The effect of Folic Acid, B12, D, and E Vitamins and Melatonin levels in the follicular fluid taken by the Intracytoplasmic Sperm Injection method on pregnancy.

Objective: It has been demonstrated that the composition of the follicular fluid and many internal/external factors affect success in subfertile couples undergoing intracytoplasmic sperm injection (ICSI). We examined the effect of folic acid, B12, D, and E vitamins and melatonin values in follicular fluid on pregnancy in women with low, normal, and high ovarian reserves who underwent ICSI. Methods: Our study was conducted at Samsun Medical Park Hospital between January 2021 and February 2022. Follicular fluid induction samples were taken from 96 infertile women with low, normal, and high ovarian reserve, and ICSI was applied. Folic acid, B12, D, and E vitamins and melatonin levels were measured in follicular fluid samples by ELISA method. Statistical analyzes were done with SPSS, and ROC curve analyses were used. Results: Nine people with poor reserve, 19 people with normal reserve and 14 people with high reserve became pregnant. Folic acid, Vitamin-D, B12, E and melatonin levels were lower in those with poor ovarian reserve than in those with normal and high ovarian reserve (p<0.05). According to the pregnancy test, the probability of pregnancy was 43,783 times higher with high levels of folic acid, while it was 8,096 times higher for vitamin D. While vitamin B12 levels were 31,474 times more likely to be pregnancies, vitamin E levels were 35,227 times higher. For melatonin, the values showed that the probability of pregnancy increased by 11,564 times. Conclusions: High antioxidants may increase the likelihood of conception in infertile women undergoing ICSI. Therefore, couples who will be treated should be advised to increase these markers, especially melatonin in the follicular fluid.

Effect of candesartan treatment on echocardiographic indices of cardiac remodeling in post-myocardial infarction patients.

OBJECTIVE: Myocardial infarction has unfavorable effect on structural and functional properties of the myocardium, referred to as cardiac remodeling. Left ventricular mass, left ventricular mass index, and relative wall thickness are important predictors of cardiac remodeling. In this study, we investigated the effect of candesartan treatment in comparison with zofenopril treatment on echocardiographic indices of cardiac remodeling in post myocardial infarction patients. MATERIAL AND METHODS: In this prospective study, patients who underwent successful percutaneous coronary intervention were randomly assigned to a candesartan or zofenopril treatment. After randomization, echocardiographic indices of cardiac remodeling including left ventricular mass, left ventricular mass index, and relative wall thickness were evaluated before the start of treatment along with 1- and 6-month follow-ups. RESULTS: According to our study, candesartan group showed significant reduction of estimated left ventricular mass and left ventricular mass index at 6-month follow-up visit compared to baseline values (199.53±38.51 g vs. 212.69±40.82 g; 99.05 g/m2 (90.00-116.5) vs. 106.0 g/m2 (96.0∼123.00), p<0.05, respectively). This trend was also observed in zofenopril group during the 6-month period (201.22±40.07 g vs. 207.52±41.61 g; 101.0 g/m2 (92.25-111.75.0) vs. 104.50 g/m2 (95.0∼116.75), p<0.05, respectively). Although both classes of drugs had favorable effects on post-myocardial infarction cardiac remodeling, the absolute benefit was more prominent in candesartan group as compared to zofenopril group (p<0.05). CONCLUSION: Our results suggest that candesartan treatment following myocardial infarction may potentially be useful in terms of improving post-myocardial infarction cardiac remodeling.

Effect of candesartan treatment on echocardiographic indices of cardiac remodeling in post-myocardial infarction patients

