OBJECTIVES: This study sought to determine whether the natural decrease in sex hormones that occurs during menopause in hypertensive women plays a role in aortic root stiffness. BACKGROUND: The effect of menopause-induced sex hormone deprivation on aortic root function is not known; however, it is of special interest in hypertensive subjects, whose aortic elastic properties are already compromized. METHODS: Eighteen women with essential hypertension were followed-up for 3 years, during which time they went through menopause (group A) and were compared with 22 age-matched hypertensive women with normal menses (group B) and 20 hypertensive men (group C). Blind echocardiographic tracings and simultaneous blood pressure measurements were obtained after at least 30 medication-free days, both at baseline and 3.5 years later. RESULTS: Aortic root function tended to be aggravated in both groups B and C, but not significantly so, with no between-group differences (p = NS), whereas it deteriorated in group A. Thus, in menopausal hypertensive subjects, aortic root systolodiastolic percent change decreased (from 6.7% to 4.9%, p < 0.0001 [p = 0.002 vs. group B; p = 0.006 vs. group C]); cross-sectional compliance decreased (from 18 to 13 cm2/mm Hg, p < 0.0001 [p = 0.002 vs. group B; p = 0.03 vs. group C]); Peterson's elastic modulus increased (from 1.2 to 1.9 dynes/cm2, p = 0.0006 [p = 0.003 vs. group B; p = 0.005 vs. group C]); aortic stiffiness index increased (from 7.0 to 10.8, p = 0.0008 [p = 0.004 vs. group B; p = 0.007 vs. group C]); and aortic root distensibility decreased (from 1.8 to 1.2 dynes/cm2, p < 0.0001 [p = 0.0003 vs. group B; p = 0.007 vs. group C]). Serum lipids did not change significantly in any group (p = NS). CONCLUSIONS: In hypertensive women, the effect of menopause on the elastic properties of the aortic root is abrupt and devastating.
OBJECTIVES: This study sought to determine whether the natural decrease in sex hormones that occurs during menopause in hypertensivewomen plays a role in aortic root stiffness. BACKGROUND: The effect of menopause-induced sex hormone deprivation on aortic root function is not known; however, it is of special interest in hypertensive subjects, whose aortic elastic properties are already compromized. METHODS: Eighteen women with essential hypertension were followed-up for 3 years, during which time they went through menopause (group A) and were compared with 22 age-matched hypertensivewomen with normal menses (group B) and 20 hypertensivemen (group C). Blind echocardiographic tracings and simultaneous blood pressure measurements were obtained after at least 30 medication-free days, both at baseline and 3.5 years later. RESULTS: Aortic root function tended to be aggravated in both groups B and C, but not significantly so, with no between-group differences (p = NS), whereas it deteriorated in group A. Thus, in menopausal hypertensive subjects, aortic root systolodiastolic percent change decreased (from 6.7% to 4.9%, p < 0.0001 [p = 0.002 vs. group B; p = 0.006 vs. group C]); cross-sectional compliance decreased (from 18 to 13 cm2/mm Hg, p < 0.0001 [p = 0.002 vs. group B; p = 0.03 vs. group C]); Peterson's elastic modulus increased (from 1.2 to 1.9 dynes/cm2, p = 0.0006 [p = 0.003 vs. group B; p = 0.005 vs. group C]); aortic stiffiness index increased (from 7.0 to 10.8, p = 0.0008 [p = 0.004 vs. group B; p = 0.007 vs. group C]); and aortic root distensibility decreased (from 1.8 to 1.2 dynes/cm2, p < 0.0001 [p = 0.0003 vs. group B; p = 0.007 vs. group C]). Serum lipids did not change significantly in any group (p = NS). CONCLUSIONS: In hypertensivewomen, the effect of menopause on the elastic properties of the aortic root is abrupt and devastating.