Correlation between some metabolic markers of vascular risk and carotid artery intima-media thickness in postmenopausal women
Introduction
Cardiovascular mortality is higher in postmenopausal than fertile women [1], [2], [3], [4], [5] and in the former reaches the incidence observed in men of the same age [2], [5]. Diverse mechanisms have been called upon to explain this phenomenon, and attention has been focused on the elevated concentrations of low density proteins that are very sensitive to oxidation [4], [6]. Moreover, reduced release of endothelial vasodilatating hormones (e.g., prostacyclin) and increased release of vasoconstrictors and proaggregants (e.g., inflammatory leucotriens and thromboxan A2) that occur when estrogen production ceases have been considered relevant [7], [8], [9], [10]. In addition, the variations in the metabolic processes of glucose and insulin metabolism between the pre and postmenopausal periods have been investigated.
A decrease of pancreatic insulin production has been reported in postmenopausal women [11], accompanied by reduced hormone elimination [12] and followed by changes in plasma insulin concentrations [11], [12], [13], [14], [15], [16], [17]. Thus, the menopause is directly associated with metabolic dysfunctions, such as elevated insulin levels and insulin resistance, both of which are considered independent variables of cardiovascular risk [18].
Several studies have underlined that increased carotid wall intima-media thickness can be considered a sensitive marker of cardiovascular risk [19]. The aim of this study was to assess insulin and insulin sensitivity in postmenopausal women and correlate them with vascular wall status and metabolic patterns.
Section snippets
Study series
Thirty one postmenopausal women (minimum duration of menopause 2 years) between 40 and 55 years (mean age 51.2±1.4 years) were recruited for this study on their first outpatients visit to the Menopause Unit at the Department of Obstetrics and Gynecology, Catania University, Italy. None of the women presented diabetes mellitus, arterial hypertension, chronic liver disease, chronic kidney insufficiency or cancer, nor had any ever been on hormone replacement therapy. None of the women were smokers.
Methods
Total cholesterol, LDL cholesterol, HDL cholesterol, plasma triglycerides and plasma fibrinogen concentrations were determined using commercially available kits. Insulin was determined by immunologic test using electrochemical luminescence test “Eglia” (Roche Lab.) and insulin sensitivity (HOMA) by applying the formula: insulin (microU/ml) × glycemia (mmol/l/22.5) [20], [21].
Body mass index (BMI) was also assessed in all subjects.
Ultrasound B mode imaging of the extracranial carotids was
Statistical analysis
Uni and multivariate analysis and correlations were realized for all the parameters under examination using specializes software (Statistica, Stat soft version 5/Windows 97). A value of P<0.05 was considered significant.
Results
The metabolic findings (mean values±S.D.) observed in our postmenopausal series of women are reported in table (Table 1).
Conclusions
The aim of this study on postmenopausal women was to see whether life-threatening cardiovascular risk factors (elevated insulin levels, insulin sensitivity, BMI, triglyerides, LDL) were correlated with carotid artery IMT that has also become a marker of atherosclerosis and is correlated with cardiovascular events [23], [24], [25], [26].
Univariate analysis demonstrated a direct correlation between the metabolic parameters investigated and carotid artery IMT. In fact, there was a direct linear
References (36)
- et al.
The effects of the menopause transition on insulin sensitivity secretion and elimination in non-obese healthy women
Eur. J. Clin. Invest
(1993) - et al.
Asymptomatic atherosclerosis and insulin resistance
Arterioscler. Thromb
(1991) - et al.
Duration of menopause and behaviour of malondialdehyde, lipids, lipoproteins and carotid wall intima-media thickness
Maturitas
(2001) - et al.
Effects of long-term hormone replacement therapy on arterial wall thickness, lipids, lipoproteins and fibrinogen and antithrombin III
Gynecol. Endocrinol
(2001) Sex differences in coronary heart disease. Why are women so superior? The 1995 Ancel Keys Lecture
Circulation
(1997)- et al.
Increased risk of atherosclerosis in women after menopause
BMJ
(1989) Spontaneous premature menopause: ischemic heart disease and serum lipids
Lancet
(1963)et al.Menopause and coronary heart disease. The Framingham study
Ann. Intern. Med
(1978)- et al.
Effects of postmenopausal estrogen replacement on the concentration and metabolism of lipoproteins
N. Engl. J. Med
(1991) - et al.
Decreased mortality in users of estrogen replacement therapy
Arch. Int. Med
(1991) - Van Baal WM, Kooistra T, Stehouwer CD, Cardiovascular disease risk and hormone replacement therapy (HRT): a review...
Menopause and the aging female reproductive system
Endocrinol. Metab. Clin. North Am
Estrogen improves endothelium-dependent flow-mediated vasodilatation in postmenopausal women
Ann. Intern. Med
17 β estradiol augments endothelium-dependent contractions to archidonic acid in rabbit aorta
Am. J. Physiol
Estrogen-induced uterine vasodilatation of nitric oxide synthesis
Am. J. Obstet. Gynecol
Influence of female sex steroids on glucose metabolism and insulin action: human studies
J. Intern. Med
Effect of menopausal status on insulin-stimulated glucose disposal
Diabetes Care
Relationship of regional fat distribution to insulin sensitivity in postmenopausal women
Fertil. Steril
Different sensitivity of glucose and amino acid metabolism to insulin in NIDDM
Diabetes
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