Vascular dysfunction across the stages of the menopausal transition is associated with menopausal symptoms and quality of life.

OBJECTIVE: The menopausal transition is associated with somatic symptoms and increased rates of depression, which can impair quality of life (QOL) and increase cardiovascular disease (CVD) risk. This period is also associated with accelerated vascular aging (arterial stiffening and endothelial dysfunction), an antecedent to CVD. This secondary analysis sought to explore associations between depression, menopausal symptoms and QOL, and vascular aging across menopause stages. METHODS: Arterial stiffness (carotid artery compliance), endothelial function (brachial artery flow-mediated dilation [FMD]), menopausal symptoms (Menopausal Symptom List [MSL]), depression (Center for Epidemiologic Studies Depression Scale [CES-D]), and QOL (Utian QOL Scale [UQOL]) were measured in 138 women (19-70 years) classified as premenopausal (n = 41, 34 ±â€Š8 years; mean ±â€ŠSD), early (n = 25, 49 ±â€Š3 years), or late perimenopausal (n = 26, 50 ±â€Š4 years), or early (n = 22, 55 ±â€Š4 years) or late postmenopausal (n = 24, 61 ±â€Š5 years). Differences across menopause stages were determined using one-way analysis of variance; associations between vascular measures and MSL, CES-D, and UQOL were tested using Pearson's correlation analyses. RESULTS: Menopausal symptoms, depression, and QOL worsened across menopause stages, particularly in late perimenopausal women. Vasosomatic symptom frequency, and general somatic symptom frequency and severity were inversely correlated with carotid artery compliance and FMD (r = -0.27 to -0.18, all P < 0.05). Only correlations with general somatic symptoms were significant after adjusting for multiple comparisons. Total QOL was positively correlated with carotid artery compliance (r = 0.23, P = 0.01). CES-D scores were not correlated with carotid artery compliance or FMD (r = -0.08, -0.03, P = 0.35). CONCLUSIONS: Vascular dysfunction across the stages of menopause was associated with greater frequency and severity of menopausal symptoms, and lower QOL, but not depression. Mechanisms underlying these associations (eg, inflammation, oxidative stress) should be explored.

Oxidative stress contributes to large elastic arterial stiffening across the stages of the menopausal transition.

OBJECTIVE: It is unclear how changes in ovarian hormones during the menopausal transition contribute to age-associated arterial stiffening. We sought to evaluate differences in arterial stiffness and the role of oxidative stress across the stages of the menopausal transition in healthy women. METHODS: Arterial stiffness (carotid artery compliance and ultrasound) was measured during immediate infusions of saline (control) and ascorbic acid (experimental model to immediately decrease oxidative stress) in 97 healthy women (22-70 y) classified as premenopausal (n = 24; mean [SD] age, 33 [7] y), early perimenopausal (n = 21; 49 [3] y) or late perimenopausal (n = 21; 50 [4] y), or postmenopausal (n = 31; 57 [5] y). RESULTS: Basal carotid artery compliance was different among the groups (P < 0.001). Mean [SD] compliance was highest in premenopausal women (1.31 [0.25] mm/mm Hg × 10), with progressive decrements in perimenopausal (early perimenopausal, 0.98 [0.31] mm/mm Hg × 10; late perimenopausal, 0.90 [0.25] mm/mm Hg × 10) and postmenopausal (0.75 [0.24] mm/mm Hg × 10) women. Ascorbic acid infusion improved compliance in late perimenopausal (15% [18%] increase, P = 0.001) and postmenopausal (17% [26%] increase, P = 0.002) women but not in early perimenopausal or premenopausal women. CONCLUSIONS: Arterial stiffening worsens across the stages of the menopausal transition in healthy women. This seems to be mediated, in part, by oxidative stress, particularly during the late perimenopausal and postmenopausal periods. It remains uncertain whether this is specifically caused by loss of ovarian function or aging.