Vascular and endocardial endothelial dysfunction in heart failure

Heart failure is defined as a clinical syndrome due to disorders in the structure or function of the heart that prevents it from meeting the needs of the organism for the oxygen necessary for the balanced metabolism of all tissues. In the pathogenesis of cardiac insufficiency, the activation and dysfunction of the endocardial and vascular endothelium are significant. Activation and endothelial dysfunction are followed by functional changes, including changes in auto- and paracrine signaling, in the distribution and number of receptors, anti-inflammatory, and anticoagulant features. It is considered that endothelial dysfunction occurred when the expected vasodilatation mediated by nitric oxide of endothelial origin in response to acetylcholine, bradykinin, P and/or serotonin does not appear. The endothelin-1 endotin-1 endocrine endothelial capillary as well as in cardiomyocytes has an increased heart rate. Neuregulin-1 plays a role in the proliferation, differentiation, and preservation of the cardiomyocyte function. The effects were mediated through a set of tyrosine kinases of receptors ErbB2, ErbB3, and ErbB4. Patients with metastatic tumor of breast cancer who received anti-ErbB2 monoclonal antibodies, the drug trastuzumab alone or in combination with anthracyclines were more likely to have cardiac insufficiency and systolic dysfunction of the chamber. The effects were mediated through a set of tyrosine kinases of ligand-dependent receptors ErbB2, ErbB3, and ErbB4. Coronary vascular endothelial dysfunction leads to coronary vasoconstriction, proliferation and remodeling of smooth muscle cells, an increase in lipid deposits in the wall of blood vessel, and possible coronary thrombosis. These processes damage_ coronary arteries, exacerbate myocardial perfusion and indirectly contribute to progressive heart failure and ischemic myocardiopathy. Dysfunction and lesion of the endocardial endothelium are always associated with strong changes in the mechanical performance of the myocardium. Endothelial dysfunction is an early occurrence that leads to the progression of heart failure. With moderate pressure loads in case of left ventricular hypertrophy, ventricular relaxation was completely suppressed due to the absence of endothelial NO release. Protection of coronary endothelium from oxidative stress is improved by bioavailability of NO. This significantly improves the relaxant response of the chamber to endogenous NO, inhibits the development of left ventricular hypertrophy and cardiac insufficiency.