Abstract
ObjectiveLoss of sex hormones has been suggested to underlie menopause-associated increment in cardiovascular risk. We investigated associations of sex hormones with arterial stiffness in 19–58-years-old women. We also studied associations of specific hormonal stages, including natural menstrual cycle, cycle with combined oral contraceptives (COC) and menopausal status with or without hormone therapy (HT), with arterial stiffness.MethodsThis study includes repeated measurements of 65 healthy women representing reproductive (n=16 natural, n=10 COC-users) and menopause (n=5 perimenopausal, n=26 postmenopausal, n=8 HT-users) stages. Arterial stiffness outcomes were aortic pulse wave velocity (PWVao) and augmentation index (AIx%) assessed using Arteriograph-device. Generalized estimating equation models were constructed to investigate associations of each hormone (wide age-range models) or hormonal stage (age-group focused models) with arterial stiffness. PWVao models with cross-sectional approach, were adjusted for age, relative fitness, fat mass and mean arterial pressure, while models with longitudinal approach were adjusted for mean arterial pressure. AIx% models used the same approach for adjustments and were also adjusted for heart rate.ResultsNegative and positive associations with arterial stiffness variables were observed for estradiol and follicle-stimulating hormone, respectively, until adjustment for confounding effect of age. In naturally menstruating women, AIx% was higher at ovulation (B=3.63, p<0.001) compared to the early follicular phase. In COC-users, PWVao was lower during active (B=-0.33 - -0.57, p<0.05) than inactive pills. In menopausal women, HT-users had higher PWVao (B=1.43, p=0.03) than postmenopausal non-HT-users.ConclusionsWhen using wide age-range assessments covering reproductive to menopausal lifespan it is difficult to differentiate age- and hormone-mediated associations, because age-mediated influence on arterial stiffness seemed to overrule potential hormone-mediated influences. However, hormonal status associated differentially with arterial stiffness in age-group focused analyses. Thus, the role of sex hormones cannot be excluded. Further research is warranted to resolve potential hormone-mediated mechanisms affecting arterial elasticity.
Highlights
Cardiovascular (CV) disease is the leading cause of death in postmenopausal women [1]
We investigated the associations of the menstrual cycle, contraception pill cycle and menopausal status with pulse wave velocity (PWV) and augmentation index (AIx)
Our results indicated that sex hormones, especially E2 and follicle-stimulating hormone (FSH), may associate with arterial stiffness
Summary
Cardiovascular (CV) disease is the leading cause of death in postmenopausal women [1]. Lack of sex steroid estradiol (E2), either due to natural or surgical menopause, has been found to associate with an increased risk of CV diseases [2,3,4]. Potential mechanisms include both indirect and direct hormone-mediated effects affecting endothelial and smooth muscle cell signaling as well as the extracellular matrix properties of the vasculature [5, 6]. PWV has been found to be lower in women than in aged-matched men throughout reproductive years since puberty until early postmenopause [12], indicating that PWV may be a valuable marker for the arterial stiffening affected by the availability of the sex hormones. AIx, on the other hand, has been shown to be higher in women compared to men throughout adulthood and to adopt a steeper increasing curve at middle-age in both sexes [13]
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