Acute pericarditis and severe acute respiratory syndrome coronavirus 2: Case report.

We present the case of a 51-year-old patient with acute pericarditis as the dominant manifestation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The patient was admitted to the emergency department during a coronavirus disease 2019 (COVID-19) outbreak with a suspected ST-elevation myocardial infarction. A coronary angiogram was normal. Real-time reverse transcriptase PCR for the detection of nucleic acid from SARS-CoV-2 in a nasopharyngeal swab was positive. Laboratory tests revealed an increased white blood cell count, with neutrophilia and lymphocytopenia, elevated level of C-reactive protein, borderline elevated erythrocyte sedimentation rate, and slightly elevated interleukin 6. Echocardiography showed a hyperechogenic pericardium posterolaterally with minimal localized pericardial effusion. A chest computed tomography scan showed a small zone of ground-glass opacity in the right lower lobe (classified as CO-RADS 3). In patients with chest pain, ST elevation on electrocardiogram, a normal coronary angiogram, and suspected COVID-19, we should think of pericarditis as an unusual presentation of SARS-CoV-2 infection.

Introduction

The association between cardiovascular diseases and the new viral agent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been a matter of debate since the coronavirus disease 2019 (COVID-19) pandemic began in Wuhan, China in December 2019. This issue has mainly concerned the prognosis and treatment of COVID-19 in patients with cardiovascular diseases (CVD) (Zeng et al., 2020, Tian-Yuan et al., 2020). On the other hand, several studies have suggested that SARS-CoV-2 might be an independent cause of myocardial damage in some patients through pathophysiological mechanisms that are not yet fully understood (Chen et al., 2020). Although the virus mainly induces lung injury, autopsy studies have confirmed that the heart, kidneys, vessels, liver, brain, and other organs may also be affected (Yao et al., 2020, Puelles et al., 2020, Cizgici et al., 2020, Hua et al., 2020, Kim et al., 2020, Doyen et al., 2020, Farina et al., 2020, Inciardi et al., 2020). Viral infections are the major cause of myocarditis and pericarditis in developed countries and it is also evident that SARS-CoV-2 has cardiotropic properties. Most of the case reports published so far have investigated cardiac involvement in COVID-19 patients with severe respiratory tract infections (Zeng et al., 2020, Chen et al., 2020, Cizgici et al., 2020, Kim et al., 2020, Puelles et al., 2020, Cizgici et al., 2020, Hua et al., 2020, Kim et al., 2020, Doyen et al., 2020, Farina et al., 2020, Inciardi et al., 2020). The case of a patient with acute pericarditis as the dominant manifestation of SARS-CoV-2 infection is presented here.

Case report

A 51-year-old Caucasian male presented to the emergency department during a COVID-19 outbreak with a suspected ST-elevation myocardial infarction. The patient complained of sudden but persistent chest pain, which had developed 1 day before hospital admission. The pain was sharp, worsened with deep breathing or a change in body position, and was alleviated while sitting. The pain lasted for several hours during the night, but then gradually and spontaneously disappeared. He did not have any respiratory symptoms and denied respiratory or any other infection or acute illness in the previous 3 months.

Apart from hypertension in the previous 5 months, the patient’s medical history was unremarkable. He was a non-smoker and he denied any substance abuse.

On admission, the patient was stable, subfebrile (37.1 °C), with a normal blood pressure (125/80 mmHg), regular heart rate (70 bpm), slight tachypnoea (18 per minute), and normal oxygen saturation on ambient air (98%). The remainder of the physical examination was unremarkable. An electrocardiogram (ECG) demonstrated sinus rhythm, minimal widespread ST elevation in leads D1, D2, aVL, aVF, and V2–V6, ST depression in leads D3 and aVR, and PR depression in leads D1, D2, aVF, and V2–V6 (Figure 1). Coronary angiography, which was performed on admission, was normal.

Figure 1

ECG on admission showing minimal widespread ST elevation in leads D1, D2, aVL, aVF, and V2–V6, ST depression in leads D3 and aVR, and PR depression in leads D1, D2, aVF, and V2–V6.

