Abstract
Studies of cardiac mechanics in compensated heart muscle suggest that muscle hypertrophy is stimulated by long-term increases in peak myocardial wall stress. 1–6 Conditions leading to either chronic left ventricular (LV) pressure or volume overload generally result in an increase in LV wall stress (expressed as force per unit area). Increased systolic stress results in decreased LV performance unless compensatory hypertrophy develops to normalize systolic wall stress. Measurements of LV wall stress in patients with chronic LV volume or pressure overload should provide an excellent index of cardiac compensation that could be followed serially to permit detection of early myocardial decompensation such as an abnormal increase in wall stress due to inadequate hypertrophy. 4–6 The objectives of this study were to examine the relation of LV peak systolic wall stress to age and body surface area in normal subjects and to establish the normal range of values for LV peak systolic stress, taking age and body surface area into account. We have shown that in normal subjects, LV wall thickness increases with increasing age and body surface area, while LV internal dimensions decrease slightly with aging, but increase with increasing body surface area. 7–9 To determine the effect of age and body surface area on LV peak systolic (meridional) wall stress, we analyzed M-mode echocardiographic data previously recorded in an adult population without evidence of cardiovascular disease. 7–9
Published Version
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