Can dysglycemia in OGTT be predicted by baseline parameters in patients with PCOS?

BackgroundPolycystic ovary syndrome (PCOS) is considered a risk factor for the development of type 2 diabetes mellitus (T2DM). However, which is the most appropriate way to evaluate dysglycemia in women with PCOS and who are at increased risk are as yet unclear. Aim of the studyTo determine the prevalence of T2DM, impaired glucose tolerance (IGT), and impaired fasting glucose (IFG) in PCOS women and potential factors to identify those at risk. Subjects and methodsThe oral glucose tolerance test (OGTT), biochemical/hormonal profile, and ovarian ultrasound data from 1614 Caucasian women with PCOS and 362 controls were analyzed in this cross-sectional multicenter study. The data were categorized according to age and BMI. ResultsDysglycemia (T2DM, IGT, and IFG according to World Health Organization criteria) was more frequent in the PCOS group compared to controls: 2.2% vs 0.8%, P = 0.04; 9.5% vs 7.4%, P = 0.038; 14.2% vs 9.1%, P = 0.002, respectively. OGTT was essential for T2DM diagnosis, since in 88% of them basal glucose values were inconclusive for diagnosis. The presence of either T2DM or IFG was irrespective of age (P = 0.54) and BMI (P = 0.32), although the latter was associated with IGT (P = 0.021). There was no impact of age and BMI status on the prevalence of T2DM or IFG. Regression analysis revealed a role for age, BMI, fat deposition, androgens, and insulin resistance for dysglycemia. However, none of the factors prevailed as a useful marker employed in clinical practice. ConclusionsOne-third of our cohort of PCOS women with either T2DM or IGT displayed normal fasting glucose values but without confirming any specific predictor for dysglycemic condition. Hence, the evaluation of glycemic status using OGTT in all women with PCOS is strongly supported

Impact of spironolactone on vascular, myocardial, and functional parameters in untreated patients with a hypertensive response to exercise

Background Although a hypertensive response to exercise (HRE) is associated with cardiac risk and masked hypertension (MHT), its mechanisms and appropriate treatment remain unclear. We investigated spironolactone as a treatment for abnormal vascular and myocardial stiffness in HRE. Methods In this randomized, double-blind, placebo-controlled study of 115 patients (54±9 years, 57% men) with an HRE (≥210/105mm Hg in men; ≥190/105mm Hg in women) but no prior history of hypertension or myocardial ischemia, MHT prevalence was 40%. Patients were randomized to spironolactone 25mg daily (n = 58) or placebo (n = 57) and underwent evaluation at baseline and 3 months with exercise echocardiography, VO pulse wave velocity (PWV), exercise and central blood pressure (BP), and 24-hour ambulatory BP. Changes in left ventricular mass index (LVMI), Doppler-derived E/e ratio (LV filling pressure), and myocardial strain were assessed. Results Baseline 24-hour systolic BP (SBP) was 133±10mm Hg and peak-exercise SBP was 219±16mm Hg. Peak systolic strain (0.3±3.6% vs.-0.1±3.2, P = 0.56), E/e (-1.1±2.3 vs.-0.6±1.7, P = 0.30), VO (0.4±4.9 vs.-0.9±4.1ml/kg/min, P = 0.15), and adjusted PWV did not significantly change with treatment, despite reduction in exercise SBP, 24-hour SBP, and LVMI. The change in exercise E/e was of borderline significance (-0.3±2.4 vs. 0.8±2.8, P = 0.06) and became significant after adjustment for baseline differences (P = 0.01). Patients with higher LVMI significantly increased VO (1.1±5.6 vs.-2.4±4.4ml/kg/min, P < 0.05) and reduced exercise E/e (-0.7±2.7 vs. 1.9±2.8, P < 0.05). Conclusions In HRE patients without previous hypertension, short-term spironolactone reduced exercise BP, 24-hour ambulatory BP, LVMI, and E/e but did not significantly alter exercise capacity or myocardial strain

Improvement of left ventricular function by lifestyle intervention in obesity: contributions of weight loss and reduced insulin resistance

Weight excess and insulin resistance mediate the link between obesity and left ventricular dysfunction. We investigated the effect and mechanisms of lifestyle modification on left ventricular function changes in obese patients