Pericarditis in patients with COVID-19: a systematic review : Journal of Cardiovascular Medicine

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Research articles: COVID-19

Pericarditis in patients with COVID-19: a systematic review

Diaz-Arocutipa, Carlosa,b,c; Saucedo-Chinchay, Josed; Imazio, Massimoe

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Journal of Cardiovascular Medicine 22(9):p 693-700, September 2021. | DOI: 10.2459/JCM.0000000000001202



Coronavirus disease 2019 (COVID-19), which is caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), continues to spread rapidly across the globe despite the containment efforts.1 Up to 17 December 2020, the current pandemic was responsible for more than 1.6 million deaths worldwide.2 The clinical spectrum of COVID-19 ranges from asymptomatic infection to multiorgan failure. The cardiovascular system is increasingly recognized as an important target of the SARS-CoV-2 infection, leading to many diseases, such as acute coronary syndrome, cardiac arrhythmias, thromboembolism, and myocarditis.3 Although pericarditis is another cardiac manifestation of COVID-19, clinical information about this presentation is still lacking.4 Therefore, we conducted a systematic review to summarize the clinical features, diagnostic methods, treatment, and outcomes of COVID-19 patients with pericarditis.


This review was reported according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement.5 We searched in the following databases: PubMed, Embase, Scopus, and Web of Science. The search was conducted from inception to 17 December 2020. The complete search strategy is available in Supplemental Digital Content, Table 1, There were no restrictions on language or publication date. Additionally, we conducted a hand-searching of reference lists of all included studies and relevant reviews to identify further studies.

The inclusion criteria were the following: studies that included adult patients (≥18 years old) diagnosed with COVID-19 by reverse transcription--PCR (RT-PCR) and pericarditis based on the European Society of Cardiology (ESC) criteria,6 studies that reported clinical data on pericarditis, and original articles and congress abstracts. We excluded animal studies, editorials, commentaries, systematic reviews, and narrative reviews.

We downloaded all articles from electronic search to EndNote X8 software and duplicate records were removed. All unique articles were uploaded to Rayyan QCRI ( for the selection process. Titles and abstracts were independently screened by two review authors (C.D.A. and J.S.C.) to identify relevant studies. Moreover, the same review authors (C.D.A. and J.S.C.) independently examined the full text of each eligible study and registered reasons for the exclusion. Any disagreement on title/abstract and full-text selection was resolved by consensus.

The information from each study was independently extracted by two review authors (C.D.A. and J.S.C.) using a standardized data extraction form that was previously piloted. Any disagreement was resolved by consensus. If additional data were needed, the corresponding author was contacted through e-mail. We extracted the following data: first author name, publication year, country, study design, sample size, age, sex, comorbidities, symptoms, electrocardiogram (ECG), laboratory, echocardiography, treatment, and outcomes.

Data are presented as frequencies and proportions for categorical variables. Continuous variables are summarized as mean ± standard deviation or median (interquartile range). As an exploratory analysis, we compared clinical characteristics between patients with acute pericarditis and myopericarditis. Acute pericarditis was defined by the presence of two or more of the following features: chest pain, pericardial friction rub, diffuse concave upward ST-elevation or PR depression on ECG, and new or worsening pericardial effusion.6 Myopericarditis was defined as the presence of acute pericarditis more elevation of troponin and/or new or presumed new focal or global left ventricular systolic dysfunction on cardiac imaging.6 Pearson's chi-squared test or Fisher's exact test were used for categorical variables and unpaired Student's t test or Mann--Whitney U test for continuous variables. All statistical analyses were performed using the statistical software R 3.6.3 ( A two-tailed P less than 0.05 was considered statistically significant.


Our electronic search retrieved 734 articles. After the removal of duplicates, 287 articles were screened by title/abstract, and of those, 234 were excluded. After a full-text assessment of the 53 remaining articles, 20 were excluded because of other population (17), incomplete data (2), and review (1). Finally, 33 articles (32 case reports and 1 case series)7–39 were selected (Fig. 1).

Fig. 1:
Flow diagram of study selection.

Thirty-four COVID-19 patients diagnosed with pericarditis were included. The mean age was 51.6 ± 19.5 years and 62% of patients were men (Table 1). Hypertension (32%), dyslipidemia (18%), and diabetes (15%) were the most frequent comorbidities. In 10 patients (30%), pericarditis was diagnosed after COVID-19 with a range from 5 to 56 days. The most common symptoms were chest pain (68%), fever (65%), and dyspnea (56%). Pericardial friction rub was reported in four cases (two with acute pericarditis and two with myopericarditis). Thirteen patients (38%) were diagnosed with acute pericarditis, whereas the rest (62%) were diagnosed with myopericarditis (Table 1).

