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Prevalence, clinical characteristics, and outcomes associated with eccentric versus concentric left ventricular hypertrophy in heart failure with preserved ejection fraction.
Concentric or Eccentric Hypertrophy: How Clinically Relevant Is the Difference? Different combinations of volume and pressure overloads cause different left ventricular (LV) geometric adaptations.
This eccentric hypertrophy creates a dilated ventricular chamber with relative wall thinning. In contrast, concentric hypertrophy is more often associated with chronic pressure overload states like hypertension or aortic stenosis.
Left ventricular hypertrophy changes the structure of the heart and how the heart works. The thickened left ventricle becomes weak and stiff. This prevents the lower left heart chamber from filling properly with blood. As a result, blood pressure in the heart increases.
In this blog we describe left ventricular hypertrophy (LVH) and identify the different categories of concentric, eccentric and concentric remodeling.
Concentric left ventricular hypertrophy is an abnormal increase in left ventricular myocardial mass caused by chronically increased workload on the heart, most commonly resulting from pressure overload-induced by arteriolar vasoconstriction as occurs in, chronic hypertension or aortic stenosis.
Whether modifications of LV geometry from concentric to eccentric are beneficial beyond the reduction of LV mass has been debated; however, the conclusion has been, in general, that concentric LV hypertrophy is also characterized by greater LV mass than eccentric LV hypertrophy; therefore, these 2 features (ie, concentric geometry and LV ...
The heart of the strength-trained athlete responds to sudden and large pressure overload with concentric left ventricular hypertrophy, in some cases accompanied by increases in left ventricular diameters.
Three main patterns of LVH have been first described: concentric hypertrophy, eccentric hypertrophy and concentric remodelling. Concentric LVH is when LVM predominantly increases by wall thickening in response to pressure overload.
It is now generally accepted that distinct signaling pathways are responsible for the different outcomes in pathological and physiological hypertrophy. In this review, we compare structural remodeling of the athlete's heart with the cardiac remodeling that occurs in settings of disease.