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Objective: Cardiac resynchronization therapy (CRT) induces structural and electrical reverse remodeling of the failing heart. However, the association between native QRS narrowing and cardiac fibrosis markers has not been investigated in patients with an implanted CRT device. Methods: A total of 41 symptomatic patients diagnosed with systolic heart failure who underwent CRT implantation were included in this study. Electrocardiogram findings and cardiac fibrosis marker levels [galectin-3, growth-differentiation factor-15 (GDF-15) and procollagen III N-terminal propeptide (P3TD)] were collected before and 12 months after initiation of biventricular pacing. Reverse electrical remodeling was defined as a decrease in 12-month intrinsic QRS (iQRS) duration by ≥20 milliseconds after CRT implantation. Results: The median QRS duration decreased from 155 milliseconds (interquartile range [IQR]: 142–178 milliseconds) before CRT to 142 milliseconds (IQR: 130–161 milliseconds) (p=0.001) after 12 months of CRT. According to the predefined criteria, electrical remodeling was detected in 16 (39.0%) patients. The median galectin-3, GDF-15, and P3TD levels were significantly decreased after CRT implantation in patients with electrical remodeling [27.65 ng/mL (IQR: 24.4–35.2 ng/mL) vs 23.00 ng/mL (IQR: 16.0-36.7 ng/mL), p=0.017; 3104 pg/mL (IQR: 2923–4825 pg/mL) vs 2276 pg/mL (IQR: 1294–3209 pg/mL), p=0.002; 0.43 ng/mL (IQR: 0.23–0.64) vs 0.15 ng/mL (IQR: 0.04–0.29 ng/mL), p=0.034, respectively]. The galectin-3, GDF-15, and P3TD levels were not significantly changed in patients without electrical remodeling [26.80 ng/mL (IQR: 23.9–31.5 ng/mL) vs 28.80 ng/mL (IQR: 23.0–34.8 ng/mL), p=0.211; 4221 pg/mL (IQR: 2709–4995 pg/mL) vs 3035 pg/mL (IQR: 2038–4872 pg/mL), p=0.143; and 0.34 ng/mL (IQR: 0.11–0.68 ng/mL) vs 0.21 ng/mL (IQR: 0.09–0.37 ng/mL), p=0.112, respectively]. Conclusion: The results from the small sample used in this study indicated that electrical reverse remodeling after CRT was associated with a decrease in cardiac fibrosis.

The aim of the study was to measure platelet-activating factor acetyl hydrolase (PAF-AH) and paraoxonase (PON1) enzyme activity levels in patients with high Psa values to compare with healthy peers and also to determine the efficacy of these parameters in predicting pathologic results of patients with high Psa values. This study included 66 patients with Psa value > 4 ng/dl (Group 1) and 44 patients with Psa

Objective: The aim of this study was to examine the relationship between vitamin D levels in patients with heart failure (HF) and response to cardiac resynchronization therapy (CRT). Methods: We studied 57 patients (mean age: 60.47+-13.09 years) with New York Heart Association Class II or III heart failure, QRS duration ≥120 milliseconds, and ejection fraction 15% decrease in left ventricular end-systolic volume at 6 months compared with baseline measurements. Vitamin D levels were evaluated before CRT implantation with ELISA. Results: Of the 57 patients, 34 patients (59.6%) were classified as responders and 23 patients (40.4%) were classified as non-responders. Baseline features, laboratory findings, and echocardiographic characteristics were nearly the same in both groups. High vitamin D level was detected in responder group compared to non-responder group (26.17+-7.5 vs 21.15+-5.9; p=0.009). Age, hypertension, diabetes mellitus, ischemic cardiomyopathy, QRS morphology and duration, and levels of B-type natriuretic peptide (BNP) and vitamin D were associated with CRT response in our study population. In multivariate regression analysis, preimplantation QRS duration, and BNP and vitamin D levels remained independent predictors (QRS duration Odds ratio [OR]: 1.047, CI: 1.019–1.417, p=0.006; BNP OR: 0.997, 95% CI: 0.994–0.999, p=0.029; vitamin D OR: 1.121, 95% CI: 1.011–1.242, p=0.030). Conclusion: In the present study, preimplantation level of vitamin D was found to be predictor of response to CRT, independent of BNP.