Table 1 - Characteristics of coronavirus disease 2019 patients with pericarditis
Total Acute pericarditis Myopericarditis P value
Age (years), mean ± SD 51.6 ± 19.5 49.7 ± 21.6 52.8 ± 18.6 0.66a
Male 21/34 (62%) 8/13 (61%) 13/21 (62%) 0.63c
 Hypertension 11/34 (32%) 4/13 (31%) 7/21 (33%) 1c
 Dyslipidemia 6/34 (18%) 2/13 (15%) 4/21 (19%) 1c
 Diabetes 5/34 (15%) 1/13 (7%) 4/21 (19%) 0.63c
 Others (CAD, AF, among others) 12/34 (35%) 4/13 (31%) 8/21 (38%) 0.73c
 Chest pain 23/34 (68%) 11/13 (85%) 12/21 (57%) 0.14c
 Fever 22/34 (65%) 9/13 (69%) 13/21 (62%) 0.73c
 Dyspnea 19/34 (56%) 7/13 (54%) 12/21 (57%) 0.84b
 Cough 14/34 (41%) 5/13 (38%) 9/21 (43%) 0.81b
 Others (fatigue, myalgia, among others) 14/34 (41%) 5/13 (38%) 9/21 (43%) 0.81b
Timing of pericarditis diagnosis
 After COVID-19 10/33 (30%) 5/13 (38%) 5/20 (25%) 0.46c
 Simultaneous with COVID-19 23/33 (70%) 8/13 (62%) 15/20 (75%) 0.46c
 CRP (mg/l), median (IQR) 77 (12–177) 105 (44–277) 30 (11–124) 0.28d
 WBC (cells/μl), median (IQR) 12 335 (5625–16 500) 6390 (4845–13 585) 13 700 (5400–17 900) 0.26d
 Lymphocytes (cells/μl), median (IQR) 934 (745–1100) 920 (690–1180) 1040 (640–1100) 0.69d
 Diffuse ST-elevation and PR depression 18/32 (56%) 7/12 (58%) 11/20 (55%) 0.86b
 Focal T-wave inversion 7/32 (22%) 2/12 (17%) 5/20 (25%) 0.68c
 Diffuse T-wave inversion 2/32 (6%) 0/12 (0%) 2/20 (10%) 0.52c
 Others (focal PR depression, among others) 5/32 (16%) 3/12 (25%) 2/20 (10%) 0.34c
Pericardial effusion 26/34 (76%) 11/13 (85%) 15/21 (71%) 0.44c
 Small 8/23 (35%) 3/11 (28%) 5/12 (42%) 0.67c
 Moderate 6/23 (26%) 4/11 (36%) 2/12 (16%) 0.37c
 Large 9/23 (39%) 4/11 (36%) 5/12 (42%) 1c
Cardiac tamponade 12/34 (35%) 6/13 (46%) 6/21 (28%) 0.46c
Abnormal lung parenchyma on chest imaging 18/30 (60%) 6/11 (55%) 12/19 (63%) 0.71c
Pharmacological treatment
 Hydroxychloroquine 13/34 (38%) 5/13 (38%) 8/21 (38%) 1c
 Lopinavir/ritonavir 6/34 (18%) 2/13 (15%) 4/21 (19%) 1c
 Azithromycin 5/34 (15%) 3/13 (23%) 2/21 (9%) 0.35c
 Corticosteroids 8/34 (23%) 1/13 (8%) 7/21 (33%) 0.12c
 NSAIDs 13/34 (38%) 8/13 (61%) 5/21 (24%) 0.04c
 Colchicine 18/34 (53%) 11/13 (85%) 7/21 (33%) <0.01b
Oxygen requirement 15/34 (44%) 5/13 (38%) 10/21 (48%) 0.60b
Mechanical ventilation 7/34 (20%) 2/13 (15%) 5/21 (24%) 0.68c
Pericardial drainage 12/34 (35%) 6/13 (46%) 6/21 (28%) 0.46c
Extracted volume (ml), median (IQR) 450 (300–540) 480 (397–737) 400 (290–470) 0.23d
 Discharged 26/34 (76%) 11/13 (84%) 15/21 (71%) 0.44c
 Hospitalized 6/34 (18%) 1/13 (8%) 5/21 (24%) 0.37c
 Dead 2/34 (6%) 1/13 (8%) 1/21 (5%) 1c
AF, atrial fibrillation; CAD, coronary artery disease; COVID-19, coronavirus disease 2019; CRP, C-reactive protein; IQR, interquartile range; NSAIDs, nonsteroidal anti-inflammatory drugs; SD, standard deviation; WBC, white blood cell.
aStudent's t test.
bPearson's chi-squared test.
cFisher's exact test.
dMann--Whitney U test.

