Heart failure (heart failure) is a result of initial myocardial injury from any cause (e.g., myocardial infarction, cardiomyopathy, hemodynamic overload, inflammation, etc.) causing structural and functional changes in the myocardium, culminating in ventricular pumping and/or filling hypoperfusion. The main manifestations are dyspnea and weakness leading to decreased exercise tolerance, as well as fluid retention leading to pulmonary stasis and peripheral edema [1]. Heart failure manifests itself on the one hand by reduced forward ejection leading to tissue and organ ischemia and hypoxia, and on the other hand by posterior stasis leading to pulmonary or body circulation stasis and edema, in parallel with activation of the neuroendocrine system, clinically manifested by activation of the sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS) and cytokines, compensating for decreased cardiac function and insufficient cardiac ejection. At the same time, the secretion of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) increases due to increased left ventricular end-diastolic pressure, which plays a role in the regulation of peripheral resistance and volume load. The results of a random sample of 15,518 urban and rural residents aged 35-74 years in China: the prevalence of heart failure was 0.9%, and there were about 4 million patients with heart failure according to calculation, of which 0.7% were men and 1.0% were women, and women were higher than men (P