Calcific pericarditis strangling the heart, an answer to unexplained heart failurediagnostic modalities.

Pericardial calcification is often found incidentally from imaging studies and may be a clue to constrictive pericarditis. Constrictive pericarditis often mimics other causes of heart failure, pulmonary, or liver disease, making it hard to diagnose. Tuberculosis is the most common infectious aetiology of Constrictive Pericarditis. Living in developing countries, such as Indonesia, should warn us of the possibility of tuberculous constrictive pericarditis as a differential diagnosis of unexplained heart failure. The presented case came with complaints of shortness of breath, especially on exertion for five years, which worsened in the last 6 months. The past history of pulmonary Tuberculosis with the Cardiac CT findings confirmed the diagnosis of Constrictive Pericarditis.

"Ghost imaging" in pericardial cavity: Disappeared "tumor-like" masses in tuberculous pericarditis.

A 66-year-old woman was admitted to our hospital due to chest distress and shortness of breath during 1 week. Transthoracic echocardiography (TTE) revealed massive pericardial effusion and multiple, irregular and high-density echo "tumor-like" masses on the heart, with the largest one on the apex. However, there were no masses found by computed tomography (CT) scan, except for increased lipids around the coronary artery. We performed emergency pericardiocentesis and drainage to relieve symptoms. The positron emission tomography/CT (PET/CT) also showed several ununiformly high accumulations in pericardial cavity. However, the high-density echo "tumor-like" masses cannot be seen by TTE after pericardiocentesis, and also cannot be detected when surgery. Pericardiotomy was performed due to severe pericardial adhesion. The diagnosis of tuberculosis (TB) was confirmed by pericardiotomy and pericardial biopsy.

Pericarditis caused by Mycobacterium africanum: case report.

BACKGROUND: Mycobacterium africanum is a member of the Mycobacterium tuberculosis complex (MTBC) and is endemic in West Africa, where it causes up to half of all cases of pulmonary tuberculosis. Here, we report the first isolation of Mycobacterium africanum from the pericardial effusion culture of a patient with tuberculous pericarditis. CASE PRESENTATION: A 31-year-old man, native from Senegal, came to the emergency room with massive pericardial effusion and cardiac tamponade requiring pericardiocentesis. M. africanum subtype II was identified in the pericardial fluid. The patient completed 10 months of standard treatment, with a favorable outcome. CONCLUSIONS: We report the first case of tuberculous pericarditis caused by Mycobacterium africanum, which provide evidence that this microorganism can cause pericardial disease and must be considered in patients from endemic areas presenting with pericardial effusion.

Unusual cause for loss of left ventricular capture in patient with cardiac resynchronization due to tuberculous pericarditis.

We report a case of 37-year-old man implanted with cardiac resynchronization therapy-defibrillator presented with persistent low-grade fever and sudden loss of left ventricular (LV) capture from coronary sinus lead after generator replacement. 18 F-fluorodeoxyglucose positron emission tomography with computed tomography scan showed increased uptake at posterolateral region of the pericardium adjacent to the LV lead, suggestive of possible lead-related infection. Combined percutaneous and surgical lead extraction revealed purulent pericarditis and polymerase chain reaction testing confirmed tuberculous (TB) pericarditis. TB pericarditis is an unusual cause of loss of LV capture, but should be considered in countries where TB is still endemic.

[Tuberculous pericarditis an infrequent extrapulmonary manifestation of TB]. / Pericarditis tuberculosa: una manifestación extrapulmonar infrecuente de TBC.

Extrapulmonary tuberculosis (TB) contributes to 15% of total cases, representing a great diagnostic and therapeutic challenge. Pericardial involvement is present in 1 to 2% of TB patients and is considered an unusual presentation form of TB. We report a 67-year-old male presenting with fever and progressive dyspnea. A chest CAT scan showed a bilateral pleural effusion and an extensive pericardial effusion. An echocardiogram showed signs of tamponade. Therefore, an emergency pericardiectomy was performed. The pathological report of pericardial tissue showed caseating necrosis and its Koch culture was positive. The patient was treated with anti-tuberculous drugs with a favorable evolution.

A case report of a child with probable drug resistant tuberculous pericarditis with a review of challenges involved in diagnosis, treatment and follow up of children with DR-TB pericarditis.

