Left ventricular hypertrophy in hypertension: stimuli, patterns, and consequences.
Review
Overview
abstract
Left ventricular (LV) size in childhood closely parallels body size, whereas in adulthood LV mass is increasingly affected by effects of obesity, hypertension, the level of cardiac volume load, and the level of LV myocardial contractility. Recently, additional independent associations of diabetes, arterial structure and function and as yet unknown genes with higher LV mass have been defined; angiotensin II and insulin have also been suggested to be additive stimuli to LV hypertrophy. Consideration of the level of LV mass and of the LV wall thickness/chamber radius ratio (relative wall thickness) has identified four different geometric patterns of LV adaptation to hypertension, including concentric LV hypertrophy (increased mass and wall thickness), eccentric hypertrophy (increased mass, normal relative wall thickness), concentric remodeling (increased relative wall thickness with normal mass) and normal LV geometry. Concentric hypertrophy is associated with especially high arterial pressure while eccentric hypertrophy is associated with obesity and elevated volume load. Numerous studies show that increased LV mass predicts cardiovascular events and death independently of all conventional risk factors; initial studies have also identified adverse implications of low LV midwall function and high relative wall thickness. Pioneer studies strongly suggest that reversal of LV hypertrophy is associated with an improved prognosis.
