Cardiac tamponade as a cause of cardiac arrest in severe COVID-19 pneumonia.

Descriptive studies of patients with SARS-CoV-2 infection show that in addition to cardiovascular disease as a predisposing factor, the infection itself seems to trigger acute myocardial injury. Previous studies on MERS-CoV and SARS-CoV, with a similar pathogenic mechanism, already describe the development of myocardial damage in an infected patient and the complexity of managing them.

We present a 65-year-old man with no relevant history who presented with community acquired pneumonia by SARS-CoV-2. He associated distributive shock with an hyperinflammatory picture (ferritin 3233 mg/dl, IL-6 996 pg/ml, fibrinogen 8.8 g/L, D-dimer 895 ng/ml). He received Tocilizumab, Ceftriaxone, Azithromycin and Hydroxychloroquine for five days. He required invasive mechanical ventilation, prone position and low-dose vasoactive drugs.

He developed myocarditis secondary to viral infection with elevated highly sensitive troponin (hs-cTnI) (192 ng/L) and right overload with hyperbilirubinemia and cytolysis. The echocardiography did not show abnormalities.

On the sixth day meanwhile in a prone position, the patient presented suddenly progressive arterial hypotension without response to norepinephrine followed by pulseless electrical activity. Transthoracic ultrasound revealed a 3-centimeter-thick pericardial effusion in the anterior and posterior compartment without right ventricular dilation. Advanced life support was started and pericardiocentesis was performed with serous fluid extraction from the anterior pericardial compartment, without return of spontaneous circulation (ROSC). After 30 min without ROSC, the patient was deceased. It was oriented as cardiac tamponade secondary to pericardial effusion due to viral myocarditis. Necropsy could not be performed due to epidemiological issues.

Patients affected by COVID-19 are predisposed to myocardial injury, especially in severe forms and including fulminant presentation. Those with preexisting cardiovascular diseases have a significantly increased risk of death with SARS-CoV-2. It has also been seen that critically ill patients generally have significantly higher Troponin I and pro-BNP values, and that this could be related to prognosis.

Myocarditis is present in 12–23% of cases. The key element is ACE-2, which is expressed in myocytes and endothelial cells (in addition to the gastrointestinal, kidney and lung systems) and acts as a functional receptor for the coronavirus, which would explain direct injury to the myocardium and blood vessels. The gold standard diagnostic test is endomyocardial biopsy, which cannot be performed in our patient. Pericardial fluid culture is also included as a diagnostic element, however, our result was negative, as well as the result of the only case of pericardial effusion due to COVID-19 published to date.

In COVID-19 patients, the myocarditis also could be due an adverse effect of drugs, mainly hydroxychloroquine and azithromycin; however, these effects are associated with chronic treatments and the pericardial effusion has not been described.

This case report highlights that myocarditis and secondary pericardial effusion can be a complication of SARS-CoV-2 infection, so it must enter the differential diagnosis of the deteriorating patient. Myopericardial injury must be evaluated initially and consecutively.

Statement of ethics

We complied with the guidelines for human studies and our research was conducted ethically in accordance with the World Medical Association Declaration of Helsinki. Information revealing the subject's identity is to be avoided. Consent for the publication of the clinical case has been obtained through the patient's immediate family.

Funding

No funding.

Authors’ contribution

We were all involved in providing care for the patient. We were all involved in writing and reviewing the manuscript.

Conflict of interest

The authors have no conflicts of interest to declare.