Laboratory tests revealed a white blood cell (WBC) count of 15.0 × 109/l (normal range 4.0–10.0 × 109/l), with an elevated neutrophil count of 13.04 × 109/l (normal range 2.06–6.49 × 109/l) and a low lymphocyte count of 0.85 × 109/l (normal range 1.19–3.35 × 109/l), elevated levels of C-reactive protein (90.7 mg/l; cut off <6.0 mg/l), borderline elevated erythrocyte sedimentation rate (ESR) (14 mm/1 h), and a slightly elevated interleukin (IL)-6 of 8.7 pg/ml (<6.0 pg/ml). Other blood tests, including levels of high-sensitivity troponin I and other markers of myocardial injury, as well as N-terminal pro-brain natriuretic peptide (NT-proBNP), were within the normal ranges during the patient’s entire hospitalization. Real-time reverse transcriptase PCR for the detection of nucleic acid from SARS-CoV-2 in a nasopharyngeal swab showed positive results and was followed by serology testing, which also returned positive for both IgM and IgG SARS-CoV-2 antibodies. Laboratory investigations for common cardiotropic viral agents (coxsackievirus, cytomegalovirus, adenovirus, and parvovirus) were negative.

Echocardiography showed a hyperechogenic pericardium posterolaterally with minimal localized pericardial effusion. The cardiac chambers were of normal size with normal left ventricular systolic function (left ventricular ejection fraction of 65%) and without regional wall abnormalities or more than mild valve disease. A chest computed tomography (CT) scan showed a small zone of ground-glass opacity in the right lower lobe, covering 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 the COVID-19 Reporting and Data System (CO-RADS) for the assessment of pulmonary involvement in COVID-19 on a non-enhanced chest CT scan, the finding was classified as CO-RADS 3 (Prokop et al., 2020).

Considering the clinical presentation and the ECG, laboratory, and echocardiography findings, the patient was diagnosed with acute pericarditis caused by SARS-CoV-2 with suspected mild viral pneumonia. The treatment included lopinavir/ritonavir (200/50 mg twice daily), aspirin (100 mg once daily), a beta-blocker (bisoprolol 2.5 mg once daily), and an antibiotic (ceftriaxone 2 g once daily).

The patient was well and afebrile without chest pain or any respiratory symptoms during the hospital stay. Serial echocardiographic studies did not demonstrate any deterioration in left ventricular systolic function or increase in pericardial effusion. The ECG 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.

Discussion

The case presented here demonstrated a patient who was diagnosed in an acute phase of pericarditis caused by SARS-CoV-2. Although cardiac involvement has been described previously in patients with COVID-19 and massive pneumonia, to our knowledge this is a rare case describing cardiac involvement in SARS-CoV-2 infection in a patient with mild pneumonia (Farina et al., 2020, Inciardi et al., 2020).

Emerging evidence suggests that SARS-CoV-2 has a tropism for myocardium and pericardium. Myocardial injury, detected by the presence of elevated high-sensitivity troponin I, has been reported to occur in about 12% of patients with COVID-19, and the virus has also been isolated in the pericardial fluid of a patient with COVID-19-associated pericarditis and cardiac tamponade (Farina et al., 2020, Huang et al., 2020). 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 (Zeng et al., 2020, Chen et al., 2020, Cizgici et al., 2020, Farina et al., 2020).

It is well established that viral agents can cause perimyocarditis either by directly affecting the heart or through mechanisms resulting from systemic inflammation during severe infections. The patient in the present case report had elevated levels of the proinflammatory cytokine IL-6, which is produced by immune cells in response to viral agents and appears to be an important mediator in the cytokine storm (Nishimoto and Kishimoto, 2006). Increased concentrations of IL-6 are also found in pericardial fluid in all forms of pericarditis (Ristić et al., 2013). Unlike previously published cases, the SARS-CoV-2 infection in our patient presented with dominantly pericardial involvement. The significance of early treatment with antiviral medication for the relatively benign course of the disease in our patient is to be established.

A limitation of this investigation is the lack of cardiac magnetic resonance imaging and pericardial biopsy that would have excluded myocarditis or confirmed pericarditis, respectively.

In conclusion, pericarditis should be considered in patients with chest pain, ST elevation on ECG, a normal coronary angiogram, and COVID-19. Accordingly, this atypical presentation of SARS-CoV-2 infection should not be forgotten. We emphasize the importance of clinical examination and ECG for decision-making in the setting of the COVID-19 epidemic. Future studies are needed to reveal in more detail the pathophysiological relationship between SARS-CoV-2 infection and the cardiovascular system, as well as the long-term outcomes of patients who have suffered perimyocardial damage due to SARS-CoV-2.

Funding source

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

Ethical approval

Approval was obtained from the local ethics committee.

Conflict of interest

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.