Wall stress and patterns of hypertrophy in the human left ventricle

Abstract

It is generally recognized that chronic left ventricular (LV) pressure overload results primarily in wall thickening and concentric hypertrophy, while chronic LV volume overload is characterized by chamber enlargement and an eccentric pattern of hypertrophy. To assess the potential role of the hemodynamic factors which might account for these different patterns of hypertrophy, we measured LV wall stresses throughout the cardiac cycle in 30 patients studied at the time of cardiac catheterization. The study group consisted of 6 subjects with LV pressure overload, 18 with LV volume overload, and 6 with no evidence of heart disease (control). LV pressure, meridional wall stress (sigma (m)), wall thickness (h), and radius (R) were measured in each patient throughout the cardiac cycle. For patients with pressure overload, LV peak systolic and end diastolic pressures were significantly increased (220±6/23±3 mm Hg) compared to control (117±7/10±1 mm Hg, P <0.01 for each). However, peak systolic and end diastolic sigma (m) were normal (161±24/23±3x103 dyn/cm2 compared to control (151±14/17±2x103 dyn/cm2, NS), reflecting the fact that the pressure overload was exactly counterbalanced by increased wall thickness (1.5±0.1 cm for pressure overload vs. 0.8±0.1 cm for control, P <0.01). For patients with volume overload, peak systolic sigma (m) was not significantly different from control, but end diastolic sigma (m) was consistently higher than normal (41±3x103 dyn/cm2 for volume overload, 17±2x103 dyn/cm2 for control, P <0.01). LV pressure overload was associated with concentric hypertrophy, and an increased value for the ratio of wall thickness to radius (h/R ratio). In contrast, LV volume overload was associated with eccentric hypertrophy, and a normal h/R ratio. These data suggest the hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress. It is proposed that increased systolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolic stress (force per unit cross sectional area) to normal. In contrast, increased resting or diastolic tension appears to result in gradual fiber elongation or lengthening which improves efficiency of the ventricular chamber but cannot normalize the diastolic wall stress.