"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.

[Diagnosis and effective surgical treatment of constrictive pericarditis].

Constrictive pericarditis is a rare and severe disease. Timely and correct differential diagnosis of this pathology facilitates choice of necessary tactics of treatment and thus improve prognosis and quality of life. In this paper we present clinical case report of a patient with constrictive pericarditis. The disease was diagnosed on the basis of clinical picture, data of X-ray and echocardiographic investigation, and confirmed by multispiral computed tomography (MSCT). The patient was subjected to pericardioectomy with positive clinical effect and results of repeated echocardiography and MSCT.

Melioidosis pericarditis mimicking tuberculous pericarditis.

Cases of melioidosis (N = 2) and tuberculous pericarditis (N = 33) during 1996-2006 were reviewed. Clinical presentations were similar, but pericardial pathological findings were not. Nine of 12 patients with melioidosis required pericardectomy. In areas where these diseases are endemic, pericardial fluid culture and pericardial biopsy can differentiate between melioidosis and tuberculosis.

Rapid diagnosis of tuberculous pericarditis by ELISPOT assay.

We describe a case in which the rapid diagnosis of tuberculous pericarditis was made using the Mycobacterium tuberculosis (MTB)-specific enzyme-linked immunospot (ELISPOT) assay on pericardial effusion mononuclear cells (PEMCs). The analysis of MTB-specific T-cells in PEMCs by ELISPOT may be useful for rapid decision-making in anti-tuberculous treatment.

The immunopathogenesis of tuberculous pericarditis.

Tuberculous pericarditis is a severe form of extrapulmonary tuberculosis and is the commonest cause of pericardial effusion in high incidence settings. Mortality ranges between 8 and 34%, and it is the leading cause of pericardial constriction in Africa and Asia. Current understanding of the disease is based on models derived from studies performed in the 1940-50s. This review summarises recent advances in the histology, microbiology and immunology of tuberculous pericarditis, with special focus on the effect of Human Immunodeficiency Virus (HIV) and the determinants of constriction.

Tuberculous pericarditis mimicking multiple tumors in pericardial effusion.

Tuberculosis is still the leading cause of pericardial disease in developing nations. A definite diagnosis of tuberculosis is usually relatively difficult, especially when its manifestations are not typical. We report a 19-year-old man who presented with chest obstruction, shortness of breath, edema of the lower extremities, and mild fever for 14 days. The manifestations of tuberculosis pneumonia were not typical, except for a small high-density shadow in the left upper lung field near the pleura, with a small amount of pleural effusion on chest computed tomography. The tuberculin skin test, acid-fast stain of sputum and pericardial effusion, and bacterial culture showed negative results. Echocardiography showed three free-floating irregular masses in a large amount of pericardial effusion. The masses and exudates were removed by pericardiectomy. The masses were composed of hyperplastic granulation tissue and dead tissue without a normal architecture, mixed with numerous caseous substances, which confirmed the diagnosis of tuberculous pericarditis. This is a unique report of a patient who presented with tuberculous pericarditis with multiple solid masses in a large amount of pericardial effusion, without typical clinical manifestations of tuberculosis.

[Clinical and pathological characteristics of constrictive pericarditis in China].

OBJECTIVE: To summarize the clinical and pathological characteristics of constrictive pericarditis in China. METHOD: Data from 150 patients with constrictive pericarditis who admitted to our hospital from 2000 to 2007 were retrospectively analyzed. RESULTS: Constriction pericarditis was detected by echocardiography in 149 out of 150 patients. Pericardial effusion was evidenced in 59.3% patients (89/150). The diagnostic accuracy rate for identifying constrictive pericarditis by echocardiography (98.7%, 107/109) was comparable to that of surgical diagnosis (100%, 109/109). Tuberculosis was the main cause of constrictive pericarditis in this cohort (78.7%, 118/150) including 25 (16.7%) cases with pathological or etiological evidences of tubercular pericarditis, 8 (5.3%) cases with pathologically active tuberculous focus elsewhere in the body, 66 (44.0%) cases with typical clinical tuberculosis manifestation and responded to anti-tubercular therapy and 19 (12.7%) cases with a diagnosis of suspicious tuberculosis. Pericardiectomy was performed in 108 cases and pericardial biopsy and surgical drainage was performed in 1 patient. In hospital death rate was 8.7% (13/150, 4 tubercular patients and 9 non-tubercular). CONCLUSION: Tuberculosis is the leading cause of constrictive pericarditis in this cohort and the best diagnosis tool is echocardiography other than pathological and etiological findings in pericardium.

