Objective:We examined the change in apelin concentration and its relationship with left ventricular diastolic function in patients treated for hypertension.Methods:Ninety treatment-naive patients with newly diagnosed hypertension and 33 age- and sex-matched control subjects were prospectively enrolled. Patients with hypertension were randomized to treatment either with telmisartan 80 mg or amlodipine 10 mg. Apelin concentration was measured and echocardiography was performed at baseline and after 1 month of treatment.Results:The data of 77 patients and 33 controls were analyzed. Mean age, gender, baseline blood pressure, apelin levels, and echocardiographic measurements were similar between the treatment groups (p>0.05 for all). Apelin concentration was significantly lower in patients with hypertension than in controls. There was a significant increase in apelin level after 1 month of treatment in both groups (0.32±0.17 vs. 0.38±0.17 ng/dL in telmisartan group, p=0.009, and 0.27±0.13 vs. 0.34±0.18 ng/dL in amlodipine group, p=0.013). Diastolic function improved significantly in both groups (p<0.05) but was not significantly associated with change in apelin concentration.Conclusion:Apelin concentration increased significantly after 1 month of effective treatment with telmisartan or amlodipine to a similar extent. Change in apelin concentration was not associated with improvement in diastolic function.

Background There are limited studies on the effects of asthma on cardiac function. Right ventricular dysfunction and pulmonary hypertension are cardiovascular complications that may be seen in advanced stages of the disease. Pulmonary artery stiffness (PAS), is a promising, relatively new echocardiographic index that has been reported to increase in right ventricular failure, providing information about pulmonary vascular bed. Aim In this study, we aimed to evaluate PAS, a marker of pulmonary artery elasticity, in adult‐onset asthma. Methods Ninety‐nine nonsmokers who had a new asthma diagnosis between the ages of 18 and 65 years and 97 healthy controls with similar age and sex distribution were included in the study. PAS was calculated by dividing the maximal frequency shift of pulmonary flow (MFS) in pulmonary acceleration time (PAT). Results Clinical and demographic characteristics of both groups were similar (P ˃ 0.05). PAS values were higher in the asthma group than in the control group (25.2 ± 4.5 vs 22.4 ± 4.1, P ˂0.001). TAPSE was lower in the case group (24.9 ± 2.0 vs 25.5 ± 2.1, P = 0.043), while RV MPI was higher (0.36 ± 0.07 vs 0.32 ± 0.06, P ˂0.001). In the multivariate linear regression analysis, RV MPI, RV Em, and TAPSE variables were independent predictors of PAS. Conclusion In our study, PAS values were higher in patients with newly diagnosed adult asthma and we found a significant weak correlation between PAS values and subclinical right ventricular dysfunction.

Background: Growing evidence suggests that endothelial dysfunction plays a key role in the pathophysiology of Slow Coronary Flow (SCF). This study investigated the association between endothelial biomarkers endocan and soluble Thrombomodulin (sTM) and SCF. Methods: The study population consisted of 89 subjects (54 patients with SCF and 35 controls). Coronary flow rate was assessed using the Thrombolysis in Myocardial Infarction (TIMI) Frame Count (TFC) method. The serum endocan and sTM levels of all subjects were analysed. Results: Significantly higher endocan levels (1.14 ± 0.22 vs. 0.96 ± 0.32 ng/ml; p=0.009) and sTM levels (657.06 ± 198.18 vs. 592.76 ± 128.45 pg/ml; p=0.119) were observed in the SCF group relative to the control group. A positive correlation was detected between endocan and TFC (r=0.563; p=0.016). Multivariate logistic regression analysis revealed endocan as a predictor of SCF. Conclusions: The endocan level in SCF patients was significantly higher than in controls and the sTM level was also increased, although the difference was not significant. These results suggest that endocan may serve as a biomarker to predict SCF.

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Objective: Recent studies have focused on the probable role of oxidative stress in cardiovascular diseases. We aimed to assess the oxidant/antioxidant biomarkers in coronary slow flow (CSF). Methods: The study included 51 subjects with CSF and age and sex matched 32 controls. Detailed anamnesis of the patients in the study was taken and routine physical examinations were performed. Routine biochemical blood tests were analyzed. Total oxidative status (TOS), oxidative stress index (OSI) and lipid hydroxyperoxide (LOOH) levels as oxidant biomarkers; paraoxonase (PON1), ceruloplasmin (CP), free sulphydryl (SH) groups, and total antioxidant capacity (TAS) levels as antioxidant biomarkers were studied. Results: Baseline demographic characteristics of the study population did not differ significantly between groups.TOS, OSI and LOOH concentrations were higher in study group than in control group. However, there was no significant difference detected in levels of TAS, PON1, SH and CP. Multivariate logistic regression analysis revealed that TOS, hsCRP and smoking were indepedent risk factors of CSF. Conclusions: Although there was not any significant difference in antioxidant biomarkers (TAS, PON1, SH and CP) in CSF patients, we detected increased TOS, OSI and LOOH levels which have oxidant properties. These data supported the possible involvement of oxidative stress in pathogenesis of CSF as previous studies reported. doi: https://doi.org/10.12669/pjms.35.3.162 How to cite this:Baysal SS, Koc S. Oxidant-Antioxidant balance in patients with coronary slow flow. Pak J Med Sci. 2019;35(3):---------.  doi: https://doi.org/10.12669/pjms.35.3.162 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.