Heart failure is a chronic condition in which the heart cannot pump enough blood to meet the body’s needs. It often develops after damage from heart attacks, long standing high blood pressure, or diseases of the heart muscle and valves. The condition is common, especially in older adults, and its prevalence is increasing as populations age and survive longer with cardiovascular disease.

Researchers distinguish between heart failure with reduced ejection fraction, where the left ventricle’s pumping ability is weakened, and heart failure with preserved ejection fraction, where the heart’s squeezing appears normal but relaxation and filling are impaired. These forms differ in underlying biology, risk factors, and treatment response.

At the molecular level, heart failure involves structural remodeling of heart muscle, activation of stress hormones such as the renin angiotensin aldosterone and sympathetic nervous systems, inflammation, and changes in energy metabolism. These processes initially compensate for injury but ultimately worsen damage and symptoms such as breathlessness, fatigue, and fluid retention.

Modern treatment targets these pathways. Standard therapies include ACE inhibitors or angiotensin receptor blockers, beta blockers, mineralocorticoid receptor antagonists, and more recently angiotensin receptor neprilysin inhibitors and SGLT2 inhibitors. These drugs reduce hospitalizations and improve survival in many patients with reduced ejection fraction. Device therapies such as implantable defibrillators and cardiac resynchronization can further reduce risk in selected cases.

However, outcomes for heart failure with preserved ejection fraction remain poor, with fewer proven therapies. Ongoing research focuses on better phenotyping of patients, understanding fibrosis and microvascular dysfunction, and developing targeted drugs and personalized treatment strategies. Prevention through control of blood pressure, diabetes, obesity, and coronary disease remains crucial.