The polycystic ovary syndrome (pcos) status and cardiovascular risk in young women

Abstract

<jats:title>Abstract</jats:title><jats:p>The study investigated the presence of early vascular damage and chronic inflammation, and their relationships with hormonal and metabolic parameters in 45 young women with PCOS in comparison with thirty-two healthy age-matched controls. Hormonal and metabolic profiles, high sensitivity C-reactive protein (hsCRP), tumoral necrosis factor-alpha (TNF-α), endothelin-1 (ET-1), brachial flow-mediated vasodilation (FMD) and carotid intima-media thickness (CIMT) were determined in both groups. Compared with the controls, women with PCOS had significantly lower FMD and respectively higher ET-1 levels (p=0.001). No differences were observed between the groups in terms of CIMT or inflammatory markers. In the PCOS group, ET-1 levels were significantly correlated with only testosterone concentrations (r = 0.31, p = 0.037), whereas the hsCRP levels were independently predicted only by body mass index (BMI). Within the total group, the PCOS status was the sole significant predictor of ET-1 levels and the only independent predictor of FMD. In conclusion, there is evidence of endothelial dysfunction associated with increased levels of androgen hormones in young women with PCOS. The combination of endothelial dysfunction and coexistent obesity promoting inflammation contributes to the progression of atherogenesis in PCOS. The PCOS status should be regarded as a predictor marker of cardiovascular risk, along with well-known cardiovascular risk factors.</jats:p>

Androgen Excess as a Major Determinant of Cardiovascular Risk in Women: Evidence from the Polycystic Ovary Syndrome

“…Despite important variability of endothelial injury with patients' phenotype, with the most severe presentation in obese and insulin resistant cases, there is consistent evidence of endothelial dysfunction associated to PCOS status itself, independent of adiposity (13,(16)(17)(18) and even insulin resistance (18). In fact, both FMD and ET-1 correlated to hyperandrogenemia in our study (2), and multiple regression analyses applied to all women revealed for PCOS an independent predictive value on both endothelin-1 and FMD as hemodynamic markers of endothelial dysfunction (2). Nonetheless, as emphasized by the Androgen Excess and Polycystic Ovary Syndrome Society (AE-PCOS) consensus statement (19), association of smoking, obesity, hypertension and especially metabolic syndrome and type 2 diabetes mellitus significantly aggravates endothelial damage and increases vascular risk in women with PCOS.…”

“…Undoubtedly, polycystic ovary syndrome (PCOS) represents the main androgen excess disorder in women (70-80% of cases) featuring clinical and/or biochemical hyperandrogenism, oligo-anovulation and polycystic ovaries appearance at imagistic investigations. A significant proportion of patients with PCOS associates obesity (about 50% of cases), insulin resistance and metabolic syndrome, and emerges as a high-risk group for cardiovascular diseases (2)(3)(4).…”

“…Assessing brachial artery flow-mediated vasodilatation (FMD), a well-documented parameter of endothelial dysfunction, Ilie et al (2) demonstrated markedly reduced FMD values in both overweight/obese and lean young PCOS patients compared to age-matched controls. In the same study population, significantly higher serum endothelin-1 concentrations were obtained in PCOS, also attesting for endothelial dysfunction (2).…”

The Polycystic Ovary Syndrome Status - A Risk Factor for Future Cardiovascular Disease

“…Accumulation of visceral fat leads to insulin resistance, endothelial dysfunction and a proinflammatory status through fat-derived metabolic products, hormones (adiponectin, resistin, FFA) and cytokines (interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-18 (IL-18), tumor necrosis factor-(TNF-). Although many researches (Puder et al, 2005;Cascella et al, 2008;Svendsen et al, 2008, as cited in Penaforte et al, 2011 have advanced the idea that women with PCOS accumulate fat mainly in the upper body compared to controls matched for weight and age (Gambineri et al, 2002, as cited in Penaforte et al, 2011), other studies, including ours, did not detect any differences in total body fat, abdominal fat, visceral fat or trunk fat (Faloia et al, 2004;Glintborg et al, 2006;Barber et al, 2008, as cited in Penaforte et al, 2011Carmina et al, 2007;Ilie et al, 2011), or trunk to peripheral fat (arm fat + leg fat + head fat) ratio in obese women with and without the syndrome (Svendsen et al, 2008, as cited in Penaforte et al, 2011, either.…”

“…The most published data, but not all (Capoglu et al, 2009;Mohlig et al, 2005;Shroff et al, 2007), demonstrate increased levels of hsCRP in women with PCOS (Diamanti- Kandarakis et al, 2006a, b;Talbott et al, 2004b;Tarkun et al, 2004). However, many studies, including our previous report, have demonstrated that in women with PCOS the CRP values are primarily dependent to upon co-existent obesity and fatty mass or insulin resistance (Kelly et al, 2001, as cited in Ilie et al, 2008;Benson et al, 2008, as cited in Repaci et al, 2011;Ilie et al, 2011), rather than to PCOS status per se. Hence, increased serum CRP levels were found in obese and non-obese PCOS compared to controls (Tarkun et al, 2004;Talbott et al, 2004b;Kelly et al, 2001, Orio et al, 2005, as cited in Ilie et al, 2008) with significantly higher values in obese than in non-obese PCOS subjects (Morin-Papunen et al, 2003), decreasing after metformin (Morin-Papunen et al, 2003).…”