PATHOGENETIC ROLE OF CYTOKINE ACTIVATION AND DISORDERS OF THE HEMOSTASIS SYSTEM IN THE DEVELOPMENT OF HEART FAILURE IN PATIENTS WITH ARTERIAL HYPERTENSION

Abstract

The concept of chronic heart failure (CHF) has today shifted from a model of normal heart function to a multi-organ
disorder. This disorder affects not only the cardiovascular system, but also the musculoskeletal, renal, neuroendocrine and immune systems. Thus, it appears that the activation of neurohormones and proinflamatory cytokines in the progression of CHF leads to both heart damage and mutations in the genetic program. Increased SAS activity in patients with CHF against the background of arterial hypertension is a key "trigger" for the activation of the cytokine system. The association of the immune inflammatory response with activated SAS suggests that the use of β-blockers in this group of patients is theoretically justified.
The use of β-blockers in patients with CHF leads to a decrease in the amount of cytokines. As can be seen, the use of β-blockers in this group of patients may be considered pathogenetically correct because the activation of SAS is closely related to the immunological inflammatory response.
Carvedilol, one of the β-blockers in patients with CHF, modulates the activation of the cytokine system. The use of ACE inhibitors, β-blockers and statins in the treatment program has a significant effect.