key: cord-0772743-vugijc7r
authors: Blagojevic, Nikola R.; Bosnjakovic, Dragana; Vukomanovic, Vladan; Arsenovic, Srdjan; Lazic, Jelena Suzic; Tadic, Marijana
title: Acute pericarditis and SARS-CoV-2: case report
date: 2020-09-28
journal: Int J Infect Dis
DOI: 10.1016/j.ijid.2020.09.1440
sha: 55f6e188cdae71514c8c45031ca03693809aa996
doc_id: 772743
cord_uid: vugijc7r

We present a case of a 51-year-old patient with acute pericarditis as the dominant manifestation of SARS-CoV-2 infection. The patient was admitted to the emergency department during a COVID-19 outbreak with a suspected ST-elevation myocardial infarction. Coronary angiogram was normal. The real-time reverse transcriptase PCR assay for the detection of nucleic acid from SARS-CoV-2 in nasopharyngeal swab was positive. The laboratory tests revealed increased white blood cell count, with neutrophilia and lymphocytopenia, elevated level of C reactive protein, borderline ESR and slightly elevated interleukin-6. Echocardiography showed hyperechogenic pericardium posterolaterally with minimal localized pericardial effusion. A chest computed tomography scan showed a small zone of ground-glass opacity of the right lower lobe (classified as CO-RADS 3). In patients with chest pain, ST elevation on ECG, normal coronary angiogram, and suspected COVID-19, we should think of the pericarditis, as unusual SARS-CoV-2 infection presentation.

The association between cardiovascular diseases and the new viral agent has been a matter of debate since the coronavirus disease 2019 (COVID-19) pandemic began in Wuhan, China in December 2019. This issue mainly concerned prognosis and treatment of COVID-19 in patients with cardiovascular diseases (CVD) (1, 2) . On the other hand, several studies suggested that Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) might be an independent cause of myocardial damage in some patients through pathophysiological mechanisms that have not yet been fully understood (3) . Even though the virus mainly induces lung injury, the autopsy study confirmed that the heart, kidneys, vessels, liver, brain, and other organs may also be affected (4) (5) (6) (7) (8) (9) (10) (11) . Viral infections are the major cause of myocarditis and pericarditis in developed countries and it is also evident that the SARS-CoV-2 has cardiotropic properties.

Most of the case reports published so far investigated cardiac involvement in COVID-19 patients with severe respiratory tract infection (1, 3, 6, (8) (9) (10) (11) . We are presenting a case of a patient with acute pericarditis as dominant manifestation of SARS-CoV-2 infection.

A 51-year-old Caucasian male was presented to the emergency department during a COVID-19 outbreak with a suspected ST-elevation myocardial infarction. The patient complained of the sudden, but persistent chest pain, which appeared one day before hospital admission. The pain was sharp and worsened with deep breathing and changing the body position-alleviating while sitting. The pain lasted for several hours during the night and gradually spontaneously disappeared. He did not have any (LVEF 65%) and without regional wall abnormalities or more than mild valve disease. A chest computed tomography scan showed a small zone of ground-glass opacity of the right lower lobe which covers less than 5% of the volume of the lobe (according to the severity score index 1 point out of a maximum of 5 for a given lobe and 25 for the lung as a whole) without any other pulmonary or upper abdomen pathology. According to COVID-19 Reporting and Data System (CO-RADS) for the assessment of pulmonary involvement of COVID-19 on a non-enhanced chest CT scan, the finding was classified as CO-RADS 3 (12) .

Considering clinical presentation, ECG, laboratory and echocardiographic findings, the patient was diagnosed as acute pericarditis caused by SARS-CoV-2 with suspected mild viral pneumonia. The treatment included lopinavir/ritonavir (200/50mg b.i.d.), aspirin (100mg q.d.), beta-blocker (bisoprolol 2.5mg q.d.), and antibiotic (ceftriaxone 2g q.d.).

The patient was well, afebrile without chest pain or any respiratory symptoms during the hospital stay.

Serial echocardiographic studies did not demonstrated any deterioration in left ventricular systolic function or increase in pericardial effusion. Electrocardiographic changes (ST and PR segments) gradually resolved and were followed by T wave inversion in lead D3. Laboratory markers of inflammation were normalized and the patient was discharged.

The present case demonstrated a patient who was diagnosed in an acute phase of pericarditis caused by a SARS-CoV-2. Although cardiac involvement was previously described in patients with COVID-19 and massive pneumonia, to our knowledge this is a rare case describing cardiac involvement of SARS-CoV-2 infection in the patient with mild pneumonia. (10, 11) J o u r n a l P r e -p r o o f Emerging evidence suggests that SARS-CoV-2 has a tropism for myocardium and pericardium. Myocardial injury, detected by the presence of elevated high sensitive troponin I was present in about 12% of patients with COVID-19, and the virus was also isolated in the pericardial fluid of patient with COVID-19associated pericarditis and cardiac tamponade. (10, 13) However, previous reports are scarce and in the majority of cases pulmonary involvement in COVID-19 is dominant, accompanied by perimyocardial damage. In these patients, perimyocarditis was mainly diagnosed due to clinical deterioration caused by heart failure. (1, 3, (6) (7) (8) (9) (10) It is well established that viral agents can cause perimyocarditis either directly affecting the heart or by mechanisms in systemic inflammation during severe infections. Our patient has elevated proinflammatory cytokine interleukin-6 (IL-6) which is produced by immune cells in response to the viral agent, and appears to be important mediator in the cytokine storm. Limitation of our investigation is lack of cardiac magnetic resonance imaging and pericardial biopsy that would exclude myocarditis or confirm pericarditis, respectively.

Pericarditis should be considered in patients with chest pain, ST elevation in ECG, normal coronary angiogram and COVID-19. Accordingly, the atypical SARS-CoV-2 infection presentation should not be forgotten. We emphasized the importance of clinical examination and electrocardiogram for decision making in the setting of the COVID-19 epidemic. Future studies are to reveal in more details the J o u r n a l P r e -p r o o f long term outcome of patients who suffered myopericardial damage due to SARS-CoV-2.

The authors declare that they have no known competing financialinterestsor personal relationships that could have appeared to influence the work reported in this paper.

First case of COVID-19 complicated with fulminant myocarditis: a case report and insights

Coronaviruses and the cardiovascular system: acute and long-term implications

SARS-CoV-2: a potential novel etiology of fulminant myocarditis

Multiorgan and Renal Tropism of SARS-CoV-2

COVID-19 myopericarditis: It should be kept in mind in today's conditions

Life-threatening cardiac tamponade complicating myopericarditis in COVID-19

COVID-19-related myocarditis in a 21-year-old female patient

Myocarditis in a patient with COVID-19: a cause of raised troponin and ECG changes

SARS-CoV-2 detection in the pericardial fluid of a patient with cardiac tamponade

Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)

CO-RADS -A categorical CT assessment scheme for patients with suspected COVID-19: definition and evaluation

Clinical features of patients infected with 2019 novel coronavirus in Wuhan

Interleukin 6: from bench to bedside

Pericardial cytokines in neoplastic, autoreactive, and viral pericarditis

Figure 1. ECG on admission showed minimal widespread ST elevation in leads D1, D2, aVL, aVF, V2-V6, ST depression in lead D3 and aVR, and PR depression in leads D1, D2, aVF

This work was supported by the Ministry of Education and Science of the Republic of Serbia.

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

This research did not receive any specific grant from funding agencies in the public, commercial, or notfor-profit sectors.

Approval was obtained from the local ethics committee.J o u r n a l P r e -p r o o f