Aim The association of metabolic abnormalities and polycystic ovarian syndrome (PCOS) has been documented, but few studies have focused on cardiovascular risk in these women. The aim of this study was to compare arterial stiffness by using the cardio‐ankle vascular index (CAVI) in PCOS women with controls, and to evaluate whether any clinical or laboratory variables had independent associations with it. Methods A group of 160 women, matched for age and body mass index were recruited. Diagnosis of PCOS was made according to the Rotterdam criteria. Arterial stiffness using CAVI was evaluated in non‐obese young woman, with and without PCOS. Results In the PCOS group (n = 80), 60 cases (75%) had findings of hyperandrogenism, 59 (73.8%) had ovulatory dysfunction, and 70 (87.5%) had an ultrasonographic appearance of polycystic ovaries. Women with PCOS had significantly higher mean CAVI values when compared to subjects without PCOS (5.78 ± 0.64 vs 5.28 ± 0.77, P < 0.001). Multiple regression analysis revealed that androgen excess was associated with increased arterial stiffness, independent of ovulatory dysfunction, polycystic ovaries, body mass index and age. Conclusion This data suggests that vascular compliance is decreased in young women with PCOS. Androgen excess is independently associated with increased arterial stiffness.
Background and aims Interarm blood pressure difference (IABPD) was associated with increased cardiovascular and all-cause mortality in various cohorts previously. In this study, we planned to explore the association between the IABPD obtained with simultaneous measurements in both arms and the risk of mortality over a 2-year follow-up of patients with acute coronary syndrome (ACS). Methods Simultaneous blood pressure (BP) measurements were performed during initial admission in patients with ACS. Systolic ≥10 mmHg and diastolic ≥5 mmHg absolute IABPD was defined as cutoff values in this study. The relationship of IABPD and all-cause mortality was assessed using Kaplan–Meier curves and Cox analysis. Results A total of 532 patients with ACS were included in the study. Mean age of the study participants was 60.1 ± 12.6. Patients included in the study were followed for 23.2 ± 7.2 months (median 25.3, min: 0, max: 28.7 months). Survival was assessed using Kaplan–Meier curves. Patients with systolic IABPD ≥ 10 mmHg and systolic IABPD < 10 mmHg had an average survival time of 25.94 ± 0.84 and 25.92 ± 0.38 months (P = 0.925), respectively. Survival times of diastolic IABPD ≥5 mmHg and diastolic IABPD <5 mmHg were 26.44 ± 0.62 and 25.71 ± 0.41 (P = 0.251) months, respectively. Conclusions In the current study, we did not find a significant association between IABPD and all-cause mortality in patients with ACS in 2-years follow-up. Future studies may be required for further evaluation of the prognostic importance of IABPD in patients with ACS.
Background The aim of the current study is to compare electrocardiographic and echocardiographic changes in patients with severe preeclampsia (PE) and those with uncomplicated pregnancies. Methods This is a case-controlled prospective study consisting of 21 pregnant women with severe preeclampsia and a control group consisting of age- and gestational age-matched 24 healthy pregnant women. All patients underwent electrocardiographic and echocardiographic investigation. Results QRS intervals were shorter and PR intervals were longer in the PE group (QRS duration: 80 (60–120) ms and 80 (40–110) ms, p=0.035; PR duration: 160 (100–240) ms and 120 (80–200) ms, respectively; p=0.046). The left ventricular end-systolic diameters of the patients with severe PE group were significantly larger than the control group (31 (24–36) mm and 30 (24–33) mm, respectively; p=0.05). Similarly, posterior wall thickness values of the PE group were significantly higher compared to the control group (9 (7–11) mm vs. 8 (6–10) mm, respectively; p=0.020). Left ventricular mass (146.63±27.73 g and 128.69±23.25 g, respectively; p=0.033) and relative wall thickness values (0.385±0.054 and 0.349±0.046, respectively; p=0.030) were also higher in the PE group. In addition, patients with early-onset severe PE had significantly a higher left ventricular end-diastolic diameter and volume compared with late-onset PE patients. Conclusions The structural changes detected in the severe PE group suggest a chronic process rather than an acute effect. In addition, diastolic dysfunction and left ventricular remodeling are most marked in patients with severe early-onset PE.
Aim: Recent studies have shown that increased circulating concentrations of fibroblast growth factor 21 (FGF21) are associated with obesity, metabolic disorder, and atherosclerosis. However, the studies which investigate the relationship between serum FGF21 levels and coronary artery disease (CAD) include conflicting data. In this study, we planned to investigate the role of FGF21 in CAD development and CAD severity. Method: Seventy-eight patients with stable angina pectoris (SA) (lesion positive) and 40 control patients (lesion negative) with similar cardiovascular risk factors who underwent coronary angiography were included in the study. Serum FGF21 levels were measured by ELISA method. CAD severity was evaluated by using SYNTAX and GENSINI risk scores. Results: Although there was a statistically significant difference between serum FGF21 levels in the SA and the control groups [101.18 ± 141.62 vs. 47.93 ± 58.74 pg/mL; p = 0.03], no correlation was found between the SYNTAX (r = 0.146 and p = 0.134) and GENSINI (r = 0.211 and p = 0.084) scores with serum FGF21 levels. The SA group had lower serum HDL-C levels (41.57 ± 11.40 vs. 54.90 ± 34.47; p = 0.02). There was a significant and negative relationship between serum FGF21 and serum HDL-C levels in correlation analysis (r = - 0.272; p = 0.026). Conclusion: The serum FGF21 levels are different between SA diagnosed and control patients. FGF21 may be a marker for CAD diagnosis, but not for the evaluation of CAD severity. To the best of our knowledge, this is the first study to evaluate coronary artery disease severity together with a lipid profile.
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