Heart Failure

Heart failure means the heart fails to pump sufficient blood for the body's demands — it does not mean the heart has stopped. In the reduced-ejection-fraction form, the weakened left ventricle pumps out a smaller fraction of its contents with each beat; in the preserved form, the stiffened ventricle fills poorly despite a normal ejection fraction. Either way, pressure backs up: fluid accumulates in the lungs causing breathlessness on exertion, lying flat or at night, and in the legs causing ankle swelling, while fatigue reflects under-supplied muscles. Coronary artery disease and previous heart attacks are the leading cause, followed by long-standing hypertension, valve disease, diabetes, atrial fibrillation and, less commonly, alcohol, chemotherapy and viral myocarditis. Treatment has been transformed: the four-pillar drug regimen — an ARNI or ACE inhibitor, a beta-blocker, an MRA and an SGLT2 inhibitor — each independently reduces death and hospitalisation in reduced-ejection-fraction disease, and cardiac devices help selected patients. Daily weight monitoring catches fluid retention days before symptoms. Salt and fluid discipline, vaccination, and cardiac rehabilitation complete the picture. Supplements must be handled carefully in heart failure; several common ones interact with its medications.

• •Breathlessness on exertion, then at rest as disease progresses
• •Needing extra pillows to breathe at night, or waking gasping (orthopnoea and paroxysmal nocturnal dyspnoea)
• •Ankle, leg and abdominal swelling from fluid retention
• •Rapid weight gain over days from fluid — a key monitoring signal
• •Fatigue and reduced exercise capacity
• •Persistent cough, worse lying down
• •Palpitations where atrial fibrillation coexists
• •Poor appetite and nausea from gut congestion in advanced disease

• •Coronary artery disease and previous heart attacks — the leading cause
• •Long-standing hypertension
• •Heart valve disease
• •Diabetes and metabolic disease
• •Atrial fibrillation and other persistent arrhythmias
• •Cardiomyopathy: genetic, viral, alcohol-related or peripartum
• •Chemotherapy agents, particularly anthracyclines
• •Chronic kidney disease and anaemia as amplifiers
• •Sleep apnoea contributing to progression
• •Thyroid disease

The failing heart triggers compensatory systems that become part of the disease: the renin-angiotensin and sympathetic systems retain salt and water and constrict vessels, maintaining pressure short-term while overloading the ventricle long-term. The modern drug pillars work by blocking these compensations. Structural damage from infarction, pressure overload from hypertension, volume overload from leaking valves and direct toxicity from alcohol or chemotherapy each initiate the same final pathway of remodelling and decline.