Whilst troponins may not always be raised in myocarditis, serial troponins showing a plateau more than 24 hours after an initial rise can be suggestive of ongoing inflammation – again, other more time sensitive diagnoses must always be investigated in the presence of raised cardiac markers [7].
B-type natriuretic peptide (BNP) and N Terminal Pro-BNP levels are raised in the presence of ventricular hypertrophy or dilatation and can signify progression to dilated cardiomyopathy in patients with myocarditis[7].
Echocardiography is non-specific in patients with myocarditis and is, rather, a useful tool to exclude valvular pathologies or other explanations for the clinical presentation. Acute myocarditis may demonstrate biventricular wall thickening with progression to impaired Right Ventricular function having an associated high mortality rate in patients with previously biopsy proven myocarditis[7].
The gold standard for diagnosis is the endomyocardial biopsy (EMB). The Dallas Criteria states that the presence of inflammatory infiltrate with or without myocyte necrosis (that is not otherwise characteristic of an ischaemic event) is required to diagnose myocarditis [7,9]. The Dallas Criteria has been criticised however for its inability to include the presence of the viral genome, within cardiac myocytes, as a potential diagnostic feature in symptomatic individuals [9]. Further sensitivity has also been found in the detection of focal or diffuse mononuclear infiltrate (CD3 stained T Lymphoctes or CD68 stained macrophages) [7]. While being the gold standard, EMB may mean referring patients to more specialist centres who have the capabilities to perform such an investigation.
A less invasive investigative tool is Cardiac MRI (CMR) imaging. This can be used to assess myocyte inflammation and differ