What is heart failure?

Heart failure is a condition in which the heart cannot pump blood as well as the body needs. The classic features are shortness of breath (especially with exertion or when lying flat), fatigue, swelling in the legs or abdomen, and reduced exercise tolerance. Heart failure is one of the most common reasons for hospitalisation in older adults.

The two main types. Heart failure with reduced ejection fraction (HFrEF) means the heart's pumping chamber is not squeezing out enough blood with each beat (ejection fraction below about 40%). Heart failure with preserved ejection fraction (HFpEF) means the heart pumps normally but does not relax and fill properly. The two have somewhat different therapy approaches, though some medicines now help in both.

The four-pillar foundation for HFrEF. Modern HFrEF therapy is built around four foundational classes of medicines, started early and up-titrated to target dose.

Angiotensin receptor-neprilysin inhibitor (sacubitril/valsartan) or, alternatively, an ACE inhibitor or ARB: these block hormones that constrict blood vessels and harm the heart over time.

Evidence-based beta-blocker (carvedilol, metoprolol succinate, bisoprolol): slows the heart rate and improves long-term function.

Mineralocorticoid receptor antagonist (spironolactone, eplerenone): blocks aldosterone signalling that contributes to fluid retention and harmful heart remodelling.

SGLT2 inhibitor (dapagliflozin, empagliflozin): originally developed for diabetes but with substantial heart failure benefits independent of diabetes.

Other medicines and devices. Vericiguat is an additional class for high-risk patients despite optimised foundational therapy. Hydralazine plus isosorbide dinitrate is used in selected populations. Implantable cardioverter-defibrillators and cardiac resynchronisation therapy are devices used in eligible patients. Several procedural options exist for specific situations.

The genetic dimension. A growing fraction of heart failure has identifiable inherited contributors, particularly in younger patients and those with a family history. Genetic testing is increasingly used to identify the underlying cause; for some inherited cardiomyopathies, mechanism-targeted therapy is in late-stage trials.

What to expect. Heart failure has been transformed by modern therapy. Patients on appropriate four-pillar therapy live substantially longer with better symptom control than was possible 15 years ago. The next several years are likely to add additional mechanism-targeted options, particularly for inherited cardiomyopathy and for refractory disease.