Obstructive sleep apnea (OSA) is associated with increased cardiovascular (CV) morbidity and mortality. Endocan is a surrogate endothelial dysfunction marker that may be associated with CV risk factors. In this study, we tested whether serum endocan is a biomarker for OSA. Serum endocan levels were measured at baseline in 40 patients with OSA and 40 healthy controls and after 3 months of continuous positive airway pressure (CPAP) treatment in the patients with OSA. All participants were evaluated by full polysomnography. Flow-mediated dilatation (FMD) and carotid intima media thickness (cIMT) were measured in all participants. Endocan levels were significantly higher in patients with OSA than in healthy controls. After adjusting confounders, endocan was a good predictor of OSA. Endocan levels correlated with OSA severity (measured by the apnea–hypopnea index [AHI]). After 3 months of CPAP treatment, endocan levels significantly decreased. Endocan levels were significantly and independently correlated with cIMT and FMD after multiple adjustments. The cIMT and FMD also had significant and independent correlation with AHI. Endocan might be a useful marker for the predisposition of patients with OSA to premature vascular disease.
Objective: We investigated whether post-exercise first minute abnormal heart rate recovery (HRR1) helps to predict the presence and severity of CAD, because of some confounding data. Methods: A cross-sectional, retrospective study was performed. Two hundred individuals were included. Gensini scores and the number of coronary artery involvements were used to evaluate the severity of CAD. Student's t-test, Mann-Whitney U test and chi-square test were used for the analysis continuous and categorical data. Spearman's correlation analysis was used to determine whether there is correlation between Gensini scoring and HRR1. Univariate and multivariate logistic regression were used to determine predictors for abnormal HRR1. ROC curve analysis was performed to detect the best sensitivity and specificity value of HRR1 in predicting CAD presence. Results: Seventy subjects (35%) did not have CAD, and CAD was present in 130 patients (65%). HRR1 ≤21 beats with ROC analysis was determined to be the best cut off point. After adjustment between the two groups in terms of age, gender, diabetes, hypertension, dyslipidemia or smoking (all p>0.05), there was relationship CAD presence and abnormal HRR1 (OR=2.1, 95% CI: 1.1-3.9, p=0.02), but not between CAD severity and HRR1 (r=-0.13, p=0.112). The sensitivity, specificity, and the positive and negative predictive values of abnormal HRR1 ≤21 beats at first minute for predicting CAD presence were 76.1%, 41.3% (AUC=0.588, CI 95%: 0.517-0,657, p=0.039), 70.7% and 48.3%, respectively. Conclusion: In the study abnormal HRR1 predicted the presence of CAD, but not the severity of it. (Anadolu Kardiyol Derg 2014; 14: 351-6)
Statins have multiple effects (also known as pleiotropic effects) on inflammation, plaque stabilization, endothelial function, and hemostasis. We evaluated the effects of rosuvastatin on mean platelet volume (MPV)--a marker for platelet activity--in patients with diabetes mellitus (DM) on rosuvastatin medication. Patients (n = 178) who were to be prescribed high-intensity rosuvastatin were retrospectively enrolled according to their medical records. Baseline and 6-month biochemical tests, automated blood count, cell-volume analysis, and their cardiovascular risk factors were recorded. Rosuvastatin significantly reduced the MPV and the lipid parameters including total cholesterol, triglyceride, and low-density lipoprotein cholesterol (LDL-C). However, there was no correlation between MPV and LDL-C before (r = -.66; P = .383) and after (r = -.112; P = .135) rosuvastatin treatment or between ΔMPV and ΔLDL-C after 40 mg rosuvastatin daily therapy (r = -.155; P = .073). Rosuvastatin significantly decreases the MPV as well as cholesterol levels. The antiplatelet activation properties of high-dose rosuvastatin treatment in patients with DM are not lipid dependent.
To date, there is no available information on the protective effect of onion (Allium cepa) extract (AcE) on cadmium (Cd)-induced cardiotoxicity. The present study was performed to assess the possible antioxidant and anti-apoptotic roles of AcE in Cd-induced cardiotoxicity in rats. A Cd group was injected subcutaneously with CdCl2 dissolved in saline at a dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in the AcE-treated group were given 1 ml of AcE via intragastric intubation for 30 days. The rats intoxicated with Cd for 30 days showed increased tissue malondialdehyde (MDA) levels and decreased levels of the enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in cardiac tissue. AcE attenuated these adverse effects of Cd. After Cd exposure, histological abnormalities were observed, including myofibrillar loss, vacuolization of cytoplasm and irregularity of myofibrils. These histological alterations were effectively attenuated by the treatment with AcE. Furthermore, our data indicate a significant reduction of apoptosis in the cardiomyocytes of the Cd group treated with AcE therapy. Animal studies show antioxidant effects of AcE. But to date, no study reported the effect of AcE on biochemical and histopathological changes due to Cd induced on rat heart. Our study showed that AcE therapy reduced Cd-induced oxidative stress and apoptosis, possibly through its antioxidant and anti-apoptotic activity.
This study investigated whether there is a relationship between atrial fibrillation (AF), mean platelet volume (MPV), and apnea hypopnea index (AHI) in patients who have obstructive sleep apnea syndrome (OSAS). We enrolled patients who had OSAS with either AF or normal sinus rhythm (NSR). We divided 90 patients (aged 50-80 years) into 2 groups: group 1 consisted of 40 patients with OSAS having AF and group 2 of 50 patients with OSAS having NSR. Mean platelet volume was higher in patients with AF than in those with NSR (9.8 ± 0.6 vs 8.4 ± 0.6 fL; P < .001). The MPV and AHI were substantial variables associated with AF (odds ratio [OR] = 2.41; 95% confidence interval [CI], 1.36-5.26; P < .004 and OR = 1.91; 95% CI, 1.26-3.32; P = .02). Elevated MPV value of ≥9.4 fL is associated with AF (70% sensitivity and 63% specificity). More research is needed to establish the clinical relevance of this association.
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