Aim: Psoriasis is a skin disease with metabolic and cardiac comorbidities. Adropin is a peptide hormone which is thought to play arole in metabolic diseases, energy homeostasis, endothelial function and cardiac diseases in recent years. In this study, we aimed toevaluate adropin levels in psoriasis patientsMaterials and Methods: The study included 51 plaque psoriasis patients aged 18-65 years who had no systemic disease and hadnot received systemic treatment in the last three months and 37 healthy controls matched by sex, age and body mass index (BMI).Serum adropin, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), andtriglyceride (TG), fasting blood glucose (FBG), fasting serum insulin, BMI, systolic blood pressure (SBP) and diastolic blood pressure(DBP) values were recorded.Results: Serum adropin level was 73.04 ± 46.21 pg / ml in the patient group. In the control group, serum adropin level was 77.26 ±43.69 pg / ml. Serum adropin levels were lower in the patient group, but this was not statistically significant (p = 0.667). PASI valuewas negatively correlated with serum adropin level. There was no correlation between serum adropin level and other variables.Insulin level, Homa-IR level, systolic and diastolic pressure were significantly higher in the patient group (p

Background and Objective Mechanical ventilation (MV) can induce oxidative stress, which plays a critical role in pulmonary injury in intubated neonates. Ischemia-modified albumin (IMA)—a variant of human serum albumin—is a novel biomarker of myocardial ischemia that occurs due to reactive oxygen species during ischemic insult. This study aimed to investigate IMA production due to oxidative stress induced during MV in neonates. Materials and Methods This study included 17 neonates that were ventilated using synchronized intermittent mechanical ventilation (SIMV; SIMV group) and 20 neonates ventilated using continuous positive airway pressure (CPAP; CPAP group). Blood samples were collected from each neonate during ventilation support and following cessation of ventilation support. Total antioxidant capacity (TAC) and total oxidant status (TOS) were measured using the Erel method. IMA was measured via an enzyme-linked immunosorbent assay kit (Cusabio Biotech Co., Ltd., Wuhan, China). The oxidant stress index (OSI) was calculated as OSI = TOS/TAC. Statistical analysis was performed using SPSS v.18.0 (SPSS Inc., Chicago, IL) for Windows. Results Among the neonates included in the study, mean gestational age was 34.7 ± 3.8 weeks, mean birth weight was 2,553 ± 904 g, and 54% were premature. There were not any significant differences in mean gestational age or birth weight between the SIMV and CPAP groups. Among the neonates in both the groups, mean IMA, TOS, and OSI levels were significantly higher during ventilation support (102.2 ± 9.3 IU mL–1, 15.5 ± 1.3 µmol H2O2 equivalent L–1, and 0.85 ± 0.22 arbitrary units [ABU], respectively), as compared with following cessation of ventilation support (82.9 ± 11.9 IU mL–1, 13.4 ± 1.3 µmol H2O2 equivalent L–1, and 0.64 ± 0.14 ABU, respectively) (p = 0.001). Among all the neonates in the study, mean TAC was significantly lower during ventilation support than the postventilation support (1.82 ± 0.28 mmol 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid [Trolox] equivalent L–1 vs. 2.16 ± 0.31 mmol Trolox equivalent L–1) (p = 0.001). There were no significant differences in mean TAC, OSI, or IMA levels between the SIMV and CPAP groups. The mean TOS level during ventilation support and the mean difference in TOS between during and postventilation support was significantly greater in the CPAP group than in the SIMV group. There were no significant relationships between the mean TOS, TAC, OSI, or IMA levels, and gestational age of the neonates. Conclusion SIMV and CPAP activated the oxidative stress and increased the IMA level in neonates; therefore, measurement of IMA and oxidant markers may be useful in the follow-up of lung injury in neonates due to ventilation support. Additional prospective studies are needed to compare the effects of various ventilation methods on oxidative stress and the IMA level in neonates.