BACKGROUND: There are unique challenges in the diagnosis and management of multi drug resistant tuberculosis (MDR-TB) in children. It is difficult to obtain confirmatory microbiological diagnosis in TB pericarditis. It is essential to differentiate between drug sensitive and drug resistant forms of TB as it has a major bearing on the regimen used, and inappropriate TB treatment combined with steroid use for pericarditis can lead to deterioration. With lack of samples, the treatment decision relies on the drug resistance pattern of the close contact if available. Therapeutic challenges of MDR-TB management in a child involve use of toxic drugs that need to be judiciously handled. We report a 2 years 4 months old male child who was diagnosed with TB pericarditis and treated based on the resistance pattern of his mother who was on treatment for pulmonary MDR-TB. CASE PRESENTATION: This 2 years 4 months old male child was diagnosed with TB involving his pericardium. Getting him started on an appropriate regimen was delayed due to the difficulty in establishing microbiological confirmation and drug susceptibility. He was commenced on a regimen based on his mother's drug resistance pattern and required surgery due to cardiac failure during the course of his treatment. He successfully completed 2 years of therapy. CONCLUSIONS: This child's case demonstrates that despite unique challenges in diagnosis and management of drug resistant extra pulmonary tuberculosis in children, treatment of even complex forms can be successful. The need for high suspicion of MDR-TB, especially when there is close contact with pulmonary TB, careful design of an effective regimen that is tolerated by the child, indications for invasive surgical management of pericarditis, appropriate follow-up and management of adverse effects are emphasised.

Sensitivity analysis for the generalized shared-parameter model framework.

In this paper, we assess the effect of tuberculosis pericarditis treatment (prednisolone) on CD4 count changes over time and draw inferences in the presence of missing data. We accounted for the missing data and performed sensitivity analyses to assess robustness of inferences, from a model that assumes that the data are missing at random, to models that assume that the data are not missing at random. Our sensitivity approaches are within the shared-parameter model framework. We implemented the approach by Creemers and colleagues to the CD4 count data and performed simulation studies to evaluate the performance of this approach. We also assessed the influence of potentially influential subjects, on parameter estimates, via the global influence approach. Our results revealed that inferences from missing at random analysis model are robust to not missing at random models and influential subjects did not overturn the study conclusions about prednisolone effect and missing data mechanism. Prednisolone was found to have no significant effect on CD4 count changes over time and also did not interact with anti-retroviral therapy. The simulation studies produced unbiased estimates of prednisolone effect with lower mean square errors and coverage probabilities approximately equal the nominal coverage probability.

Diagnostic performance of interferon-gamma release assay for diagnosis of tuberculous pericarditis: A meta-analysis.

BACKGROUND: The diagnosis of tuberculous pericarditis is difficult to set, not only for its non-specific clinical presentation, but also for the lack of useful diagnostic tests. We comprehensively evaluate the overall diagnostic accuracy of Interferon-gamma release assays (IGRA) upon tuberculous pericarditis by meta-analysis. METHODS: We searched PubMed, Embase and Cochrane Library database from the earliest available date of indexing through April 30, 2019. The study quality was evaluated using the Quality Assessment of Diagnostic Accuracy Studies (QUADAS2) checklist. We determined the sensitivities and specificities across studies, calculated positive and negative likelihood ratios (LR+ and LR-) and constructed summary receiver operating characteristic curves parameters. RESULTS: Across six results from five studies (415 patients), the pooled sensitivity for IGRA methods was 0.94 (95% confidence interval [CI]; 0.87-0.98) with heterogeneity (χ2  = 69.9, P = .01) and a pooled specificity of 0.94 (95% CI; 0.75-0.94) without heterogeneity (χ2  = 41.1, P = .13). Likelihood ratio (LR) syntheses gave an overall positive likelihood ratio (LR+) of 16.8 (95% CI; 8.0-35.4) and negative likelihood ratio (LR-) of 0.06 (95% CI; 0.03-0.13). The pooled diagnostic odds ratio was 278 (95% CI; 114-6806). CONCLUSIONS: Interferon-gamma release assays demonstrated good sensitivity and specificity for diagnosis of tuberculous pericarditis. At present, the literature regarding remains the use of IGRA for diagnosis of tuberculous pericarditis still limited; thus, further large multicenter studies would be necessary to substantiate the diagnostic accuracy of IGRA test for the diagnosis of tuberculous pericarditis.

