Advances in research on the central mechanism of heart failure

Heart failure is a complex clinical syndrome, and impaired filling or ejection disorders result from any ventricular structure or dysfunction can cause heart failure. The prevalence of heart failure in adult populations in developed countries has reached 1% to 2%, while the prevalence in elderly people over 70 years of age has increased to ≥10%. With the population aging and the prevalence of coronary heart disease increased, the prevalence of heart failure has increased, becoming a disable and fatal disease. The changes of the central nervous system hormones such as renin-angiotensin system (RAS), inflammatory cytokines (proinflammatory cytokines, PIC), and reactive oxygen species (ROS) may be closely related to increased central activity in heart failure, which can significantly alter the activities of peripheral sympathetic nerves. Constant sympathetic nervous activity is an important cause of development of heart failure, so reducing the sympathetic excitability of heart failure is regarded as one of the focuses of treatment and research. This paper focuses on the influence of central neurohormone on heart failure and possible central mechanism.