AbstractPolycystic ovary syndrome (PCOS) is possibly the most common endocrinopathy of reproductive age, characterized by hyperandrogenism and oligomenorrhea. Additionally, approximately one-third to one-half of all women and adolescent girls with PCOS tend to fulfill many of the metabolic syndrome criteria, and many view PCOS as a premetabolic syndrome condition, predisposing to a high risk for cardiovascular disease. Endothelial dysfunction, impaired arterial structure, or proinflammatory markers are early features of atherosclerosis, and can be used as surrogate indicators of future coronary artery disease in women with PCOS. However, as the latest studies show, these symptoms are the result of deleterious effects that cardiovascular risk factors, in particular insulin resistance and obesity, produce on the vascular wall, rather than to the presence of PCOS per se. The relationship between hyperandrogenemia and the risk of cardiovascular disease is controversial and needs to be clarified. Further research is warranted to understand the pathogenesis of cardiovascular disease in PCOS, and to identify subtypes of PCOS in which the presence of cardiovascular risk factors may result in increased cardiovascular events, leading to high morbidity or mortality rates caused by cardiovascular disease.
BackgroundWe are hereby investigating for the first time the effect of the association ethinylestradiol30μg-drospirenone 3mg (DRP/EE30μg) plus metformin and weight loss on endothelial status and C-reactive protein (hsCRP) levels in polycystic ovary syndrome (PCOS).Methods25 young women with PCOS (mean age 22.76 ± 0.83 years, body mass index (BMI): 28.44 ± 6.23) who completed the study were prospectively evaluated. The oral contraceptive- DRP/EE30μg (21 days/month) and metformin (1700 mg daily) were administered for 6 months to the PCOS group. Additionally, the 15 overweight and obese patients (BMI > 25 kg/m2) were instructed in a diet of no more than 1500 cal daily. Primary outcome measures were surrogate markers of cardiovascular disease and included endothelial function, i.e. flow-mediated dilatation (FMD) on the brachial artery and endothelin-1 levels, as well as hsCRP concentrations, body composition (measured by whole-body dual-energy X-ray-absorptiometry) and insulin resistance. Variables were assessed at baseline, as well as after our medical intervention.ResultsThe combination between DRP/EE30μg plus metformin combined with weight loss triggered a significant improvement in the FMD values (FMD-PCOSbasal 3.48 ± 1.00 vs FMD-PCOS6 months7.43 ± 1.04, p = 0.033), as well as body composition and insulin insensitivity (p < 0.05). Regarding hsCRP levels, there was no significant intragroup (PCOS6months – PCOSbasal) difference.ConclusionA 6-month course of metformin- DRP/EE30μg (associated with weight loss) improves the endothelial dysfunction in PCOS and shows neutral effects on hsCRP concentrations as an inflammation marker. These data demand for reevaluation of the medical therapy in PCOS, particularly in women with additional metabolic and cardiovascular risk factors (ClinicalTrials.gov Identifier: NCT01459445).
AbstractThe 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.
We consider mitral valve disease requiring surgery in a patient with dextrocardia and situs inversus totalis to be an exceptional finding. The transseptal approach for mitral valve surgery in dextrocardia represents a technical challenge owing to its anatomic particulars. We present the case of a 56-year-old female patient who had been diagnosed with situs inversus totalis in childhood and with chronic atrial fibrillation in adulthood and was under oral anticoagulant treatment. She was referred to our hospital for increasing dyspnea and palpitation. Transthoracic echocardiography detected severe mitral regurgitation associated with moderate tricuspid regurgitation, with normal left and right ventricular function. Contrast chest computed tomography (CT) and preoperative abdominal CT showed both dextrocardia and situs inversus totalis, with normal continuity of the inferior vena cava. Biatrial cannulation was performed with the surgeon standing on the right side of the patient, and mitral valve replacement using a transseptal approach was performed with the surgeon standing on the left side of the patient. In this case report, we emphasize the rarity of mitral valve disease in a patient with dextrocardia and the inherent potential difficulty that can appear in this particular anatomic condition.
Background and aims We studied the feto-placental interface, in Pregnancy Induced Hypertension (PIH), to present his specific structural modifications. Method We have studied the microscopical modifications of 68 placentas obtained after delivery for two equal groups representing mothers with PIH and normotensive. The samples obtained by sections were specifically prepared for the study using three types of histological stains. We used optical microscopy for observing mainly the lumen of spiral arteriole and changes in its intimate and medial tunica. Results We registered the following specific structural modifications in the pregnancies with PIH : fibrosis in the middle of the villosity, fibrinoid necrosis, condensation of stromal connective tissue, syncytial layer agglutinations of the villous or intervillous spaces (nodes, buds, or bridges), thrombosis and/or infarction of the spiral vessels and villous capillary endothelial atheromatosis. Conclusions Our study was done to find a better understanding of the histo-logical changes of the preeclamptic feto-maternal interface concerning his role in PIH. The morphological modifications of the feto-placental interface in the PIH represent a marker of the fetal and postnatal hypoxia/ischemia with an immediate and late impact upon their cerebral development.
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