The most common findings on ECG were diffuse ST-elevation and PR depression (56%) and focal T-wave inversion (22%) with a similar proportion in patients with acute pericarditis and myopericarditis (Table 1). Among patients with myopericarditis, 8 out of 17 patients had a left ventricular ejection fraction (LVEF) less than or equal to 50%. Of those cases with reduced LVEF, five out of six had global wall motion abnormality. Overall, 26 patients had pericardial effusion and 12 of them developed cardiac tamponade without significant difference between patients with acute pericarditis and myopericarditis (Table 1). The size of pericardial effusion was reported as small in eight patients, moderate in six patients, and large in nine patients. In 60% of cases, abnormal lung parenchyma was reported on chest imaging (X-ray or computed tomography). Cardiovascular magnetic resonance was performed in eight patients12,20,23–25,28,35 (two patients with pericarditis and six patients with myopericarditis). Subepicardial late gadolinium enhancement was reported in five patients.12,24,25,28,35 Endomyocardial biopsy was not performed in any case. Invasive coronary angiography was performed in six patients and none showed obstructive coronary artery disease. The median values of C-reactive protein and white blood cells were above the normal range. In contrast, the median value of lymphocytes was below the normal range (Table 1). Although the type of reported troponin was different across studies, 20 patients had elevated levels of troponins. Fifty-six percent of patients with pericarditis had mild/moderate COVID-19 and 44% had severe/critical disease. In Fig. 2, we show our proposal for the diagnostic process of pericarditis and myopericarditis in patients with COVID-19.

Fig. 2:
Diagnostic process of pericarditis and myopericarditis in patients with coronavirus disease 2019. CK, creatine kinase; CMR, COVID-19, coronavirus disease 2019; cardiovascular magnetic resonance; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; RT-PCR, reverse transcription–PCR; SARS-CoV-2, severe acute respiratory coronavirus-2; WBC, white blood count.

The most used drugs for COVID-19 management were hydroxychloroquine (38%), lopinavir/ritonavir (18%), and azithromycin (15%) (Table 1). Other used drugs were corticosteroids (n = 8), empirical antibiotics (n = 7), immunoglobulin (n = 2), and remdesivir (n = 2). In six patients,20,26,28,30,34,36 corticosteroids were administered as part of the COVID-19 treatment, while in the remaining two patients,16,18 it was given for myopericarditis. Thirteen patients (38%) were treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and 18 patients (53%) with colchicine. Only one patient received aspirin 325 mg and heparin 5000 IU on admission as ST-segment elevation myocardial infarction was suspected.15 The NSAIDs used were aspirin in six patients [dosage: 500 mg twice-daily (n = 1) and 600 mg four times daily (n = 1)], ibuprofen in five patients [dosage: 600 mg three times daily (n = 3) and 800 mg three times daily (n = 1)], and indomethacin in three patients [dosage: 25 mg three times daily (n = 2) and 50 mg three times daily (n = 1)]. The dosage of colchicine was 0.5 mg twice-daily in seven patients and 0.5 mg once-daily in three patients. NSAIDs and colchicine were more frequently used in patients with acute pericarditis compared with myopericarditis (Table 1). One patient received anakinra (an interleukin-1 receptor antagonist) after the failure of initial therapy with colchicine.21 Oxygen supplementation and mechanical ventilation were required in 44% and 20% of cases, respectively. Among the 12 patients who needed pericardial drainage, the median volume extracted was 455 ml (300–540 ml). The macroscopic aspect of the pericardial fluid was reported as serosanguineous (n = 5) and serous (n = 5). The RT-PCR for SARS-CoV-2 in the pericardial fluid was tested in seven patients and in two of them, the result was positive. Overall, only two patients (6%) died during hospitalization without difference between patients with acute pericarditis and myopericarditis (Table 1). The cause of death was septic shock for both cases.


To our knowledge, this is the first systematic review of pericarditis in COVID-19 patients. We found that approximately half of the patients had ST-elevation and PR depression on ECG and LVEF less than 50% on echocardiography. Sixty-two percent of cases were diagnosed as myopericarditis. Pericardial effusion and cardiac tamponade were present in 76 and 35% of cases, respectively. Almost half of the patients received NSAIDs and colchicine, more frequently in acute pericarditis compared with myopericarditis. Overall, the in-hospital mortality was 6% without difference between patients from both groups.

