ALTERATIONS IN THE PERIPHERAL CIRCULATION IN HEART FAILURE: CURRENT VIEW ON ENDOTHELIAL DYSFUNCTION AND PHARMACOLOGICAL IMPLICATIONS INVOLVING ITS PATHOPHYSIOLOGICAL ASPECTS

Abstract

Introduction. Despite the significant advances in the pharmacotherapy of cardiovascular diseases, the increasing prevalence of heart failure (HF) and its poor prognosis constitute one of the leading medical problems worldwide. The complex pathophysiology of HF involves the alterations in the peripheral circulation, particularly the development of endothelial dysfunction (ED). The deepening of understanding the pathology of ED and the spectrum of pharmacological implications, involving its certain pathophysiological aspects, could favor the optimization of the personalized approach to the management of such challenging HF patients. Aim: to provide a literature review of the current data on the alterations in peripheral circulation in HF with the focus on ED, and to outline possible pharmacological implications involving certain pathophysiological aspects of ED in HF patients. Material and methods. The thematic scientific papers, published predominantly during the last decade, constituted the study material. The research methodology involved bibliosemantic method and structural and logical analysis. Results and discussion. Currently, the ED considered as a stage of a specific continuum, which is initiated in the form of «activation» of the endothelium, and moves through the stage of its actual «dysfunction» to the stage of endothelial «damage». Taking into account the important pathogenetic and prognostic significance of ED in HF, the endothelium is considered as a target of various pharmacological influences, including renin-angiotensin-aldosterone inhibitors and statins. Among the modern approaches to pharmacological treatment of HF, the correction of reduced nitric oxide (NO) bioavailability by modulating the «NO-soluble guanylate cyclase-cyclic guanosine monophosphate» signaling pathway is a perspective option in terms of preventing the occurrence and progression of ED. Conclusion. The deepening of knowledge about the pathophysiological features of ED in HF allows both to improve the understanding of the pharmacodynamic effects of already approved cardiovascular drugs, and to outline the perspectives for pharmacological direct or indirect impact on endothelium.