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Circulation
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Data sources: UnpayWall
Circulation
Article . 2000 . Peer-reviewed
Data sources: Crossref
Circulation
Article . 2000
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Left Ventricular Hypertrophy

Pathogenesis, Detection, and Prognosis
Authors: B H, Lorell; B A, Carabello;

Left Ventricular Hypertrophy

Abstract

When the heart faces a hemodynamic burden, it can do the following to compensate: (1) use the Frank-Starling mechanism to increase crossbridge formation; (2) augment muscle mass to bear the extra load; and (3) recruit neurohormonal mechanisms to increase contractility. The first mechanism is limited in its scope, and the third is deleterious as a chronic adjustment. Thus, increasing mass assumes a key role in the compensation for hemodynamic overload. This increase in mass is due to the hypertrophy of existing myocytes rather than hyperplasia, because cardiomyocytes become terminally differentiated soon after birth. In response to pressure overload in conditions such as aortic stenosis or hypertension, the parallel addition of sarcomeres causes an increase in myocyte width, which in turn increases wall thickness. This remodeling results in concentric hypertrophy (increase in ratio of wall thickness/chamber dimension). According to LaPlace’s Law, the load on any region of the myocardium is given as follows: (pressure×radius)/(2×wall thickness); thus, an increase in pressure can be offset by an increase in wall thickness. Because systolic stress (afterload) is a major determinant of ejection performance, the normalization of systolic stress helps maintain a normal ejection fraction even when needing to generate high levels of systolic pressure.1 Volume overload in conditions such as chronic aortic regurgitation, mitral regurgitation, or anemia engenders myocyte lengthening by sarcomere replication in series and an increase in ventricular volume. This pattern of eccentric hypertrophy (cavity dilatation with a decrease in ratio of wall thickness/chamber dimension) is also initially compensatory, such that the heart can meet the demand to sustain a high stroke volume. However, chronic hypertrophy may be deleterious because it increases the risk for the development of heart failure and premature death. This review will focus on the pathogenesis of pressure- versus volume-overload types of left ventricular hypertrophy (LVH), detection, …

Related Organizations
Keywords

Humans, Hypertrophy, Left Ventricular

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
933
Top 0.1%
Top 0.1%
Top 1%
bronze