New data on the pathogenesis of chronic cor pulmonale were obtained. The reduction of pulmonary capillaries at the site of the tuberculosis process beyond this site was found to contribute much to the development of pulmonary artery hypertension. Irreversible injuries to the vessels are due to both the pneumosclerotic changes and the specific circulating immune complexes (CIC) effects. Acting on the peripheral veins (in Koch's test), CICs influence the central hemodynamics, decreasing circulating blood volume by 30-40% and reducing cardiac output, thus resulting in deficit of the blood inflow to the right compartments of the heart. In this case the atrium functions at a higher load, like a suction pump, thus leading to cardiac hypertrophy. Peripheral vasodilators (apressin, nitrong) combined with cardiac glycosides (digoxin), favorably influencing the central hemodynamics, are recommended for the prevention and treatment of chronic cor pulmonale.