Tuberculous pericarditis develops either via hematogenous or lymphangeal spread, or directly from pulmonary lesions. Tuberculous pericarditis begins with fibrin deposits, granuloma formation, and the presence of live acid-fast bacilli. A pericardial effusion, which is serous but often contains some blood with a high level of protein. Recently, PCR technology has been employed to amplify M. Tuberculosis DNA from pericardial fluid. The elevation of ADA (> 45 U/l) is supportive of the diagnosis. Tuberculous pericarditis is detected clinically either in the effusive stage by nonspecific systemic syndrome or after the development of constrictive pericarditis. The short-course treatment of tuberculous pericarditis should consist of three-drug regimen, such as INH, RFP, PZA, SM, EB. The use of prednisolone is controversial. Tuberculous myocarditis is extremely rare because of low affinity between M. Tuberculosis and myocardium. Most cases of tuberculous pericarditis are clinically silent and diagnosed at autopsy.