Lack of association between aortic sclerosis and left ventricular hypertrophy in elderly subjects

The presence of aortic sclerosis has been associated with increased LV mass, particularly in hypertensive subjects. However, aortic sclerosis has also been associated with endothelial dysfunction, which may provide stimuli for development of left ventricular hypertrophy independent of afterload. Thus, we have sought to determine whether aortic sclerosis is a determinant of increased left ventricular mass in a non-hypertensive cohort of aging subjects.

79 subjects, mean age 68 ± 6 years, without existing cardiovascular disease or previous antihypertensive therapy were studied. LV volumes were calculated from the short axis stack of cardiac MRI and LV mass was indexed to height(2.7). The presence of aortic sclerosis was assessed with echocardiography using backscatter from the aortic valve (AV(BS)) and visual scoring. Plasma asymmetric dimethylarginine levels and vascular responses to salbutamol were used to assess endothelial function. ANCOVA was used to test the relationship between LV mass index and afterload. Univariate and multivariate analyses were performed to find determinants of increased LV mass.

15 (19%) of subjects had aortic sclerosis on the basis of AV(BS); none had aortic valve areas <1.5 cm(2). There was no significant difference in LV mass between subjects with and without aortic sclerosis. While LV mass was directly related to systolic blood pressure, this relationship was independent of the presence/absence of aortic sclerosis. On multivariate analysis, significant correlates of increased LV mass were male gender, systolic blood pressure and increased BMI, but not presence of aortic sclerosis.

In this aging normotensive population free of established cardiovascular disease, aortic sclerosis is not associated with left ventricular hypertrophy.