Characterization of the immunological features of tuberculous pericardial effusions in HIV positive and HIV negative patients in contrast with non-tuberculous effusions.

OBJECTIVE: To investigate the immunopathogenesis of pericardial tuberculosis (TB) and the influence of human immunodeficiency virus (HIV) on the anti-tuberculous immune response. DESIGN: Consecutive patients presenting with large pericardial effusions were subjected to a full clinical examination and pericardiocentesis. Aspirated fluid was sent for biochemistry, differential leukocyte count, flow cytometric analysis and determination of cytokine levels. Pericardial tissue was sent for TB culture and histopathological evaluation. Diagnoses were made according to pre-determined criteria. RESULTS: Fifty-six patients were included and divided into HIV positive TB (n = 22), HIV negative TB (n = 21) and non-tuberculous effusions (n = 13). Peripheral blood neutrophil, lymphocyte and monocyte counts were significantly lower in HIV positive TB patients. Lymphocytes were the dominant cell type in tuberculous pericardial effusions. CD4+ cells dominated in HIV negative tuberculous effusions, whereas CD8+ cells dominated in HIV positive TB. The difference in the concentration of IFN-gamma levels in the tuberculous and non-tuberculous pericardial effusions was statistically significant. Despite significant differences in pericardial CD4+ cell counts, IFN-gamma levels were similarly elevated in HIV negative and HIV positive tuberculous effusions. Highest levels of pericardial IL-10 were observed in samples associated with least tissue necrosis, suggesting the possibility of a tissue protective immunoregulatory role for IL-10. CONCLUSIONS: Tuberculous pericardial effusions result from a T helper1 (Th1)-dominant immune response. IFN-gamma producing CD4+ lymphocytes dominate in HIV negative patients, whereas CD8+ seem to play a more important role in HIV positive patients. Infection with HIV leads to the depletion of immunocompetent cells such as monocytes, NK cells and neutrophils.

Clinical characteristics and initial management of patients with tuberculous pericarditis in the HIV era: the Investigation of the Management of Pericarditis in Africa (IMPI Africa) registry.

BACKGROUND: The incidence of tuberculous pericarditis has increased in Africa as a result of the human immunodeficiency virus (HIV) epidemic. However, the effect of HIV co-infection on clinical features and prognosis in tuberculous pericarditis is not well characterised. We have used baseline data of the Investigation of the Management of Pericarditis in Africa (IMPI Africa) registry to assess the impact of HIV co-infection on clinical presentation, diagnostic evaluation, and treatment of patients with suspected tuberculous pericarditis in sub-Saharan Africa. METHODS: Consecutive adult patients in 15 hospitals in three countries in sub-Saharan Africa were recruited on commencement of treatment for tuberculous pericarditis, following informed consent. We recorded demographic, clinical, diagnostic and therapeutic information at baseline, and have used the chi-square test and analysis of variance to assess probabilities of significant differences (in these variables) between groups defined by HIV status. RESULTS: A total of 185 patients were enrolled from 01 March 2004 to 31 October 2004, 147 (79.5%) of whom had effusive, 28 (15.1%) effusive-constrictive, and 10 (5.4%) constrictive or acute dry pericarditis. Seventy-four (40%) had clinical features of HIV infection. Patients with clinical HIV disease were more likely to present with dyspnoea (odds ratio [OR] 3.2, 95% confidence interval [CI] 1.4 to 7.4, P = 0.005) and electrocardiographic features of myopericarditis (OR 2.8, 95% CI 1.1 to 6.9, P = 0.03). In addition to electrocardiographic features of myopericarditis, a positive HIV serological status was associated with greater cardiomegaly (OR 3.89, 95% CI 1.34 to 11.32, P = 0.01) and haemodynamic instability (OR 9.68, 95% CI 2.09 to 44.80, P = 0.0008). However, stage of pericardial disease at diagnosis and use of diagnostic tests were not related to clinical HIV status. Similar results were obtained for serological HIV status. Most patients were treated on clinical grounds, with microbiological evidence of tuberculosis obtained in only 13 (7.0%) patients. Adjunctive corticosteroids were used in 109 (58.9%) patients, with patients having clinical HIV disease less likely to be put on them (OR 0.37, 95% CI 0.20 to 0.68). Seven patients were on antiretroviral drugs. CONCLUSION: Patients with suspected tuberculous pericarditis and HIV infection in Africa have greater evidence of myopericarditis, dyspnoea, and haemodynamic instability. These findings, if confirmed in other studies, may suggest more intensive management of the cardiac disease is warranted in patients with HIV-associated pericardial disease.

Tuberculous constrictive pericarditis complicated with tuberculous mediastinitis - case report.

