Characteristic Features of Left Ventricular Hypertrophy in Valvular Disease with Volume Overload

In left ventricular hypertrophy (LVH), concentric hypertrophy is known to be associated with pressure overload, and the condition is principally brought on by increased systolic wall stress in the left ventricle. In contrast, eccentric hypertrophy has conventionally been associated with volume overload. However, incompatible with this assumption, transverse thickening of the wall of the left ventricle is often observed in LVH ascribed to volume overload. To clarify the hypertrophic pattern and elucidate the hemodynamic factors involved in the pathogenesis of LVH associated with volume overload, we investigated LVH caused by volume overload in 14 patients of mitral regurgitation (MR) and 20 patients of aortic regurgitation (AR). The MR group comprised 5 males and 9 females (60±11 years old) and the AR group was made up of 11 males and 9 females (41±11 years old). Results were compared with those found in 14 controls (8 males and 6 females, 52±11 years old). Preload was expressed most properly as end-diastolic dimension of the left ventricle (LVDd) among several indices. Although no increase in LVDd was noted in mild MR (I-II°), a marked increase was found in severe MR (III-IV°) over that of the controls (60.4±2.9 versus 47.7±5.7mm, p<0.001). In mild AR (I-II°) the LVDd was significantly increased (53.3±6.0mm, p<0.05) over that of the controls, and in severe AR (III-IV°) the increase was considerably higher (61.2±6.6mm, p<0.05) than that in mild AR. Increased afterload was noted only in severe MR, compared with that of the controls (96.8±37.0 versus 66.7±19.6g/cm^2, p<0.05). Left ventricular mass (LVM) was abnormally large in mild MR (257±68g, p<0.05), severe MR (334±79g, p<0.001) and severe AR (386±165g, p<0.001) over that of the controls (183±46g). The cross-sectional area increased with severity in a manner comparable to that of LVM. The relationship between LVDd (x) and LVM (y) in the MR cases was shown by a regression line of y=7.2x-93.0 (r=0.71) and in the AR cases by a regression line of y=14.6x-528.1 (r=0.67). In the MR cases studied, the relationship between LVSWS (x) and LVM (y) was represented by y=1.3x+194.3 (r=0.55). Thus, LVH attributable to volume-overload diseases is not only eccentric but it can be concentric. Furthermore, these results suggest that excessive preload and afterload might be not the simple pathogenesis of the development of LVH in these diseases. Neurohumoral factors possibly activated by systolic dysfunction of the left ventricle are thought to play some role in the development of LVH associated with volume overload.