Background: Several studies have investigated the effects of cardiac resynchronization therapy (CRT) on heart failure (HF), but none have evaluated the pathophysiological pathways involved in a single group of patients. Therefore, this study aims to assess the long-term effects of CRT on six different patho­physiological pathways involved in the process of HF by the use of surrogate biomarkers. Methods: In a group 44 patients with HF, six groups of biomarkers were measured, both at baseline and 1 year after CRT implantation: inflammation (interleukin [IL]-4, IL-6, tumor necrosis fac­tor [TNF]-a, high sensitive C-reactive protein [hsCRP]); oxidative stress (myeloperoxidase [MPO], oxidized low-density lipoprotein [oxLDL], uric acid); extracellular matrix (ECM) remodeling (matrix metalloproteinase [MMP]-2 and -9, galectin-3, procollagen III N-terminal propeptide [prokol-3NT]); neurohormonal pathways (endothelin-1, chromogranin-A); myocyte injury (troponin T, creatine kinase MB fraction [CK-MB]), myocyte stress (B-type natriuretic peptide [BNP]). CRT responders were de­fined as patients with ≥ 15% reduction in left ventricular end-systolic volume at 12 months post-CRT. Results: At 1-year follow-up, 72.7% (n = 32) of the patients were categorized as CRT responders. In these patients, the levels of IL-6, MPO, oxLDL, MMP-2, galectin-3, troponin T, and BNP were significantly reduced as compared to baseline values. While the biomarkers for myocyte stress (effect size = 0.357; p = 0.001), ECM remodeling (effect size = 0.343; p = 0.015) and oxidative stress (effect size = 0.247; p = 0.039) showed a significant change in the CRT responders during follow-up, the biomarkers for other pathophysiological pathways did not show a significant alteration. Conclusions: In the present study, a significant reduction was only observed in the biomarkers of myo­cardial stress, ECM remodeling, and oxidative stress among all the CRT responder subjects. (Cardiol J 2018; 25, 1: 42–51)

Yucel, Aykan/0000-0002-5888-692X WOS: 000287480300040 PubMed: 21193188 Objective: To evaluate endothelial function via serum asymmetric dimethylarginine (ADMA) levels, paraoxonase 1 (PON1) activity, and brachial artery flow-mediated dilatation (FMD) in women with polycystic ovary syndrome (PCOS). Design: Prospective case-control study. Setting: University hospital. Patient(s): Thirty patients with PCOS with a mean age of 24.33 +/- 4.50 years and 30 healthy controls matched for body mass index (BMI) and age. Intervention(s): Endothelial function was assessed biochemically with serum ADMA levels and serum PON1 activity and functionally with brachial artery FMD by ultrasonography. Main Outcome Measure(s): Serum ADMA levels, serum PON1 activity, brachial artery FMD, hormonal and biochemical parameters. Result(s): Patients with PCOS had higher levels of free testosterone and insulin, and higher waist-hip ratio and Ferriman Gallwey scores when compared with the controls. Fasting glucose and homeostasis model assessment of insulin resistance were not different between the groups. There was no statistically significant difference in ADMA levels between two groups. Serum PON1 activity and brachial artery FMD were statistically significantly lower in women with PCOS. There was negative correlation between ADMA and PON1 in patients with PCOS. Conclusion(s): Serum PON1 activity and brachial artery FMD, as markers of endothelial dysfunction and cardiovascular risk, were statistically significantly lower in women with PCOS compared with healthy controls matched for age and BMI. Endothelial dysfunction may be seen at earlier ages in patients with PCOS. (Fertil Steril (R) 2011;95:1067-72. (C) 2011 by American Society for Reproductive Medicine.)

Aim: Ibuprofen is an older agent, but its intravenous form is a very new drug. The aim of this study was to investigate whether intravenous form of ibuprofen has protective effect against renal ischemia reperfusion injury at two different doses such as 10-30 mg/kg.Material and Methods: Thirty-two Wistar Albino type female rats were divided into 4 groups as sham, control, IBU-10, IBU-30. In the control group, 60 minutes renal ischemia and 60 minutes reperfusion were performed. In the ibuprofen groups, at the 45th minute of ischemia, ibuprofen was administered in different doses at 10 mg/kg and 30 mg/kg through intraperitoneally. After 60 minutes of ischemia, the clamps were opened. Renal tissue and blood samples were collected from the rats at the end of the reperfusion period. Serum TAS, TOS and prolidase enzyme levels were analyzed in plasma samples. Both histopathological and biochemical evaluations were performed with kidney tissue. Results: In the groups given intravenous ibuprofen, less cellular damage was always detected. Cellular damage indicators were significantly lower in the treated rats than in the control group. Serum and tissue prolidase values were different between groups (p0.001, p0.001). Serum TAS and TOS levels were also different between groups (p=0.001, p=0.003). Serum OSI levels were also different between groups (p=0.017).Conclusion: The biochemical and pathological results obtained in our study suggest that intravenous ibuprofen, has a protective effect against kidney damage. We believe that our study will shed light on future clinical prospective studies.