Constrictive pericarditis is a rare and severe disease. A 37-year-old patient was admitted in the hospital for dyspnea, precordial pain, right-sided cardiac failure. Chest X-ray showed cardiac enlargement and an opacity suggestive for pleural effusion. Echocardiography revealed an adhesive-effusive-constrictive pericarditis, a very thickened pericardium and bilateral pleural effusion. After a pericardiectomy done to restore cardiac compensation and to identify etiological factors, a tuberculous pericarditis (TBP) was diagnosed. After surgery and starting anti-TB treatment, the patient presented altered clinical status, dyspnea, dry cough, fever and delayed callus formation at sternum level. Thoracic scan revealed mediastinal air collections, pericarditis and pleurisy. Thus, the TBP diagnosis was extended to mediastinal TB and anti-TB therapy was continued. After four months of treatment, another thoracic scan showed disappearance of the mediastinal air-leakage bubbles, multiple new micronodules in both lungs and lymph nodes of up to 15 mm; also increasing pericardial and pleural effusions. This case was interpreted as a TB treatment failure situation. A retreatment regimen was started, resulting in a slow favorable outcome. Pericardial TB is a rare condition, usually with delayed diagnosis and poor treatment benefits. Whenever possible, earlier diagnostic can contribute to better management of these cases.

Tuberculous pericarditis.

Tuberculous pericarditis is a rare but dangerous disease with a mortality of 20% to 40%. Early diagnosis and institution of appropriate therapy are critical, and open pericardial biopsy appears to be the most reliable diagnostic tool. Corticosteroids, in conjunction with antituberculous medication, are effective in suppressing the early granulomatous inflammatory response. Pericardiectomy should be considered early when the response to a medical regimen is delayed or inadequate.

The Effects of Angiotensin Converting Enzyme Inhibitors (ACE-I) on Human N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) Levels: A Systematic Review and Meta-Analysis.

BACKGROUND: Tuberculous pericardial effusion is a pro-fibrotic condition that is complicated by constrictive pericarditis in 4% to 8% of cases. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a ubiquitous tetrapeptide with anti-fibrotic properties that is low in tuberculous pericardial effusion, thus providing a potential mechanism for the heightened fibrotic state. Angiotensin-converting enzyme inhibitors (ACE-I), which increase Ac-SDKP levels with anti-fibrotic effects in animal models, are candidate drugs for preventing constrictive pericarditis if they can be shown to have similar effects on Ac-SDKP and fibrosis in human tissues. OBJECTIVE: To systematically review the effects of ACE-Is on Ac-SDKP levels in human tissues. METHODS: We searched five electronic databases (1996 to 2014) and conference abstracts with no language restrictions. Two reviewers independently selected studies, extracted data and assessed methodological quality. The protocol was registered in PROSPERO. RESULTS: Four studies with a total of 206 participants met the inclusion criteria. Three studies (106 participants) assessed the change in plasma levels of Ac-SDKP following ACE-I administration in healthy humans. The administration of an ACE-I was associated with an increase in Ac-SDKP levels (mean difference (MD) 5.07 pmol/ml (95% confidence intervals (CI) 0.64 pmol/ml to 9.51 pmol/ml)). Two studies with 100 participants further assessed the change in Ac-SDKP level in humans with renal failure using ACE-I. The administration of an ACE-I was associated with a significant increase in Ac-SDKP levels (MD 8.94 pmol/ml; 95% CI 2.55 to 15.33; I2 = 44%). CONCLUSION: ACE-I increased Ac-SDKP levels in human plasma. These findings provide the rationale for testing the impact of ACE-I on Ac-SDKP levels and fibrosis in tuberculous pericarditis.

Broad clonal heterogeneity of antigen-specific CD4+ T-cells localizing at the site of disease during tuberculosis.

The repertoire of CD4+ T-lymphocytes was investigated in six patients affected by tuberculosis, who had a negative PPD skin test at diagnosis. Polyclonal CD4+ T-cell lines from the peripheral blood failed to proliferate to PPD and to the 16- or 38-kDa proteins of Mycobacterium tuberculosis, while CD4+ T-cell lines from the site of disease responded to PPD, and to the 16- and 38-kDa proteins, and derived epitopes in vitro. The repertoire of CD4+ T-cells accumulating at the site of disease was found to be widely heterogeneous as demonstrated by the finding that at least seven different peptides from the 16- and 38-kDa proteins were recognized by every patient. These results indicate that CD4+ T-cells localized at the site of disease in tuberculosis recognize a vast array of M. tuberculosis epitopes.

"Acute" granulomatous pericarditis. clinical and hemodynamic correlate.

