**6.2 Treatment**

*Inflammatory Heart Diseases*

strictive pericarditis [23].

**5. Treatment**

thoracotomy.

decreasing tolerance [26].

**6. Constrictive pericarditis**

specificity of 100% for the diagnosis of TB [21].

HIV-positive and HIV-negative patients are needed [28].

response to pharmacological treatment.

culture medium, resulting in a 75% yield, compared with a 53% yield with conventional culture [18]. Pericardial biopsy specimens may also be used to diagnose tuberculous pericarditis. The polymerase chain reaction (PCR) has also been suggested for detecting *M. tuberculosis* DNA in pericardial fluid [19]. The probability of obtaining a definitive bacteriological result is greatest when pericardial fluid and

The difficulty of carrying out the diagnosis of tuberculous pericarditis, associated with its high mortality without proper treatment, has led to the use of indirect methods. Indirect methods such as dosing activity of adenosine deaminase (ADA) in the pericardial fluid, with cut-off levels between 30 and 60 U/L of ADA activity, are suggestive of tuberculous pericarditis [20]. In areas of the high endemic level of tuberculosis, a cut-off level of ADA activity <35 presents a sensitivity of 90% and a specificity of 74% for diagnosis [21]. The utility of ADA activity in pericardial fluid was also demonstrated in HIV-positive patients, although in patients with severe

Very high levels of ADA in pericardial fluid have strong association with con-

The measurement of interferon gamma (IFN-γ) levels in the pericardial fluid also helps early diagnosis. Cut-off values >200 pg/L have a sensitivity of 92% and

Pharmacological treatment increases survival in tuberculous pericarditis, even in HIV-positive patients [24]. A regimen that includes rifampicin, isoniazid, pyrazinamide, and ethambutol for at least 2 months, followed by rifampicin and isoniazid (up to 6 months), proved to be effective in extrapulmonary tuberculosis [25]. Treatments beyond 6 months do not show better results, increasing cost and

The treatment associated with corticosteroids would not be justified at present, given that the evidence for its use is not the best [27]. Although the results are inconclusive, adding corticosteroids to treatment may have benefits on morbidity and re-experiences, but randomized controlled trials with sufficient numbers of

It is obvious that if pericarditis is associated with severe pericardial effusion, with hemodynamic compromise, the first treatment option associated with antituberculous treatment is drainage by subxiphoid puncture or by minimal

It is the most feared complication of tuberculous pericarditis; it is described in about 30% of patients, even in spite of antituberculous treatment and the use of

In summary, the "definitive" diagnosis of tuberculous pericarditis is based on the presence of the tubercle bacillus in the pericardial fluid or proving it in the pericardium biopsy and "probably" when there is evidence of tuberculosis elsewhere in the body and the presence of unexplained pericarditis, with high levels of ADA or good

biopsy specimens are examined early in the effusive stage [18].

**4.3 Indirect methods for the diagnosis of tuberculous pericarditis**

CD4 lymphocyte depletion, the ADA levels observed are lower [22].

**34**

The treatment must include antituberculous medication for 6 months. Consider pericardiectomy in all patients once antibiotic treatment has been instituted [32]. Surgery should be performed early if the patient presents hemodynamic deterioration (despite antituberculous treatment) [33] or if they present pericardial calcifications, which are markers of chronicity of the disease [34].
