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. (Hypertens Res 1999; 22: 1-9) Key Words: hypertension, echocardiography, left ventricular hypertrophy, left ventricular functionSince the mid 1970s, methods to measure left ventricular (LV) mass by echocardiography or by other techniques (1) have been used to show that LV hypertrophy (LVH) is more prevalent, more heterogeneous in its anatomic and pathophysiologic patterns, and a stronger determinant of outcome in hypertensive patients than was previously recognized. In this article, we will examine stimuli of hypertensive LVH, review its geometric patterns, and discuss the consequences of LVH with respect to cardiac function and outcome.
Stimuli PromotingThe LV normally grows continuously from infancy until adulthood (2), with cellular enlargement (hypertrophy) accounting for most of the increase in size. Further increases, or at times decreases, in LV muscle mass may occur due to physiologic or pathologic alterations in hemodynamic load. In apparently normal individuals, the closest correlate of LV mass is body size in both children and adults (2-3). Body size has traditionally been taken into account by indexing LV mass for body surface area. This method of LV mass indexation is useful in detecting LVH due to hypertension, but may misclassify obesity-induced LVH as normal (4). A physiologic approach to the problem imposed by obesity is to index LV mass for lean body mass (5), but this is impractical for routine purposes. Alternatively, body height to the power of its allometric (or growth) relationship with LV mass can be used to index the latter variable (6). After puberty, men have a lar...