Carotid Atherosclerosis Progression in Postmenopausal Women Receiving a Mixed Phytoestrogen Regimen: Plausible Parallels with Kronos Early Estrogen Replacement Study
Abstract:This randomized double-blinded, placebo-controlled clinical trial evaluated the progression of intima-media thickness of common carotid artery (cIMT) and the effect of phytoestrogen therapy on atherosclerosis development in early and late postmenopausal women. The 2-year cIMT progression was evaluated in 315 early postmenopausal women aged 40–55 years and in 231 late postmenopausal women aged 60–69 years free of cardiovascular disease. B-mode ultrasound was done at baseline and after 12 and 24 months of follow… Show more
“…The search for markers of subclinical atherosclerosis is one of the fundamental factors in the identification of individuals with a high risk of cardiovascular disease (CVD). The thickness of the intimal-medial layer of the carotid arteries (cIMT) is considered to be a direct non-invasive marker of subclinical atherosclerosis, used in clinical and epidemiological studies to assess the effect of conventional and new cardiovascular risk factors (CVRFs) on the progression of atherosclerotic lesions [2,3]. However, conventional CVRFs are poorly associated with cIMT, which suggests the presence of other factors determining the risk atherosclerosis development [4,5].…”
The search for markers of predisposition to atherosclerosis development is very important for early identification of individuals with a high risk of cardiovascular disease. The aim of the present study was to investigate the association of mitochondrial DNA mutations with carotid intima-media thickness and to determine the impact of mitochondrial heteroplasmy measurements in the prognosis of atherosclerosis development. This cross-sectional, population-based study was conducted in 468 subjects from the Novosibirsk region. It was shown that the mean (carotid intima-media thickness) cIMT correlated with the following mtDNA mutations: m.15059G>A (r = 0.159, p = 0.001), m.12315G>A (r = 0.119; p = 0.011), m.5178C>A (r = 0.114, p = 0.014), and m.3256C>T (r = 0.130, p = 0.011); a negative correlation with mtDNA mutations m.14846G>A (r = −0.111, p = 0.042) and m.13513G>A (r = −0.133, p = 0.004) was observed. In the linear regression analysis, the addition of the set of mtDNA mutations to the conventional cardiovascular risk factors increased the ability to predict the cIMT variability from 17 to 27%. Multi-step linear regression analysis revealed the most important predictors of mean cIMT variability: age, systolic blood pressure, blood levels of total cholesterol, LDL and triglycerides, as well as the mtDNA mutations m.13513G>A, m.15059G>A, m.12315G>A, and m.3256C>T. Thus, a high predictive value of mtDNA mutations for cIMT variability was demonstrated. The association of mutation m.13513G>A and m.14846G>A with a low value of cIMT, demonstrated in several studies, represents a potential for the development of anti-atherosclerotic gene therapy.
“…The search for markers of subclinical atherosclerosis is one of the fundamental factors in the identification of individuals with a high risk of cardiovascular disease (CVD). The thickness of the intimal-medial layer of the carotid arteries (cIMT) is considered to be a direct non-invasive marker of subclinical atherosclerosis, used in clinical and epidemiological studies to assess the effect of conventional and new cardiovascular risk factors (CVRFs) on the progression of atherosclerotic lesions [2,3]. However, conventional CVRFs are poorly associated with cIMT, which suggests the presence of other factors determining the risk atherosclerosis development [4,5].…”
The search for markers of predisposition to atherosclerosis development is very important for early identification of individuals with a high risk of cardiovascular disease. The aim of the present study was to investigate the association of mitochondrial DNA mutations with carotid intima-media thickness and to determine the impact of mitochondrial heteroplasmy measurements in the prognosis of atherosclerosis development. This cross-sectional, population-based study was conducted in 468 subjects from the Novosibirsk region. It was shown that the mean (carotid intima-media thickness) cIMT correlated with the following mtDNA mutations: m.15059G>A (r = 0.159, p = 0.001), m.12315G>A (r = 0.119; p = 0.011), m.5178C>A (r = 0.114, p = 0.014), and m.3256C>T (r = 0.130, p = 0.011); a negative correlation with mtDNA mutations m.14846G>A (r = −0.111, p = 0.042) and m.13513G>A (r = −0.133, p = 0.004) was observed. In the linear regression analysis, the addition of the set of mtDNA mutations to the conventional cardiovascular risk factors increased the ability to predict the cIMT variability from 17 to 27%. Multi-step linear regression analysis revealed the most important predictors of mean cIMT variability: age, systolic blood pressure, blood levels of total cholesterol, LDL and triglycerides, as well as the mtDNA mutations m.13513G>A, m.15059G>A, m.12315G>A, and m.3256C>T. Thus, a high predictive value of mtDNA mutations for cIMT variability was demonstrated. The association of mutation m.13513G>A and m.14846G>A with a low value of cIMT, demonstrated in several studies, represents a potential for the development of anti-atherosclerotic gene therapy.
Postmenopausal women have an increased risk of cardiovascular disease, which is believed to correlate with lower estrogen level. There are conflicting data regarding hormone replacement therapy (HRT) based on the timing of this therapy. After large randomized trials showed no cardiovascular benefit of hormone replacement, estrogen replacement therapy was dramatically reduced even though starting hormone replacement in early postmenopausal period had shown significant benefit. There are hardly any reviews discussing in detail the effect of HRT on cardiovascular system while briefly discussing other effects of this therapy in postmenopausal women. The novelty of this review is the comprehensive discussion of this effect that can help researchers and clinicians to design future research or trials. In this manuscript, the effect of HRT on cardiovascular system in clinical trials and basic science will be reported and potentially erroneous conclusions drawn by various studies will be discussed. Furthermore, various noncardiovascular effect of HRT will be analyzed.
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