Heart failure is a chronic condition in which the heart cannot pump enough blood to meet the body’s needs. It can result from damage to the heart muscle, long standing high blood pressure, coronary artery disease, valve problems or genetic disorders. Researchers distinguish between heart failure with reduced ejection fraction, where the pumping ability is weakened, and preserved ejection fraction, where the heart becomes stiff and cannot fill properly. This distinction is crucial because the underlying biology and treatment responses differ.

Modern research shows that chronic neurohormonal activation is central. Systems such as the renin angiotensin aldosterone system and the sympathetic nervous system initially compensate for impaired pumping but eventually drive fluid retention, vascular constriction, fibrosis and further damage. Inflammation, oxidative stress and changes in cardiac metabolism also contribute, along with remodeling of the heart’s structure and electrical properties.

Diagnosis relies on clinical signs such as breathlessness, fatigue and swelling, supported by imaging, natriuretic peptide measurements and assessment of ejection fraction. Management has shifted from symptom control to targeting the disease mechanisms. Standard therapies now include ACE inhibitors or angiotensin receptor blockers, beta blockers, mineralocorticoid receptor antagonists and, more recently, angiotensin receptor neprilysin inhibitors and SGLT2 inhibitors. These treatments reduce mortality and hospitalizations by interrupting harmful neurohormonal pathways and improving cardiac efficiency.

Non drug approaches such as cardiac resynchronization therapy, implantable defibrillators, ventricular assist devices and lifestyle measures complement medication. Ongoing research explores gene based interventions, novel metabolic modulators and anti inflammatory strategies, aiming to personalize treatment and slow or reverse the progression of heart failure.