Byulleten Nauki I Praktiki · 2026
The role of endothelial dysfunction in the development of chronic heart failure in the elderly
By Tsoy L. G., Sabirov I. S., Khasanova Sh. Sh. et al.
Chronic heart failure (CHF) is currently a significant global health problem, particularly in industrialized countries. CHF has a high prevalence (estimated at 1% to 2% in the general population, particularly among the elderly), affecting over 64 million people worldwide and associated with high morbidity and mortality rates. CHF is closely linked to endothelial dysfunction, which significantly contributes to its progression. Among the mechanisms identified in the pathogenesis of heart failure, endothelial dysfunction, characterized by disruption of the normal functioning of the endothelium, which plays a key role in vascular homeostasis, is receiving increasing attention. Endothelial dysfunction in CHF is characterized by decreased nitric oxide bioavailability, increased oxidative stress, and a proinflammatory, prothrombotic phenotype, which collectively impair vascular function. It also impairs the endothelium's ability to regulate vascular tone, maintain fluid balance, and control inflammation. This disruption also affects vascular repair and regeneration processes, which exacerbates endothelial damage. Age-related endothelial dysfunction, most often indicated by impaired endothelium-dependent vasodilation, is mediated by decreased nitric oxide bioavailability and decreased sensitivity to vasodilatory prostaglandins secreted by the endothelium. Oxidative stress and inflammation are the primary macromechanisms by which aging leads to decreased nitric oxide bioavailability and endothelium-dependent vasodilation. Vascular oxidative stress develops with age as a result of increased production of reactive oxygen species, such as superoxide anion, against the background of unchanged or reduced antioxidant defenses. This is due to the oxidation of tetrahydrobiopterin, a cofactor of endothelial nitric oxide synthase necessary for nitric oxide synthesis. This leads to uncoupling of endothelial nitric oxide synthase and the production of superoxide anion rather than nitric oxide. Increased levels of the endothelial vasoconstrictor molecule endothelin-1 also contribute to the impairment of endothelium-dependent vasodilation with age.