Objective: Determination of the factors associated with the intensive care unit (ICU) prognosis and mortality has important role in the clinical follow-up of the patients. Definition of novel biomarkers, beside older biomarkers available for evaluation of the outcome of these patients has been proposed. Platelet-activating factor acetylhydrolase (PAF-AH) is an enzyme that inactivates the platelet-activating factor. A reduction in the level of the PAF-AH has been demonstrated during systemic inflammation and multiple organ failure. This research aims to determine whether measurement of PAF-AH enzyme activity in ICUs can be used as a prognostic indicator like conventional biomarkers.Methods: Eighty five adult patients have been included. Following data have been recorded: preliminary C-reactive protein (CRP), lactate, albumin and PAF-AH values, APACHE II scores and discharge forms from ICU. Patients were divided in two groups with respect to APACHE II values: Group 1 (1-19) and Group 2 (≥20).Results: Observed mortality was 51.2%. In the APACHE II Group 2 patients, the values of CRP (p=0.001) and lactate (p=0.040) were significanty high, and the values of PAF-AH (p=0.008) and albumin (p=0.001) were significantly low. A statistically significant difference was found between PAF-AH values of exitus and alive patients (p=0.001). According to ROC analysis, the sensitivity and specificity of predicting mortality was 70.5% and 70.7% for CRP, 63.6% and 70.7% for lactate, 90.2% and 61.4% for albumin and 63.6% and 70% PAF-AH, respectively.Conclusion: Our study demonstrated that, in predicting the ICU mortality risk, sensitivity of the PAF-AH is similar to the sensitivity of the lactate, and specificity of the PAF-AH is better than that of the albumin. According to our results, PAF-AH can be included in the novel biomarkers.

Objective: Paraoxonase1 (PON1), exhibits both esterase activity (PON1-AREase) and homocysteine thiolactonase activity (PON1-HTLase) which respectively prevent LDL oxidation and detoxify homocysteine thiolactone (HTL). Platelet-activating factor-acetylhydrolase (PAF-AH) is an antioxidant enzyme preventing LDL oxidation by hydrolysis of oxidized phospholipids. Both of these enzymes exhibit a proatherogenic role. ADMA is an endogenous inhibitor of nitric oxide (NO) synthesis causing endothelial dysfunction. The aim was to compare non-obese PCOS patients with a BMI matched control group using the following characteristics: serum PON1-HTLase, ADMA, PAF-AH, and lipid and hormonal parameters. Results: 77 women with PCOS and 25 healthy subject were recruited for this study, The controls were non-obese BMI and age matched with the patients. There were no significant differences with respect to age, BMI, FSH, free testosterone, DHEA, androstenadion, total cholesterol, triglycerides, HDL, LDL, VLDL, fasting glucose/insulin ratio and HOMA-IR among the groups (p > 0.05). However, total testosterone and fasting glucose levels were significantly higher in the PCOS group (p < 0.05). On the other hand, PON1-HTLase levels (39.6 +/- 5.77 vs. 33.8 +/- 8.2, p = 0.02) were significantly lower in the PCOS group while ADMA levels (1.14 +/- 0.6 vs. 3.37 +/- 6.4, p = 0.004) were significantly higher in the PCOS group. However, there was no significant difference in PAF-AH activity among the groups Conclusions: Decreased PON1-HTLase and increased ADMA levels might be a relevant marker for the development of future atherosclerotic heart disease (AHD) in non-obese PCOS patients. Further studies are needed to confirm our results.