Although there are some reports of pericardial involvement associated with COVID-19, its real frequency is not fully known. A recent meta-analysis of 2676 hospitalized patients with confirmed COVID-19 showed a pooled prevalence of pericardial effusion of 3% on chest computed tomography.40 Even though the cause of pericardial effusion was not identified, it is likely that most cases were because of pericardial inflammation. Moreover, given that a second wave of the current COVID-19 pandemic is occurring in several countries,1 the absolute number of potentially affected people with pericarditis is increasingly large. Overall, these data suggest that pericarditis is an entity under-diagnosed, and as a result, many patients are not receiving appropriate treatment. In addition, pericardial effusion was found in a significantly higher proportion of COVID-19 patients with severe/critical disease compared with the nonsevere group (16 versus 0%, P < 0.01), suggesting that it could be useful as a marker of poor outcome.41Although we found that 44% of patients with pericarditis had severe/critical COVID-19, it cannot be concluded that pericarditis is associated with more severe forms of COVID-19 as a control group was not available.

The most common etiology of pericarditis in developed countries is idiopathic (80–85%), most often presumed to be caused by viral agents, such as parvovirus B19, coxsackievirus, echovirus, among others.42 A definitive diagnosis is usually lacking as it requires the detection of the viral genome in the pericardial fluid or tissue through invasive methods, which are generally not used in routine clinical practice. Furthermore, viral serological tests have not proven to be clinically useful given that they only suggest a recent viral infection with little impact on treatment and have been shown to have a poor correlation with the detection of viral genomes in pericardial fluid.42 Although two studies14,35 have reported a positive result of RT-PCR for SARS-CoV-2 in pericardial fluid, the test was negative in the rest of the samples (n = 5). This can be explained by the low diagnostic yield of RT-PCR for samples other than upper and lower respiratory specimens as well as the timing of the test.43 Also, this low detection rate of SARS-CoV-2 in pericardial samples is comparable with other cardiotropic viruses, where most cases of pericarditis are autoreactive without detection of active viral infection.44 Given the lack of strong evidence regarding the direct role of SARS-CoV-2 for pericardial inflammation in all COVID-19 patients, other causes of pericarditis should also be considered.

Acute pericarditis is caused by an inflammatory response to an acute injury to the mesothelial cells of the pericardial layers.45 The inflammation is initiated by the viruses themselves or the release of cellular debris triggering the formation of the Nod Like Protein Receptor 3 (NLRP3) inflammasome that intensifies a local and systemic inflammatory response driven mainly by interleukin-1β.45 In addition, cardiotropic viruses can also cause myocardial inflammation through the same pathways leading to myopericarditis.6 The pathogenesis of acute pericarditis and myopericarditis in COVID-19 patients is still poorly understood. Dysregulation of the immune system is key in the pathogenesis of SARS-CoV-2 infection leading to an overproduction of pro-inflammatory cytokines in some patients, resulting in what has been called a cytokine storm.46 This increased inflammatory response may play a role in the different cardiovascular presentations associated with COVID-19, including pericarditis and myopericarditis. Amoozgar et al.8 described a case of COVID-19 where the patient developed a large pericardial effusion. In the pericardial biopsy, a thickened pericardium with reactive mesothelial cells, lymphocytes, and histiocytes was found. Furthermore, the detection of SARS-CoV-2 genome in the pericardial fluid of two COVID-19 patients has been reported. Overall, these findings suggest that COVID-19 probably shares the same pathophysiological mechanisms as seen in other cardiotropic viral infections.47

The ECG in acute pericarditis and myopericarditis commonly evolves through four stages: diffuse ST-elevation and depression of the PR segment, normalization of ST-elevation and PR depression, diffuse T-wave inversion, and normalization of ECG.48 However, this typical ECG evolution has been reported only in 60% of cases.49 We found that almost half of the patients had diffuse ST-elevation with PR depression on ECG. Although atypical ECG changes (e.g. focal ST-elevation or T-wave inversion) occur more frequently in myopericarditis than in acute pericarditis, we found no significant differences between both groups. Many factors could influence the changes in the ECG: timing of ECG evaluation, heterogeneity in the grade of epicardial inflammation, and variable exposition to anti-inflammatory therapy.48

