AIM--to develop pathogenetic methods for the correction of dysregulated erythropoesis in coronary heart disease (CHD). 20 patients with myocardial Q-infarction and 52 ones with chronic CHD. 26 patients of the CHD group suffered anemia. Ten volunteers without signs of cardiovascular pathology served as controls. Characteristics of peripheral blood and iron metabolism, serum levels of inflammation markers and erythropoietin (EPO) were measured. In most CHD patients elevated levels of TNF-alpha inhibited hepatic synthesis of EPO. Low hepcidin production was associated with increased EPO levels and low iron content in blood. Anemia developing in CHD patients may cause not only inflammation but also depletion of iron reserves. Correction of dysregulated erythropoesis in coronary heart in CHD must be performed with due regard for the above mechanisms on an individual basis.