Diagnosis and Management of Tuberculous Pericarditis: What Is New?

PURPOSE OF REVIEW: This review provides an update on the immunopathogenesis of tuberculous pericarditis (TBP), investigations to confirm tuberculous etiology, the limitations of anti-tuberculous therapy (ATT), and recent efficacy trials. RECENT FINDINGS: A profibrotic immune response characterizes TBP, with low levels of AcSDKP, high levels of γ-interferon and IL-10 in the pericardium, and high levels of TGF-ß and IL-10 in the blood. These findings may have implications for future therapeutic targets. Despite advances in nucleic acid amplification approaches, these tests remain disappointing for TBP. Trials of corticosteroids and colchicine have had mixed results, with no impact on mortality, evidence of a reduction in rates of constrictive pericarditis and potential harm in those with advanced HIV. Small studies suggest that ATT penetrates the pericardium poorly. Given that there is a close association between high bacillary burden and mortality, a rethink about the optimal drug doses and duration may be required. The high mortality and morbidity from TBP despite use of anti-tuberculous drugs call for researches targeting host-directed immunological determinants of treatment outcome. There is also a need for the identification of steps in clinical management where interventions are needed to improve outcomes.

[Pericarditis in contemporary therapeutic clinic: nosological spectrum, approaches to diagnosis and treatment].

AIM: To analyze the register of pericarditis in a therapeutic clinic, to evaluate their nosological spectrum, to optimize approaches to diagnosis and treatment. MATERIALS AND METHODS: For the period 20072018, the register includes 76 patients with the diagnosis of pericarditis (average age 53.115.7 years, 2085 years, 46 female). Patients with hydropericardium were not included in the register. Diagnostic puncture of pericardium was carried out in 5 patients, pleural puncture in 11 patients. Morphological diagnostics included endomyocardial/ intraoperative biopsy of myocardium (n=4/2), thoracoscopic/intraoperative biopsy of pericardium (n=1/6), pleural puncture (n=5), transbronchial (n=1), thoracoscopic biopsy of intrathoracic lymph nodes (n=2), lung (n=1), supraclavicular lymph node biopsy (n=1), salivary gland (n=1), subcutaneous fat and rectum biopsy per amyloid (n=6/1). The genome of cardiotropic viruses, level of anti-heart antibodies, C-reactive protein, antinuclear factor, rheumatoid factor (antibodies to cyclic citrullinized peptide), antibodies to neutrophil cytoplasm were determined, extractable nuclear antigens (ENA), protein immunoelectrophoresis, diaskin test, computed tomography of lungs and heart, cardiac magnetic resonance imaging, oncologic search. RESULTS: The following forms of pericarditis were verified: tuberculosis (14%, including in combination with hypertrophic cardiomyopathy HCM), acute / chronic viral (8%) and infectious immune (38%), including perimyocarditis in 77%, pericarditis associated with mediastinum lymphoma/sarcoma (4%), sarcoidosis (3%), diffuse diseases of connective tissue and vasculitis (systemic lupus erythematosus, rheumatoid arthritis, diseases of Horton, Takayasu, Shegren, Wegener, 12%), leukoclastic vasculitis, Loefflers endomyocarditis, AL-amyloidosis, thrombotic microangiopathy (1% each), HCM (8%), coronary heart disease (constriction after repeated punctures and suppuration; postinfection and immune, 4%), after radiofrequency catheter ablation and valve prosthetics (2%). Tuberculosis was the main causes of constrictive pericarditis (36%). Treatment included steroids (n=39), also in combination with cytostatics (n=12), anti-tuberculosis drugs (n=9), acyclovir/ganclovir (n=14), hydroxychloroquine (n=23), colchicine (n=13), non-steroidal anti-inflammatory drugs (n=21), L-tyroxine (n=5), chemotherapy (n=1). In 36 patients different types of therapy were combined. Treatment results observed in 55 patients. Excellent and stable results were achieved in 82% of them. Pericardiectomy/pericardial resection was successfully performed in 8 patients. Lethality was 13.2% (10 patients) with an average follow-up 9 [2; 29.5] months (up to 10 years). Causes of death were chronic heart failure, surgery for HCM, pulmonary embolism, tumor. CONCLUSION: During a special examination, the nature of pericarditis was established in 97% of patients. Morphological and cytological diagnostics methods play the leading role. Tuberculosis pericarditis, infectious-immune and pericarditis in systemic diseases prevailed. Infectious immune pericarditis is characterized by small and medium exudate without restriction and accompanying myocarditis. Steroids remain the first line of therapy in most cases. Hydroxychloroquine as well as colchicine can be successfully used in moderate / low activity of immune pericarditis and as a long-term maintenance therapy after steroid stop.