Ten cases of acute constrictive pericarditis from southern Iran are presented. They differed from chronic constrictive pericarditis by the absence of ascutes and edema of the lower extremities, the presence of cardiomegaly on posteroanterior chest x-ray film, the lack of calcification of the pericardium on fluoroscopic examination, and the presence of sinus rhythm in all cases. If tuberculosis is the etiologic agent, early pericardiectomy should be considered. This is especially important in areas where close follow-up of patients is difficult or impossible, since all patients in this series ultimately developed clinically significant constriction.

Surgical pathology of the parietal pericardium: a study of 344 cases (1993-1999).

Among 344 cases with surgically resected parietal pericardium, ages ranged from 1 to 87 years (mean, 55), and 64% were male. Causes of pericardial disease included neoplastic (33%), idiopathic (30%), iatrogenic (23%), and others (14%). Pericardial constriction (Group 1) represented the largest group (143 cases, 76% male). Maximal pericardial thickness was 1-17 mm (mean, 4). Fibrotic thickening occurred in 96%. Chronic lymphoplasmacytic inflammation affected 73% (mild or moderate in 97%). Calcification was uncommon (gross in 28%, microscopic in 8%), and granulomas were rare (4%, none tubercular). Constriction was idiopathic in 49% and iatrogenic (postpericardiotomy or postirradiation) in 41%. Neoplasms and cysts (Group 2) represented the second largest group (96 cases). Among 43 cases with secondary pericardial involvement, carcinomas accounted for 53% and lymphomas 21%. Forty cases (Group 3) had pericardial effusions (75% chronic), which were idiopathic in 28% and postpericardiotomy in 23%. Thirty-three cases (Group 4) had acute or recurrent pericarditis clinically, which was idiopathic in 70%. Lastly, 32 cases (Group 5) had pericardial resection for conditions unrelated to primary pericardial disease. In conclusion, pericardial constriction tended to be nontubercular (100%), nongranulomatous (96%), idiopathic or iatrogenic (90%), and noncalcific (64%), and it could occur with normal pericardial thickness (4%). Because considerable overlap in the gross and microscopic features existed among cases with noncalcific pericardial constriction (Group 1), pericardial effusions (Group 3), and pericarditis (Group 4), clinical information was necessary to provide an accurate clinicopathologic interpretation.

Myocarditis and myocardial interstitial fibrosis in constrictive pericarditis--an extended pathological spectrum?

We performed endomyocardial biopsy in six patients with constrictive pericarditis, revealing the presence of myocarditis and myocardial interstitial fibrosis in all regardless of the endocardial thickening. These findings suggest that the presence of endomyocardial involvement in the setting of restrictive heart disease should not be deemed specific for endomyocardial fibrosis when the clinical evaluation suggests constrictive pericarditis.

Myocardial and endocardial involvement in tuberculous constrictive pericarditis: difficulty in biopsy distinction from endomyocardial fibrosis as a cause of restrictive heart disease.

Differentiation of constrictive pericarditis and endomyocardial fibrosis by the available diagnostic methods is difficult at present. With this in mind, we compared autopsy data in heart specimens from 8 patients of constrictive pericarditis of tuberculous origin and 6 patients with tropical endomyocardial fibrosis. Post-mortem endomyocardial biopsies were also performed from both the ventricles. Pericardial thickening and adhesions were present in all cases of constrictive pericarditis and in none of those with endomyocardial fibrosis. Interestingly, significant endocardial thickening was seen in four, and myonecrosis, lymphohistiocytic cellular infiltration and myofibrosis were observed in seven of the eight cases of constrictive pericarditis. This suggests that the tubercular insult to heart may result in involvement of all three layers with varying severity. The endomyocardial biopsy specimens from the affected areas revealed similar histopathological changes of endocardial thickening and focal myofibrosis with cellular infiltrates in patients with both constrictive pericarditis and endomyocardial fibrosis, making distinction of the two difficult. The hallmark of differentiation between these two clinical entities appears to be a diligent attempt at identification of the thickened pericardium.

Constrictive pericarditis: case presentation and a review of the literature.

Constrictive pericarditis (CP) is a relatively rare entity, the result of a thickened, scarred and often calcified pericardium, adherent to the heart and limiting diastolic ventricular filling. Some reported etiologies for CP include pericardial involvement from cardiac trauma (including surgery), mediastinal irradiation, tuberculosis and other infectious diseases, neoplasms and myocardial infarction. However, the majority of CP cases are idiopathic. This report presents three cases of postoperative, tuberculous and idiopathic CP, highlighting the clinical and pathological changes seen in CP, and a review of the literature.