The Influence of Basic Therapy and New Drugs on NO-Dependent Mechanisms of Cardiac Destruction in Chronic Heart Failure

Abstract

Chronic heart failure (CHF) remains a leading cause of global mortality, characterized by profound molecular and biochemical disturbances, including nitric oxide (NO) system dysfunction, mitochondrial impairment, and oxidative stress. While standard therapies such as ACE inhibitors, SGLT2 inhibitors, and beta-blockers address clinical symptoms, their capacity to interrupt the underlying biochemical mechanisms of cardiomyopathy is often limited. This review examines the pathophysiological role of impaired NO production and reactive oxygen species (ROS) accumulation in exacerbating myocardial contractile dysfunction and disease progression. Special focus is directed toward the development of next-generation β1-blockers with multifunctional properties, including antioxidant, NO-mimetic, and antiapoptotic effects. Evidence suggests that the novel compound Hypertril (1-(β-phenylethyl)-4-amino-1,2,4-triazolium bromide) exhibits significant cardioprotective potential. Experimental data indicate that Hypertril improves eNOS/iNOS expression and enhances NO bioavailability more effectively than conventional β-blockers, leading to stabilized ECG parameters and restored energy metabolism. These findings underscore the clinical relevance of developing NO-mimetic agents to optimize the pharmacological management of CHF.