Heart Failure
Heart failure is a clinical syndrome in which the heart cannot pump or fill with blood well enough to meet the body's metabolic demands at normal filling pressures, producing symptoms such as breathlessness, fatigue, and fluid retention. It is the common end-point of many cardiac diseases rather than a single disease, and it is conventionally classified by left ventricular ejection fraction and by acuity.
Definition
Heart failure is a syndrome caused by a structural or functional cardiac abnormality, resulting in reduced cardiac output and/or elevated intracardiac pressures, and characterised by typical symptoms and signs of congestion and/or hypoperfusion.
Scope
This area orients the reader to heart failure as a syndrome and links to its principal topics: systolic (reduced ejection fraction) and diastolic (preserved ejection fraction) phenotypes, acute decompensation, cardiogenic shock at the severe end of the spectrum, and the compensatory mechanisms that shape its natural history. It is an educational reference map of the subfield, not a clinical management protocol.
Sub-topics
Core questions
- What distinguishes heart failure as a syndrome from the underlying diseases that cause it?
- How does left ventricular ejection fraction partition heart failure into reduced, mildly reduced, and preserved phenotypes?
- What separates chronic stable heart failure from acute decompensation and from cardiogenic shock?
- How do compensatory neurohormonal and mechanical responses initially preserve output but later drive progression?
Key concepts
- Heart failure as a syndrome, not a single disease
- Left ventricular ejection fraction classification (reduced, mildly reduced, preserved)
- Congestion versus hypoperfusion
- Acute versus chronic presentation
- Natriuretic peptides as biomarkers
- Neurohormonal activation
Key theories
- Neurohormonal hypothesis of progression
- Packer's framework holds that chronic activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, initially compensatory, ultimately exerts deleterious effects on the heart and circulation that drive the progression of heart failure, providing the rationale for antagonising these systems.
Mechanisms
A wide range of insults — ischaemic injury, hypertension, valvular disease, cardiomyopathies, and others — can impair the heart's ability to eject blood (systolic dysfunction) or to fill at normal pressures (diastolic dysfunction). The resulting fall in effective output triggers compensatory responses, notably the Frank-Starling mechanism and neurohormonal activation of the sympathetic and renin-angiotensin-aldosterone systems. These responses initially maintain perfusion but, sustained over time, promote adverse remodelling, fibrosis, and further functional decline, a process central to the neurohormonal hypothesis.
Clinical relevance
Heart failure is one of the most common and consequential cardiovascular syndromes and a major driver of hospitalisation. Understanding its classification and mechanisms underpins evidence appraisal across cardiology. This entry describes the syndrome at a conceptual level and is not a source of individualised diagnostic or treatment recommendations.
Epidemiology
Heart failure affects a substantial and growing share of adults, with prevalence rising steeply with age, and it carries high rates of hospitalisation and mortality. Reported lifetime risk is considerable in older populations, and the burden is shifting in some settings toward the preserved-ejection-fraction phenotype, as summarised in contemporary epidemiologic reviews.
Evidence & guidelines
Major society guidelines — including the 2021 ESC guidelines and the 2022 AHA/ACC/HFSA guideline — define heart failure, set out its ejection-fraction-based classification, and summarise the evidence base. They are cited here as authoritative classification and reference sources rather than as instructions for care.
History
Heart failure has been recognised clinically for centuries, but its modern understanding shifted during the twentieth century from a purely haemodynamic model toward a neurohormonal one. Packer's 1992 articulation of the neurohormonal hypothesis reframed the syndrome as a progressive disorder driven by maladaptive systemic responses, reshaping both classification and the conceptual basis of subsequent guidelines.
Key figures
- Milton Packer
- Theresa McDonagh
- Paul Heidenreich
Related topics
Seminal works
- packer-1992
- mcdonagh-2021-esc
- heidenreich-2022-aha
Frequently asked questions
- Is heart failure the same as a heart attack?
- No. A heart attack (myocardial infarction) is acute damage to heart muscle from interrupted blood supply, whereas heart failure is a chronic or acute syndrome in which the heart cannot meet the body's circulatory needs. A heart attack is one of several causes that can lead to heart failure.
- How is heart failure classified by ejection fraction?
- Guidelines group heart failure by left ventricular ejection fraction into reduced (HFrEF), mildly reduced (HFmrEF), and preserved (HFpEF) categories, which differ in their mechanisms, epidemiology, and evidence base.