Heart failure is a complex clinical syndrome that is a serious stage of various heart diseases, with high morbidity, high hospitalization rates and mortality. Heart failure is a symptomatic disease. The specific symptoms are difficulty breathing and fatigue, often accompanied by specific signs - fluid retention, and heart failure is also a progressive process. Initial myocardial damage causes hemodynamic abnormalities (preload, afterload, and abnormal myocardial contractility affect the heart's work). Improvement of hemodynamic parameters can significantly reduce symptoms, but is not beneficial for the progression of heart failure, long-term prognosis and mortality. It has gradually become clear that the basic mechanism leading to the occurrence and development of heart failure is ventricular remodeling, which is characterized by hypertrophy of cardiomyocytes, apoptosis, re-expression of embryonic genes and proteins, and changes in the quality and composition of extracellular bases. Clinical manifestations are: myocardial mass, increased ventricular volume, and changes in ventricular shape. After initial myocardial injury, a variety of endogenous neuroendocrine and cytokines are activated, including norepinephrine, angiotensin II, aldosterone, vasopressin, endothelin, and tumor necrosis factor. In heart failure, these factors increase in circulation and tissue. Long-term, chronic activation of the neuroendocrine cytokine system can promote myocardial remodeling, aggravate myocardial damage and functional deterioration, and further activate neuroendocrine cytokines, forming a vicious circle. Therefore, blocking the neuroendocrine system, blocking myocardial remodeling has become a key link in the treatment of heart failure, and more and more attention has been paid, and new treatment ideas and related drugs have emerged.
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Amino compound
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