An application of a pattern-mixture model with multiple imputation for the analysis of longitudinal trials with protocol deviations.

BACKGROUND: The benefit of a given treatment can be evaluated via a randomized clinical trial design. However, protocol deviations may severely compromise treatment effect since such deviations often lead to missing values. The assumption that methods of analysis can account for the missing data cannot be justified and hence methods of analysis based on plausible assumptions should be used. An alternative analysis to the simple imputation methods requires unverifiable assumptions about the missing data. Therefore sensitivity analysis should be performed to investigate the robustness of statistical inferences to alternative assumptions about the missing data. AIMS: In this paper, we investigate the effect of tuberculosis pericarditis treatment (prednisolone) on CD4 count changes over time and draw inferences in the presence of missing data. The data come from a multicentre clinical trial (the IMPI trial). METHODS: We investigate the effect of prednisolone on CD4 count changes by adjusting for baseline and time-dependent covariates in the fitted model. To draw inferences in the presence of missing data, we investigate sensitivity of statistical inferences to missing data assumptions using the pattern-mixture model with multiple imputation (PM-MI) approach. We also performed simulation experiment to evaluate the performance of the imputation approaches. RESULTS: Our results showed that the prednisolone treatment has no significant effect on CD4 count changes over time and that the prednisolone treatment does not interact with time and anti-retroviral therapy (ART). Also, patients' CD4 count levels significantly increase over the study period and patients on ART treatment have higher CD4 count levels compared with those not on ART. The results also showed that older patients had lower CD4 count levels compared with younger patients, and parameter estimates under the MAR assumption are robust to NMAR assumptions. CONCLUSIONS: Since the parameter estimates under the MAR analysis are robust to NMAR analyses, the process that generated the missing data in the CD4 count measurements is missing at random (MAR). The implication is that valid inferences can be obtained using either the likelihood-based methods or multiple imputation approaches.

Normal Tumor Markers and Increased Adenosine Deaminase in Pericardial Effusion Misdiagnosed as Tuberculous Pericarditis Ultimately Proven as Lung Adenocarcinoma with Pericardial Metastasis: a Case Report and Literature Review.

BACKGROUND: Elevated adenosine deaminase (ADA) and normal tumor markers in pericardial or pleural effusion are usually considered to be a specific manifestation of benign pericardial or pleural effusion. Here we report a case of lung adenocarcinoma with pericardial metastasis with elevated ADA and normal tumor markers in pericardial effusion. METHODS: Pericardiocentesis and lung puncture combined laboratory indexes and pathology were performed for diagnosis. RESULTS: Analysis of pericardial fluid revealed a white blood cell (WBC) count of 2,000 x 106/L (70% for lymphocytes) with an ADA level of 72.8 U/mL. Pathology of pericardial effusion found no malignant cells. Histopathology of percutaneous lung puncture showed adenocarcinoma. CONCLUSIONS: ADA and tumor markers were not a specific index in differential diagnosis between tuberculosis and metastasis in pericardial effusion.

Exudative-constrictive tuberculous pericarditis in combination with arthritis in cardiologist practice: thoracoscopic biopsy as a diagnosis and treatment method.

