What is the main principle behind heart failure with reduced ejection fraction (HFrEF)?

Heart failure with reduced ejection fraction (HFrEF) primarily involves the phenomenon of neurohormonal activation. In this condition, the heart's ability to pump blood effectively is compromised, leading to a decrease in cardiac output. As a compensatory mechanism, the body activates various neurohormonal pathways, primarily the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system.

When the heart fails, it triggers a series of hormonal responses aimed at preserving perfusion to vital organs. This neurohormonal activation results in vasoconstriction, increased blood volume, and elevated heart rate, which can initially help maintain blood flow. However, over time, these compensatory mechanisms can lead to adverse effects, such as fluid retention, increased afterload, and further cardiac remodeling, ultimately exacerbating heart failure.

The focus on neurohormonal activation underscores the importance of managing these compensatory responses in HFrEF to alleviate symptoms and improve long-term outcomes. Treatment strategies often target this activation, using medications such as ACE inhibitors, beta-blockers, and diuretics to counteract the negative effects of excess neurohormonal stimulation.