Heart Failure

Heart failure is a clinical syndrome arising when the heart can no longer pump or fill adequately to meet the body's circulatory needs at normal filling pressures. As a pathology topic it is the common downstream consequence of diverse cardiac insults - ischaemic injury, pressure and volume overload, valvular disease and primary myocardial disorders - that converge through cardiac remodelling on impaired pump function.

Definition

Heart failure is a syndrome of impaired cardiac output or elevated filling pressures resulting from structural or functional abnormality of cardiac filling or ejection, classified in part by left-ventricular ejection fraction into reduced, mildly reduced and preserved phenotypes.

Scope

The entry covers the structural and functional basis of pump failure, the distinction between failure with reduced and preserved ejection fraction, the maladaptive remodelling that drives progression, and the major aetiologies that culminate in the syndrome. It is reference pathology describing how the failing heart arises and evolves, not clinical management guidance; the cardiology-care view is held under a separate clinical entry.

Core questions

• What structural and functional changes underlie failure with reduced versus preserved ejection fraction?
• How do pressure overload, volume overload and ischaemic loss of myocardium drive cardiac remodelling?
• Why does compensatory hypertrophy and neurohormonal activation eventually become maladaptive?
• How do diverse cardiac diseases converge on the common syndrome of pump failure?

Key concepts

• Reduced versus preserved ejection fraction
• Pressure overload and concentric hypertrophy
• Volume overload and eccentric hypertrophy/dilation
• Cardiac remodelling and fibrosis
• Neurohormonal activation
• Systolic and diastolic dysfunction

Key theories

Maladaptive remodelling model of heart-failure progression

Cardiac injury or chronic overload triggers structural remodelling - hypertrophy, chamber dilation, fibrosis and altered myocyte biology - that is initially compensatory but becomes self-perpetuating and maladaptive, progressively worsening pump function and driving the failure syndrome.

Mechanisms

An initiating insult - myocardial infarction, chronic hypertension, valvular lesion, or primary cardiomyopathy - imposes loss of contractile tissue or sustained haemodynamic load. The heart compensates through hypertrophy (concentric with pressure overload, eccentric with volume overload), chamber remodelling and neurohormonal activation. Over time these responses become maladaptive: interstitial fibrosis stiffens the myocardium, myocyte biology and calcium handling deteriorate, and the ventricle dilates or stiffens, impairing systolic ejection, diastolic filling, or both. The result is the syndrome of inadequate output and congestion. Ejection fraction phenotypes (reduced versus preserved) reflect different dominant patterns of this remodelling.

Clinical relevance

Heart failure is a major and growing cause of morbidity, hospitalisation and mortality, and represents the shared endpoint of much cardiovascular pathology. Understanding its mechanisms supports appraisal of prevention and evidence; this entry is descriptive and does not provide individualised diagnostic or treatment advice.

Epidemiology

Heart failure affects a large and rising number of people, with prevalence increasing with age and with the burden of antecedent conditions such as coronary disease and hypertension; it is a leading cause of hospital admission among older adults.

History

The understanding of heart failure shifted over the late twentieth century from a primarily haemodynamic and fluid-retention model toward a neurohormonal and remodelling paradigm, in which chronic activation of compensatory systems and structural remodelling drive progression. This reframing, articulated in work on cardiac plasticity and remodelling, underpins the modern classification by ejection-fraction phenotype reflected in contemporary guidelines.

Key figures

• Joseph A. Hill
• Eric N. Olson
• Gregg C. Fonarow

Seminal works

• hill-olson-2008
• bloom-2017

Frequently asked questions

Does heart failure mean the heart has stopped?

No. It means the heart cannot pump or fill well enough to meet the body's needs at normal pressures. It is a syndrome of impaired function and congestion, not cardiac arrest.

What is the difference between reduced and preserved ejection fraction?

Reduced ejection fraction reflects impaired systolic emptying, often after myocyte loss and dilation, whereas preserved ejection fraction reflects a stiff, poorly relaxing ventricle with impaired filling; both produce the failure syndrome through different remodelling patterns.