AIM: The goal is to present the possibilities of diagnosis verification, the features of the clinical picture of tuberculous pericarditis in the therapeutic clinic and the results of its treatment. MATERIALS AND METHODS: The paper presents clinical observation and a general analysis of 10 cases of tuberculous pericarditis in patients aged 31-79 (mean age 58.0 ± 15.1 years), 6 women and 4 men. Diagnostic puncture pericardium was performed on two patients, pleural puncture - on three Thoracoscopic biopsy of hilar lymph nodes and lung (n=1), pleura (n=1), supraclavicular lymph node biopsy (n=1). Dyskin test was carried out, as well as sputum examination, multispiral computed tomography, oncological search. RESULTS: A 31-year-old patient with a massive effusion in the pericardial cavity, pleural lesion, arthritis of the left knee joint, whose results of the pericardial effusion and sputum were not diagnosed, tuberculosis was detected only with thoracoscopic biopsy of the lung and intrathoracic lymph nodes; the treatment via prednisolone and subtotal pericardectomy was performed. Among 10 patients with MSCT of the lung, changes were noted in general, but in only one case they were highly specific. Diaskin test is positive in 70%. In the study of punctata, bronchoalveolar flushing, Koch bacteria were not detected; at sputum in microscopy and biological sample BC was detected in two patients. The lymphocytic character of effusion in the pericardium / pleura is noted in 4 out of 5 cases. At a biopsy of lymphonoduses and a lung at 2 patients the picture of a granulomatous inflammation with a caseous necrosis. Pericarditis was predominantly large (from 2 cm and more) effusion, signs of constriction were noted in 50% of patients. CONCLUSION: Tuberculosis is one of the frequent causes of pericarditis in the Moscow therapeutic clinic. The most lymphocytic effusion with fibrin and the development of constriction. The negative results of all laboratory tests for tuberculosis do not exclude a diagnosis, It is necessary to use invasive morphological diagnostics, including thoracoscopic biopsy.

Prednisolone and Mycobacterium indicus pranii in tuberculous pericarditis.

BACKGROUND: Tuberculous pericarditis is associated with high morbidity and mortality even if antituberculosis therapy is administered. We evaluated the effects of adjunctive glucocorticoid therapy and Mycobacterium indicus pranii immunotherapy in patients with tuberculous pericarditis. METHODS: Using a 2-by-2 factorial design, we randomly assigned 1400 adults with definite or probable tuberculous pericarditis to either prednisolone or placebo for 6 weeks and to either M. indicus pranii or placebo, administered in five injections over the course of 3 months. Two thirds of the participants had concomitant human immunodeficiency virus (HIV) infection. The primary efficacy outcome was a composite of death, cardiac tamponade requiring pericardiocentesis, or constrictive pericarditis. RESULTS: There was no significant difference in the primary outcome between patients who received prednisolone and those who received placebo (23.8% and 24.5%, respectively; hazard ratio, 0.95; 95% confidence interval [CI], 0.77 to 1.18; P=0.66) or between those who received M. indicus pranii immunotherapy and those who received placebo (25.0% and 24.3%, respectively; hazard ratio, 1.03; 95% CI, 0.82 to 1.29; P=0.81). Prednisolone therapy, as compared with placebo, was associated with significant reductions in the incidence of constrictive pericarditis (4.4% vs. 7.8%; hazard ratio, 0.56; 95% CI, 0.36 to 0.87; P=0.009) and hospitalization (20.7% vs. 25.2%; hazard ratio, 0.79; 95% CI, 0.63 to 0.99; P=0.04). Both prednisolone and M. indicus pranii, each as compared with placebo, were associated with a significant increase in the incidence of cancer (1.8% vs. 0.6%; hazard ratio, 3.27; 95% CI, 1.07 to 10.03; P=0.03, and 1.8% vs. 0.5%; hazard ratio, 3.69; 95% CI, 1.03 to 13.24; P=0.03, respectively), owing mainly to an increase in HIV-associated cancer. CONCLUSIONS: In patients with tuberculous pericarditis, neither prednisolone nor M. indicus pranii had a significant effect on the composite of death, cardiac tamponade requiring pericardiocentesis, or constrictive pericarditis. (Funded by the Canadian Institutes of Health Research and others; IMPI ClinicalTrials.gov number, NCT00810849.).

Interventions for treating tuberculous pericarditis.

