The widespread of ferrum deficiency in the population of age-related patients significantly worsens the distance prognosis of major cardiovascular diseases and requires timely diagnosis and correction. The currently accepted routine approach to the diagnosis of latent and apparent ferrum deficiency does not correlate with tissue metabolic changes in cardiomyocytes and needs to be revised. The process of the aggravating effect of anemic syndrome on the course of somatic pathology, including at the tissue level, continue to be actively researched.Many experimental researches have confirmed that in order to verify ferrum deficiency in cardiomyocytes, in addition to ferritin and ferrum levels in blood serum, it is necessary to calculate the transferrin saturation coefficient with ferrum, assess the level of soluble transferrin receptors and determine the level of hepcidin.