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Definitive diagnosis of tuberculous pericarditis requires isolation of the tubercle bacillus from pericardial fluid, but isolating the organism is often difficult.To improve diagnostic efficiency for tuberculous pericarditis, using available tests.Prospective observational study.Consecutive patients (n = 233) presenting with pericardial effusions underwent a predetermined diagnostic work-up. This included (i) clinical examination; (ii) pericardial fluid tests: biochemistry, microbiology, cytology, differential white blood cell (WBC) count, gamma interferon (IFN-gamma), adenosine deaminase (ADA) levels, polymerase chain reaction testing for Mycobacterium tuberculosis; (iii) HIV; (iv) sputum smear and culture; (v) blood biochemistry; and (vi) differential WBC count. A model was developed using 'classification and regression tree' analysis. The cut-off for the total diagnostic index (DI) was optimized using receiver operating characteristic (ROC) curves.Fever, night sweats, weight loss, serum globulin (40 g/l) and peripheral blood leukocyte count (10 x 10(9)/l) were independently predictive. The derived prediction model had 86% sensitivity and 84% specificity when applied to the study population. Pericardial fluid IFN-gammaor=50 pg/ml, concentration had 92% sensitivity, 100% specificity and a positive predictive value (PPV) of 100% for the diagnosis of tuberculous pericarditis; pericardial fluid ADAor=40 U/l had 87% sensitivity and 89% specificity. A diagnostic model including pericardial ADA, lymphocyte/neutrophil ratio, peripheral leukocyte count and HIV status had 96% sensitivity and 97% specificity; substituting pericardial IFN-gamma for ADA yielded 98% sensitivity and 100% specificity.Basic clinical and laboratory features can aid the diagnosis of tuberculous pericarditis. If available, pericardial IFN-gamma is the most useful diagnostic test. Otherwise we propose a prediction model that incorporates pericardial ADA and differential WBC counts.

Traditional diagnostic tests for pericardial tuberculosis (TB) are insensitive and often require long culture periods, and this has led to more emphasis being placed on biochemical tests such as the pericardial adenosine deaminase (ADA) test. However, controversy exists as to its diagnostic utility. In addition, the use of interferon (IFN)-gamma, which is a reliable indicator of pleural and peritoneal TB, has not been explored in pericardial effusions. We investigated ADA and IFN-gamma levels in pericardial effusions of different etiologies.A prospective study was carried out from February 1995 to February 1998 at Tygerberg Hospital (South Africa), with pericardial taps being performed under echocardiographic guidance. During this period, 110 consecutive patients presenting with large pericardial effusions were included in the study. Diagnoses were made according to predetermined criteria, and they included TB (n = 64), malignancy (n = 12), nontuberculous infections (n = 5), other effusions (n = 19), and effusions of uncertain origin (n = 10). The median ADA level in the tuberculous group was 71.7 U/L (range, 10.3 to 303.6 U/L), which was significantly higher than that in any other group (p0.05). With a cutoff level for ADA activity of 30 U/L, sensitivity was 94%, specificity was 68%, and positive predictive value was 80%. IFN-gamma levels were determined in 30 subjects. The median IFN-gamma concentration in the tuberculous group was1,000 pg/L, which was significantly higher than in any other diagnostic group (p0.0005). A cutoff value of 200 pg/L for IFN-gamma resulted in a sensitivity and specificity of 100% for the diagnosis of pericardial TB.Pericardial fluid levels of ADA and IFN-gamma are useful in the diagnosis of tuberculous pericarditis.

Study objectives: To determine the biochemical characteristics of large pericardial effusions in various disease states, and to assess their utility as diagnostic tools. Setting: An academic university hospital in the Western Cape, South Africa. Design: Consecutive, prospective case series. Patients: One hundred ten hospital patients > 12 years old, who presented to the echocardiography department with large pericardial effusions, and 12 control subjects who underwent open-heart surgery (coronary artery bypass graft or aortic valve replacement). Measurements: Fluid was sent for examination of biochemistry, adenosine deaminase, microbiology, hematology, and cytology. The etiology of each pericardial fluid sample was established using predetermined criteria. Results: The biochemistry of pericardial exudates differed significantly from pericardial transudates. Light’s criteria (whereby an exudate is defined as having one or more of the following: pleural fluid/serum protein ratio > 0.5; pleural fluid/serum lactate dehydrogenase [LDH] ratio > 0.6; and/or pleural fluid LDH level > 200 U/L) were applied to pericardial fluids and demonstrated to be the most reliable diagnostic tool for identifying pericardial exudates. The corresponding sensitivity was 98%. Conclusion: Although laboratory tests are a useful guideline when assessing the etiology and pathophysiology of pericardial effusions, the majority of large, clinically significant pericardial effusions result from exudative causes. (CHEST 2002; 121:495– 499)