BACKGROUND: Tuberculous pericarditis can impair the heart's function and cause death; long term, it can cause the membrane to fibrose and constrict causing heart failure. In addition to antituberculous chemotherapy, treatments include corticosteroids, drainage, and surgery. OBJECTIVES: To assess the effects of treatments for tuberculous pericarditis. SEARCH METHODS: We searched the Cochrane Infectious Diseases Group Specialized Register (27 March 2017); the Cochrane Central Register of Controlled Trials (CENTRAL), published in the Cochrane Library (2017, Issue 2); MEDLINE (1966 to 27 March 2017); Embase (1974 to 27 March 2017); and LILACS (1982 to 27 March 2017). In addition we searched the metaRegister of Controlled Trials (mRCT) and the World Health Organization (WHO) International Clinical Trials Registry Platform (ICTRP) search portal using 'tuberculosis' and 'pericard*' as search terms on 27 March 2017. We searched ClinicalTrials.gov and contacted researchers in the field of tuberculous pericarditis. This is a new version of the original 2002 review. SELECTION CRITERIA: We included randomized controlled trials (RCTs) and quasi-RCTs. DATA COLLECTION AND ANALYSIS: Two review authors independently screened search outputs, evaluated study eligibility, assessed risk of bias, and extracted data; and we resolved any discrepancies by discussion and consensus. One trial assessed the effects of both corticosteroid and Mycobacterium indicus pranii treatment in a two-by-two factorial design; we excluded data from the group that received both interventions. We conducted fixed-effect meta-analysis and assessed the certainty of the evidence using the GRADE approach. MAIN RESULTS: Seven trials met the inclusion criteria; all were from sub-Saharan Africa and included 1959 participants, with 1051/1959 (54%) HIV-positive. All trials evaluated corticosteroids and one each evaluated colchicine, M. indicus pranii immunotherapy, and open surgical drainage. Four trials (1841 participants) were at low risk of bias, and three trials (118 participants) were at high risk of bias.In people who are not infected with HIV, corticosteroids may reduce deaths from all causes (risk ratio (RR) 0.80, 95% confidence interval (CI) 0.59 to 1.09; 660 participants, 4 trials, low certainty evidence) and the need for repeat pericardiocentesis (RR 0.85, 95% CI 0.70 to 1.04; 492 participants, 2 trials, low certainty evidence). Corticosteroids probably reduce deaths from pericarditis (RR 0.39, 95% CI 0.19 to 0.80; 660 participants, 4 trials, moderate certainty evidence). However, we do not know whether or not corticosteroids have an effect on constriction or cancer among HIV-negative people (very low certainty evidence).In people living with HIV, only 19.9% (203/1959) were on antiretroviral drugs. Corticosteroids may reduce constriction (RR 0.55, 0.26 to 1.16; 575 participants, 3 trials, low certainty evidence). It is uncertain whether corticosteroids have an effect on all-cause death or cancer (very low certainty evidence); and may have little or no effect on repeat pericardiocentesis (RR 1.02, 0.89 to 1.18; 517 participants, 2 trials, low certainty evidence).For colchicine among people living with HIV, we found one small trial (33 participants) which had insufficient data to make any conclusions about any effects on death or constrictive pericarditis.Irrespective of HIV status, due to very low certainty evidence from one trial, it is uncertain whether adding M. indicus pranii immunotherapy to antituberculous drugs has an effect on any outcome.Open surgical drainage for effusion may reduce repeat pericardiocentesis In HIV-negative people (RR 0.23, 95% CI 0.07 to 0.76; 122 participants, 1 trial, low certainty evidence) but may make little or no difference to other outcomes. We did not find an eligible trial that assessed the effects of open surgical drainage in people living with HIV.The review authors found no eligible trials that examined the length of antituberculous treatment needed nor the effects of other adjunctive treatments for tuberculous pericarditis. AUTHORS' CONCLUSIONS: For HIV-negative patients, corticosteroids may reduce death. For HIV-positive patients not on antiretroviral drugs, corticosteroids may reduce constriction. For HIV-positive patients with good antiretroviral drug viral suppression, clinicians may consider the results from HIV-negative patients more relevant.Further research may help evaluate percutaneous drainage of the pericardium under local anaesthesia, the timing of pericardiectomy in tuberculous constrictive pericarditis, and new antibiotic regimens.

IgG4-related disease manifesting as pericarditis with elevated adenosine deaminase and IL-10 levels in pericardial fluid.

A 78-year-old female with massive pericardial effusion fulfilled diagnostic criteria for immunoglobulin G4 (IgG4)-related disease. Although her adenosine deaminase (ADA) level in the pericardial effusion was high, all the tests for tuberculosis infection were negative. Immunostaining of the pericardium biopsy specimen revealed remarkably increased IgG4-positive cells. This is the first report describing IgG4-related pericarditis with elevated ADA level. We also demonstrate the elevated interleukin-10 (IL-10) level in pericardial fluid and IL-10-producing T-cells in the pericardium.