We have previously shown that left ventricular (LV) wall thickness increases with age in normotensive BLSA men. To determine whether this finding relates to the increase in systolic blood pressure (SBP) which also accompanies normal aging, LV wall thickness (Th) was measured in short axis 2-dimensional echocardiogram (2-D echo) echoes obtained from 74 participants of the Baltimore Longitudinal Aging population without evidence of hypertensive (BP < 140/90) or ischemic heart disease. The average of 3 contigous septal wall Th measurements normalized for body surface area (WTS) was related to age (WTS = 0.66 + 0.0029 (age), r = 0.26, p < 0.03), but more strongly to SBP (WTS = 0.32 + 0.0039 (SBP), r = 0.39, p < 0.001). When WTS was regressed against age and SBP (multivariate analysis) the effect of age became insignificant (p = 0.28) while SBP remained a strong determinant of WTS (r = 0.41, p = 0.0045). These data suggest that the normal LV hypertrophy associated with aging is mediated via an increase in SBP. Doppler echocardiography during isometric handgrip in 25 healthy BLSA subjects revealed that advanced age was associated with a greater rise in systolic blood pressure (r=.53, p=.008), greater increases in Lv end diastolic dimension (r=.59, p=.002) and end systolic dimensions (r=.50, p=.01), blunted fractional shortening (r=.42, p=.04) and a further augmentation of atrial contribution to LV filling (r=.48, p=.014). In a related study, MUGA end-diastolic volume (EDV) and ejection fraction (EF) in 47 women (w) and 104 men (M), and average LV end- diastolic wall thickness (EDWT) by 2-D echo (31 W and 43 M) were obtained in BLSA subjects. Both EDV and EDWT were smaller in W than in M (117 plus or minus 30 vs 146 plus or minus 38ml p<0.001 and 0.97 plus or minus 0.14 vs 1.17 plus or minus 0.16 cm, p<.001 respectively). EF was greater in W than in M (68 plus or minus 7 vs 64 plus or minus 7%, p<.005). Gender differences were eliminated by adjustment for body surface area (BSA) and systolic blood pressure (SBP). Thus, there is no distinctive gender difference in cardiac structure or function.
