COVID myocarditis

I have heard of a few cases of myocarditis associated with the SARS-CoV-2, one from a physician in Kansas reporting on a COVID-positive patient with respiratory distress, atypical chest pain, EKG changes suggestive of a STEMI but clean (ie atherosclerosis-free) coronary arteries; and an LA cardiologist responding that she has been seeing myocarditis-like presentations.

There is little written about this that i could find, but a case report from China was published in the European Society of Cardiology journal, describing a patient with fulminant myocarditis associated with coronavirus who apparently responded to glucocorticoids and human immunoglobulin (see covid myocarditis eurjcard2020 in dropbox, or doi:10.1093/eurheartj/ehaa190).

Case:

-- 37-year-old male admitted to the hospital with chest pain and dyspnea for 3 days, and diarrhea.

-- Blood pressure 80/50

-- Troponin-T was >10,000 ng/L; CK-MB 112.9 ng/L;  BNP was 21,025 ng/L

-- chest x-ray found cardiac enlargement. Chest CT showed pulmonary infection, enlarged heart, and pleural effusion. EKG showed ST elevation consistent with acute MI (leads 3, AVF). Emergent CT coronary angiogram showed no coronary stenosis.

-- Echo showed a large heart with ejection fraction 27%; left atrium 39 mm, right ventricle 25 mm, right atrium 48 mm, 2 mm of pericardial effusion

-- sputum was examined for 13 respiratory viruses: only coronavirus positive. negative for: influenzas A (including H1N1 and H3N2) and B, Mycoplasma pneumoniae, adenovirus, bocavirus, rhinovirus, parainfluenza, chlamydia, and RSV

-- clinical diagnosis was coronavirus fulminant myocarditis with cardiogenic shock and pulmonary infection

Therapy:

-- methylprednisolone 200 mg per day for 4 days to suppress inflammation

-- immunoglobulin 20 g per day for 4 days to regulate immune status

-- norepinephrine to raise blood pressure

-- diuretics (torsemide and furosemide)

-- milrinone to increase myocardial contractility

-- piperacillin sulbactam for infection

-- pantoprazole

-- with above, symptoms improved significantly. Chest x-ray one week later showed normal size heart, echo showed size and function of the heart had returned to normal, with LVEF 66%

-- troponin-T decreased to 220.5, CK MB to 9, BNP to 1587

-- by 3 weeks all of the myocardial injury markers had fully normalized

Commentary:-- I bring this up just because myocarditis may be an important and serious complication of coronavirus, as it is with many different viral infections. And some of the clinical presentation for myocarditis may be incorrectly attributed to the more common ARDS or some other severe pulmonary complications. And though this was only one patient, their results are intriguing, should be studied more rigorously, and the therapy they used may be an option for a severely ill person with fulminant myocarditis

-- they did not check for many of the other common viral etiologies of myocarditis. in the setting of China (or other more endemic coronavirus areas), for a person with myocarditis, and with evaluation finding a positive coronavirus and negative flu and several other infections, the putative role of the coronavirus is pretty likely

-- however, they did not definitively confirm myocarditis (no cardiac MRI, endomyocardial biopsy), though clinically seems very likely

--  the role of steroids is not so clear even in ARDS, with observational trials on both sides:

    -- a study finding that steroids may be harmful, and not recommending their use (see covid steroids not likely help lancet2020 in dropbox, or doi.org/10.1016/ S0140-6736(20)30317-2), and another finding twice the mortality in those on steroids (see covid mortality risk factors lancet2020, or doi.org/10.1016/S0140-6736(20)30566-3)

     -- but another study finding a 60% lower death rate with steroids (see covid steroids help ards jamaintmed2020 in dropbox, or doi:10.1001/jamainternmed.2020.0994)

-- a longer term issue: though it is important to figure out the best treatment regimen for the acute situation, it is also unclear what the long-term consequences of this viral myocarditis will be (ie, is this likely to progress to a dilated cardiomyopathy?)

--so, the big issue here is that most of what we are doing is in an evidence-free zone. we really need good RCTs to guide us. 

    -- for example: in the above observational steroid studies, were those put on steroids sicker (ie, doing poorly so they tried everything?), or perhaps they were they less sick (more hope for recovery in a situation where people are being triaged for therapies/care being rationed??? and mostly giving up on the sickest ones??).

    -- should we even try the combination of steroids/immunoglobulins in a patient who seems to be dying of fulminant myocarditis?? that may be reasonable, but we really don't know if that person may have recovered spontaneously and in fact the steroids did nothing or may even have been harmful. 

    -- and maybe they did not have myocarditis by more specific testing (though this was a pretty likely diagnosis). and was it the steroids, the immunoglobulin, or both that was potentially beneficial.

but i thought it was useful to put myocarditis on our radar screens as a possible complication of SARS-CoV-2 infection

geoff​

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