When left ventricular failure occurs and there is increase in end systolic volume due to which dilation of ventricle or cardiomegaly occurs is it the same as eccentric hypertrophy
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left ventricular systolic failure end systolic volume ventricular dilation eccentric hypertrophy pathophysiology
Not exactly, but they are often related.
In left ventricular systolic failure, reduced contractility means the LV ejects less blood, so end-systolic volume (ESV) increases. Over time, retained blood and neurohormonal remodeling can increase end-diastolic volume (EDV) too, producing LV chamber dilatation and cardiomegaly.
Eccentric hypertrophy is a structural remodeling pattern in which:
- LV chamber size increases
- LV myocardial mass increases
- Relative wall thickness is normal or reduced
- Myocytes become longer, with sarcomeres added in series
So, dilatation from chronic LV failure may be accompanied by eccentric hypertrophy, but the terms do not mean the same thing:
| Term | What it describes |
|---|---|
| Increased ESV | A functional/volume consequence of poor systolic emptying |
| LV dilatation | Increased chamber size |
| Cardiomegaly | Enlarged heart, which may result from dilation, hypertrophy, or both |
| Eccentric hypertrophy | Dilated LV plus increased LV muscle mass in a characteristic geometry |
A simple sequence in chronic HFrEF can be:
↓ Contractility -> ↑ ESV -> ↑ EDV / LV dilatation -> eccentric remodeling or eccentric hypertrophy
But advanced dilated cardiomyopathy can eventually have a very dilated, thin-walled LV with inadequate effective muscle mass. In that situation, calling it simply “eccentric hypertrophy” can be misleading. Eccentric hypertrophy is classically the compensatory response to chronic volume overload, such as chronic aortic or mitral regurgitation. The medical texts define it as increased LV mass with normal relative wall thickness, and describe volume overload as causing disproportionate myocyte lengthening.
A useful contrast:
- Pressure overload such as hypertension or aortic stenosis -> concentric hypertrophy: thicker walls, initially smaller or normal cavity.
- Volume overload such as regurgitant valve disease, or chronic dilated remodeling -> eccentric hypertrophy/remodeling: larger cavity, relatively normal or thinner walls.
So the heart can just dilate without eccentric hypertrophy
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Yes. The ventricle can dilate without meeting the definition of eccentric hypertrophy.
Eccentric hypertrophy requires both:
- Increased LV cavity size, and
- Increased LV myocardial mass
If the LV enlarges but muscle mass does not increase adequately, or is lost because of myocyte death/fibrosis, this is better termed dilatation with eccentric remodeling, not necessarily eccentric hypertrophy.
For example, in advanced dilated cardiomyopathy or post-myocardial-infarction remodeling, the LV may become large and relatively thin-walled. It can look “hypertrophied” in the sense that the whole heart is enlarged, but its actual LV mass may be normal, mildly increased, or insufficient for the chamber size.
A useful progression:
- Early chronic volume overload -> dilation + compensatory increase in muscle mass = eccentric hypertrophy
- Advanced systolic failure -> progressive dilation, wall thinning relative to cavity, fibrosis and loss of contractile cells = adverse eccentric remodeling / dilated ventricle, possibly without true hypertrophy
So “dilation” is a chamber-size finding. “Eccentric hypertrophy” is a specific mass-and-geometry pattern.
How does LV dilates
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left ventricular dilation pathophysiology volume overload systolic dysfunction remodeling authoritative source
LV dilates when it is repeatedly exposed to excess volume, excessive wall stress, or weak contraction. It is not simply a balloon filling with blood. It is a gradual structural change of the muscle and chamber.
In left ventricular systolic failure
-
Contractility falls
The LV cannot eject normally. -
More blood remains after systole
So ESV increases. -
More blood enters during the next diastole
Normal venous return is added to the residual blood. Thus EDV increases too. -
The larger filling volume stretches the LV wall
Initially, this raises stroke volume through the Frank-Starling mechanism. -
With persistent stress, remodeling occurs
Cardiomyocytes lengthen, matrix and collagen change, fibrosis may develop, and the chamber progressively becomes wider and more spherical. This is LV dilatation. -
Dilatation then worsens the problem
By Laplace's law:[ \text{Wall stress} \propto \frac{\text{LV pressure} \times \text{LV radius}}{2 \times \text{wall thickness}} ]When radius increases, wall stress rises unless wall thickness increases proportionately. Higher wall stress makes ejection harder, increases oxygen demand, and promotes further remodeling.
So the self-perpetuating cycle is:
[
\text{Reduced contractility}
\rightarrow \uparrow \text{ESV}
\rightarrow \uparrow \text{EDV}
\rightarrow \text{LV stretch and dilatation}
\rightarrow \uparrow \text{wall stress}
\rightarrow \text{further reduced contractility}
]
Other major ways the LV dilates
- Chronic volume overload: aortic regurgitation, mitral regurgitation, left-to-right shunts. The LV must accommodate an abnormally large diastolic volume.
- Myocardial infarction: dead/scarred myocardium cannot contract and may expand. Surviving myocardium remodels, enlarging the LV.
- Dilated cardiomyopathy: genetic disease, myocarditis, alcohol/toxins, persistent tachycardia, etc., can weaken myocytes and lead to dilation.
- Long-standing pressure overload: severe hypertension or aortic stenosis initially produces concentric hypertrophy, but late decompensation can lead to dilatation.
In short, ESV rises because the LV cannot empty; EDV then rises because residual volume plus incoming blood accumulates. Persistent stretch and wall stress cause physical remodeling of the LV into a larger chamber.
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