Currently, the mainstay anti-inflammatory therapy for acute pericarditis is the combination of NSAIDs with colchicine.6 Although there were initial concerns about the safety of NSAIDs in COVID-19, recent evidence has shown that the use of NSAIDs was not associated with worse clinical outcomes in patients with COVID-19;50–52 therefore, NSAIDs should not be contraindicated in these patients.53 Colchicine is an old anti-inflammatory drug with a good safety profile that acts by blocking microtubule polymerization and NLRP3 inflammasome activity in inflammatory cells.42 Interestingly, some observational studies have reported that the use of colchicine reduced mortality in COVID-19 patients.54–56 Recently, three randomized controlled trials (RCTs) evaluating the use of colchicine in COVID-19 patients have been published with conflicting results.57–59 On 5 March 2021, the RECOVERY trial closed the enrollment of COVID-19 patients in the colchicine arm as no convincing evidence of mortality benefit was found (; accessed 13 March 2021). Two additional RCTs [COLCOVID (NCT04350320) and CONVINCE (NCT04516941)] are still ongoing. Corticosteroids are recommended as a second-line therapy at low-to-moderate doses (e.g. prednisone 0.2–0.5 mg/kg/day or equivalent) for acute pericarditis in patients with contraindications or failure to NSAIDs.6 Corticosteroids are not used as a first option as these are associated with an increased risk of recurrence and a more prolonged disease course, especially at high doses.6 Recently, the RECOVERY trial has provided evidence that the use of dexamethasone at a dose of 6 mg per day reduced mortality in COVID-19 patients who required oxygen support.60 We found that 23% of patients were treated with corticosteroids; however, data on episodes of pericarditis recurrence were not available. Hence, given the clear benefit of corticosteroids in severe COVID-19 cases, their use should be continued in this group of patients even if they have acute pericarditis.53 Our review shows that 38 and 53% of patients with pericarditis were treated with NSAIDs and colchicine, respectively. One of the main reasons for the low utilization of proven therapies for pericarditis may be related to initial concerns that these medications are harmful in patients with COVID-19. In addition, despite there being limited data for the treatment of myopericarditis, lower doses of NSAIDs are generally recommended to control symptoms. Also, colchicine has insufficient evidence for use in this clinical entity. Accordingly, we found that COVID-19 patients with myopericarditis received NSAIDs and colchicine in a lower proportion than patients with acute pericarditis.

Most patients with acute idiopathic pericarditis and myopericarditis have a good long-term prognosis.6 The most common complication is a recurrence, which can occur in 20–30% of cases.42 As previously mentioned, our review did not identify any cases of recurrence at follow-up, although there is a possibility that it will be increasingly reported in the future. Constrictive pericarditis and cardiac tamponade rarely occur in these patients.6 Accordingly, only one case of constrictive pericarditis associated with SARS-CoV-2 infection has been reported in the literature.61 Despite cardiac tamponade being a rare presentation, our review showed a higher proportion (35%) of cardiac tamponade in patients with COVID-19 compared with other cardiotropic viral infections in which the pericardial effusion is usually mild.48 Although this could be overestimated as the information is derived from case reports, it is possible that the large inflammatory response observed in COVID-19 patients contributes to the development of this complication. Overall, only two patients with COVID-19 and pericarditis died during hospitalization; however, the cause was extracardiac (septic shock by viral pneumonia) in both cases. This low short-term mortality could be explained by the fact that our patients were relatively young and had a low proportion of comorbidities.


Our review has some limitations. First, although the definition of myopericarditis was based on troponin levels and the left ventricular systolic function, there were other mechanisms not related to myocardial inflammation (such as acute coronary thrombosis and Takotsubo cardiomyopathy) that could also result in elevation of troponins and/or systolic dysfunction in COVID-19 patients.47 However, we expected that this will occur only in a minority of cases. Second, because of the lack of endomyocardial biopsy, a histopathological diagnosis of myopericarditis was not possible. Third, given that all included studies were case reports or case series, selection and publication bias would be probably present as only patients with unusual characteristics and worse outcomes may have been published. Fourth, although we have reported clinical outcomes in the short term, the mid-term to long-term prognosis remains unknown. Finally, our study was composed of a small sample (n = 34), limiting the generalizability of the results.


Our systematic review shows that almost half of COVID-19 patients with pericarditis had ST-elevation and PR depression on ECG and reduced LVEF. Sixty-two percentage of cases were diagnosed as myopericarditis. Pericardial effusion was present in nearly 80% of cases. However, approximately half or less of the patients were treated with NSAIDs and colchicine. Overall, the short-term prognosis was good across groups. Importantly, all data came from case reports and case series, thus prospective studies with larger samples are needed to confirm our findings and guide the clinical care of these patients.

Conflicts of interest

There are no conflicts of interest.


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acute pericarditis; coronavirus disease 2019; myopericarditis; systematic review

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