Aim: Paraoxonase-1 (PON1) is an antioxidant enzyme located in high density lipoprotein (HDL). PON1 was defined as a protective factor against atherosclerosis. The aim of this study was to investigate the possible relationship between serum paraoxonase (PONase), homocysteine thiolactonase (HTase) activities and PON1 Q192R polymorphism, and the extent and severity of atherosclerosis. Methods: Blood specimens were collected from 142 individuals who had no coronary artery lesions angiographically (control group) and 128 individuals who had angiographically documented coronary artery disease of several degrees (patient group). The extent and severity of arterial lesions were evaluated by the Gensini scoring system. PONase and HTase activities were measured in serum using a spectrophotometric method. PON1 Q192R polymorphism was evaluated using PCR-RFLP after DNA isolation from blood. Results: Serum PONase and HTase activities were significantly lower in the patient group than in healthy controls (135.7 +/- 56.0 U/mL vs 153.8 +/- 62.0 U/mL, p < 0.05; 36.0 +/- 6.1 U/mL vs 43.0 +/- 4.04 U/mL, p < 0.01; respectively). In the patient group, there was a negative correlation between PONase, HTase activities and the Gensini score (r = -0.168, p = 0.039; r = -0.164, p = 0.006, respectively). In both groups, there was no significant difference in the distribution of PON1 Q192R polymorphism. In the patient group, the distribution of Gensini scores according to genotypes was not significant. Conclusion: It has been concluded that serum PONase and HTase activities might be a more relevant marker than PON1 genotype in evaluating the extent and severity of atherosclerosis.

Estrogen replacement therapy alters the lipid profiles favorably for delaying atherosclerosis in postmenopausal women. The effects of estrogen plus progesterone combination therapy on lipids are controversial. This study was designed to evaluate the effect of female sex hormones on lipids and lipoproteins and to clarify the influence of progesterone on the effect of estrogen in postmenopausal women. Of the 60 postmenopausal women admitted to our menopause clinic, 40 had intact uterus and received continuous 0.625 mg conjugated equine estrogen (CEE) plus 2.5 mg medroxyprogesterone acetate (MPA), whereas the remaining 20 were hysterectomized and received 0.625 mg CEE daily. To assess the alterations in lipids and lipoproteins during menopause, 45 healthy premenopausal women were investigated. Lipid and lipoprotein levels were assessed in each subject at baseline and at the 6th and 18th months of therapy. In menopause, a shift towards more atherogenic lipid and lipoprotein profiles than those of the premenopausal state was found. Following 18 months of treatment, both regimens reduced total cholesterol (TC) levels as compared with the baseline (6.4 vs. 6.9% in the CEE/MPA and CEE groups, respectively). The CEE group had a more pronounced increase in high-density lipoprotein (HDL) cholesterol than the CEE/MPA group (10.3 vs. 8.8%, respectively). Both groups displayed reduced TC, low-density lipoprotein (LDL) cholesterol and apolipoprotein-B (ApoB) concentrations, whereas triglycerides increased, with a greater tendency to increase in the CEE/MPA group at the end of the trial. Also, the lipoprotein (a) [Lp(a)] levels decreased significantly (27.6 vs. 24.5% in the CEE/MPA and CEE groups, respectively). This decrease was more pronounced in subjects with a relatively higher basal Lp(a) concentration. Both treatment regimens caused positive alterations in the lipid and lipoprotein profiles. This association might play a pivotal role in the postmenopausal increases in atherosclerotic diseases and cardioprotective effect of estrogen in postmenopausal women.

Objective: Paraoxonase-2 (PON2) is a cellular enzyme that has antioxidant properties similar to PON1, an HDL-associated serum enzyme playing an important role in the prevention of atherosclerosis. 1. The aim of this study is to investigate whether serum paraoxonase activity and PON2 Ser311Cys polymorphism are related to coronary artery disease and the extent of atherosclerosis. Methods: Blood specimens were collected from 131 individuals who had no coronary artery lesions angiographically and 110 individuals who had angiographically-documented coronary artery disease at several degrees. The extent and severity of arterial lesions were evaluated by Gensini scoring system. Paraoxonase and arylesterase activities were measured in serum using a spectrophotometric method. PON2 Ser311Cys polymorphism was evaluated using PCR-RFLP after DNA isolation from samples. Results: Serum paraoxonase and arylesterase activities were significantly lower in the patient group than controls (respectively, 135.6±55.4 U/ml vs 152.9±61.2 U/ml, p