Heart failure: hypertrophy and remodelling
- Mechanism
A strained heart first grows thicker or wider to cope. Over time the enlarged muscle becomes stiff, starved of oxygen and weak.
What it is
Heart failure is the inability of the heart to pump enough blood for the body's needs, or to do so only at high filling pressures. It is the end of many diseases: ischemic heart disease, hypertension, valve disease and cardiomyopathies. The myocardium first adapts by hypertrophy and by neurohormonal activation (sympathetic system, renin–angiotensin–aldosterone, natriuretic peptides). Pressure overload adds sarcomeres in parallel (concentric hypertrophy); volume overload adds them in series (eccentric hypertrophy with dilation). Sustained adaptation becomes maladaptive remodelling: myocyte death, fibrosis and a failing pump.
Structure
- Gross: a heavy heart; thick left ventricle in pressure overload, dilated chambers in volume overload or end-stage failure.
- H&E: enlarged myocytes with large hyperchromatic boxcar nuclei; interstitial fibrosis; in end stage, attenuated and stretched myocytes.
Step by step
- An injury or a load (infarct, high pressure, leaking valve) reduces output or raises wall stress.
- Frank–Starling: higher filling stretches fibres and raises output in the short term.
- Sympathetic and renin–angiotensin–aldosterone activation raise heart rate, contractility and fluid retention.
- Myocytes hypertrophy; pressure adds sarcomeres in parallel, volume adds them in series.
- Oxygen demand outstrips the capillaries; myocytes die and are replaced by fibrosis.
- The ventricle dilates or stiffens; output falls and filling pressures rise: clinical heart failure.
Two patterns of cardiac hypertrophy
| Pattern | Causes | Sarcomeres | Ventricle |
|---|---|---|---|
| Concentric (pressure overload) | Hypertension, aortic stenosis | Added in parallel; myocytes wider | Thick wall, small or normal cavity, diastolic dysfunction |
| Eccentric (volume overload) | Mitral or aortic regurgitation, shunts, after infarction | Added in series; myocytes longer | Dilated cavity, weight up, systolic dysfunction late |
Clinical notes
- Physiological hypertrophy of athletes has normal capillary density and no fibrosis, unlike pathological hypertrophy.
- Natriuretic peptides (BNP, NT-proBNP) measure ventricular wall stress and help diagnose heart failure.
Test yourself
Think of the answer, then tap the question to see it.
How does the arrangement of new sarcomeres differ between pressure and volume overload?
Pressure overload adds sarcomeres in parallel (concentric thickening); volume overload adds them in series (eccentric dilation).
Why does a hypertrophied heart become ischemic?
Myocyte mass and oxygen demand grow faster than the capillary supply, and the thick wall is harder to perfuse.
What does BNP reflect?
Stretch of the ventricular wall; it is released by myocytes when filling pressure or volume rises.
Elsewhere in DurgiPedia
- Heart failure physiology
- Cardiac output and what sets it
- The ventricular pressure–volume loop
- Cardiac muscle: intercalated discs
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Heart Failure | Congestive Heart Failure | CHF | MedlinePlus (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.