Abstract

Abstract Thyroid and cardiovascular system are inextricably related and cardiovascular complications can occur in both subclinical and overt thyroid dysfunction. We report the case of a 42–year–old woman presenting with chest pain. She had a positive SARS–CoV–2 swab in June and she was hospitalised in suspicion of COVID–related pneumonia and pericarditis in July: treatment with ibuprofen and colchicine was started and patient was discharged. On July 26th, the patient came back to emergency department due to worsening chest pain and myalgias after therapy decalage. She had face edema and hoarse voice. 12–leads EKG was normal; echocardiography showed 8 mm pericardial effusion and normal ejection fraction. Blood testing revealed no inflammatory signs, a mild increase of Troponin (peak value 19.1 ng/L, n.v. 0–14) and a high value of CPK (peak value 2299 U/L, 464 U/L at time of discharge, n.v. 30–150). Moreover, she had a biohumoral profile of Hashimoto thyroiditis: severe hypothyroidism with increase in TSH levels (538 microU/ml peak value, 322 microU/ml at time of discharge, n.v. 0.27–4.2) and positivity to thyroid autoantibodies. The patient underwent a cardiac magnetic resonance imaging that was suggestive for acute perimyocarditis with biventricular diffuse myocardial edema, preserved biventricular function and mild–to–moderate pericardial effusion. Low dose L–T4 therapy was started together with liothyronine that was stopped after few days, once acceptable FT3 concentrations were obtained. At echocardiography control after 8 days, we registered a significant reduction of pericardial effusion (2 mm). Myocarditis is an inflammatory disease of the myocardium and it is predominantly mediated by viral infection. A rare cause of myocarditis is represented by dysthyroidism. In our case, the severe hypothyroidism seems to be the cause of myocardial and pericardial edema. The failure in diagnosis of this endocrinological disorder can determine a delay in specific therapy with possible serious cardiovascular manifestations. So, it would be reasonable to check the thyroid status of all patients presenting with myopericarditis, in the absence of another clearly identifiable aetiology. The role of to the prior SARS–CoV–2 infection in not certain in our case, but the quick recovery after specific endocrinological therapy suggests the low probability of perimyocarditis as SARS–CoV2 related manifestation.

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