Background Effusive-constrictive pericarditis (ECP) is traditionally diagnosed by using the expensive and invasive technique of direct pressure measurements in the pericardial space and the right atrium. The aim of this study was to assess the diagnostic role of echocardiography in tuberculous ECP. Methods Intrapericardial and right atrial pressures were measured pre- and post-pericardiocentesis, and right ventricular and left ventricular pressures were measured post-pericardiocentesis in patients with tuberculous pericardial effusions. Echocardiography was performed post-pericardiocentesis. Traditional, pressure-based diagnostic criteria were compared with post-pericardiocentesis systolic discordance and echocardiographic evidence of constriction. Results Thirty-two patients with tuberculous pericardial disease were included. Sixteen had ventricular discordance (invasively measured), 16 had ECP as measured by intrapericardial and right atrial invasive pressure measurements and 17 had ECP determined echocardiographically. The sensitivity and specificity of pressure-guided measurements (compared with discordance) for the diagnosis of ECP were both 56%. The positive and negative predictive values were both 56%. The sensitivity of echocardiography (compared with discordance) for the diagnosis of ECP was 81% and the specificity 75%, while the positive and the negative predictive values were 76% and 80%, respectively. Conclusion Echocardiography shows a better diagnostic performance than invasive, pressure-based measurements for the diagnosis of ECP when both these techniques are compared with the gold standard of invasively measured systolic discordance.

Aims : To establish the influence of human immunodeficiency virus (HIV) infection on the histopathological features of patients presenting with tuberculous pericarditis. Methods and results : A prospective study was carried out at Tygerberg Academic Hospital, South Africa; 36 patients with large pericardial effusions had open pericardial biopsies under general anaesthesia and were included in the study. Patients underwent pericardiocentesis, followed by daily intermittent catheter drainage; a comprehensive diagnostic work-up (including histopathology of the pericardial tissue) was also performed. Histological tuberculous pericarditis was diagnosed according to predetermined criteria. Tuberculous pericarditis was identified in 25 patients, five of whom were HIV+. The presence of granulomatous inflammation (with or without necrosis) and/or Ziehl–Neelsen positivity yielded the best test results (sensitivity 64%, specificity 100% and diagnostic efficiency 75%). Conclusions : Co-infection with HIV impacts on the histopathological features of pericardial tuberculosis and leads to a decrease in the sensitivity of the test. In areas which have a high prevalence of tuberculosis, the combination of a sensitive test such as adenosine deaminase, chest X-ray and clinical features has a higher diagnostic efficiency than pericardial biopsy in diagnosing tuberculous pericarditis.

The aim of this study was to describe the clinical, echocardiographic and laboratory characteristics of large pericardial effusions and cardiac tamponade secondary to systemic lupus erythematosus (SLE). An ongoing prospective study was conducted at Tygerberg Academic Hospital, South Africa between 1996 and 2002. All patients older than 13 years presenting with large pericardial effusions (.10 mm) requiring pericardiocentesis were included. Eight cases (out of 258) were diagnosed with SLE. The mean (SD) age was 29.5 (10.7) years. Common clinical features were Raynaud’s phenomenon, arthralgia and lupus nephritis class III/IV. Echocardiography showed Libman-Sacks endocarditis (LSE) in all the mitral valves. Two patients developed transient left ventricular dysfunction; both these patients had pancarditis. Typical serological findings included antinuclear antibodies, anti-double stranded DNA antibodies, low complement C4 levels and low C3 levels. CRP was elevated in six cases. Treatment consisted of oral steroids and complete drainage of the pericardial effusions. No repeat pericardial effusions or constrictive pericarditis developed amongst the survivors (3.1 years follow up). This study concludes that large pericardial effusions due to SLE are rare, and associated with nephritis, LSE and myocardial dysfunction. Treatment with steroids and complete drainage is associated with a good cardiac outcome.

The pregnancy outcome of 59 pregnancies in 38 women with prosthetic heart valves, managed at a tertiary referral centre from 1989-98 were reviewed. Ten women underwent valve replacement during pregnancy. The main outcome measures were major maternal complications and perinatal outcome. The maternal mortality rate for pregnancies following valve replacement surgery was 6.1%, with a 21% pregnancy loss before viability and a perinatal loss of 8%. Major morbidity in this group was as follows: haemorrhage 29.8%, cardiac failure 12.8%, thromboembolism 8.5%, infective endocarditis 6.4% and valve thrombosis 4.3%. No maternal mortality occurred among those who underwent valve replacement during pregnancy but their perinatal loss was 25%. We conclude that although maternal mortality and morbidity rates in women with prosthetic heart valves who became pregnant were high, the perinatal outcome was good except for women who underwent valve replacement during pregnancy who experienced a high perinatal loss rate.