SUMMARY Objective: Myocardial infarction has unfavorable effect on structural and functional properties of the myocardium, referred to as cardiac remodeling. Left ventricular mass, left ventricular mass index, and relative wall thickness are important predictors of cardiac remodeling. In this study, we investigated the effect of candesartan treatment in comparison with zofenopril treatment on echocardiographic indices of cardiac remodeling in post myocardial infarction patients. Material and Methods: In this prospective study, patients who underwent successful percutaneous coronary intervention were randomly assigned to a candesartan or zofenopril treatment. After randomization, echocardiographic indices of cardiac remodeling including left ventricular mass, left ventricular mass index, and relative wall thickness were evaluated before the start of treatment along with 1- and 6-month follow-ups. Results: According to our study, candesartan group showed significant reduction of estimated left ventricular mass and left ventricular mass index at 6-month follow-up visit compared to baseline values (199.53±38.51 g vs. 212.69±40.82 g; 99.05 g/m2 (90.00-116.5) vs. 106.0 g/m2 (96.0∼123.00), p<0.05, respectively). This trend was also observed in zofenopril group during the 6-month period (201.22±40.07 g vs. 207.52±41.61 g; 101.0 g/m2 (92.25-111.75.0) vs. 104.50 g/m2 (95.0∼116.75), p<0.05, respectively). Although both classes of drugs had favorable effects on post-myocardial infarction cardiac remodeling, the absolute benefit was more prominent in candesartan group as compared to zofenopril group (p<0.05). Conclusion: Our results suggest that candesartan treatment following myocardial infarction may potentially be useful in terms of improving post-myocardial infarction cardiac remodeling.

Assessment of arterial stiffness and epicardial adipose tissue thickness in predicting the subclinical atherosclerosis in patients with ankylosing spondylitis.

OBJECTIVE: Atherosclerosis is a chronic, progressive, inflammatory disease. Recognition of subclinical atherosclerotic vascular changes before clinical manifestation in an asymptomatic population is important for risk stratification and optimal management, which finally leads to the prevention of cardiovascular disease. We aimed to determine the risk of premature subclinical atherosclerosis by evaluating epicardial adipose tissue thickness (EATT) and arterial stiffness parameters in patients with ankylosing spondylitis (AS). METHODS: We performed a prospective study of 60 consecutive patients meeting modified New York criteria for AS compared to 60 controls matched for age and sex. Patients with traditional cardiovascular risk factors were excluded. Arterial stiffness parameters and EATT (examined via echocardiography) values of all patients and control groups were measured. RESULTS: There was no difference between basal characteristic and echocardiographic parameters in patients with AS and in the control group. EATT and pulse wave velocity (PWV) were higher in the AS patients compared to the control group. EATT was 5.74 ± 1.22 mm and 4.91 ± 1.21 mm (p < .001) and PWV was 9.90 ± 0.98 m/s and 6.46 ± 0.83 m/s (p = .009) in the AS and control groups, respectively. Also, PWV was significantly correlated with EATT, age, and central blood pressure in patients with AS. CONCLUSIONS: EATT and PWV, markers of atherosclerosis and cardiovascular disease, were significantly higher in patients with AS than the control group. In addition, in this study, it has been shown that there is a significant relationship between PWV and EATT in patients with AS.

Decrease in Pulse Wave Velocity is Associated with Clinical Improvement in Patients with Ischemic Stroke.

BACKGROUND: Arterial stiffness is an independent determinant of cardiovascular and cerebrovascular risks. The relationship between the increase in arterial stiffness parameters and the severity of stroke has been shown in previous studies. We aimed to investigate the association between clinical improvement and changes in arterial stiffness parameters in patients presenting acute ischemic stroke. METHODS: A total of 107 patients were enrolled in this study. On the first and seventh day of the hospitalization, 24 h non-invasive blood pressure was monitored and arterial stiffness parameters were measured. The National Institutes of Health Stroke Scale (NIHSS) was used to determine the severity of stroke, and the Modified Rankin Scale was used to determine dependency and to evaluate functional improvements. RESULTS: Arterial stiffness parameters of augmentation index (AIx@75) and pulse wave velocity (PWV) were significantly higher in patients who died during hospitalization than patients who were discharged (respectively p <0.001, p = 0.04). In the group with clinical improvement, PWV values measured on the seventh day were significantly lower than PWV values measured on the first day (p = 0.032). When the changes in PWV value measured on the first and seventh day for both groups were analyzed using mixed ANOVA test, p value were significant (p = 0.033). Multivariate binary logistic regression analyses showed that negatively change in PWV and CDBP independently predicts the clinical improvement. CONCLUSIONS: Increased AIx@75 and PWV appear to be associated with higher in-hospital mortality rates in patients with acute ischemic stroke. Additionally, clinical improvement in patients with ischemic stroke is associated with a decrease in PWV .

The Prognostic Utility of Plasma NGAL Levels in ST Segment Elevation in Myocardial Infarction Patients.

INTRODUCTION: Plasma neutrophil gelatinase-associated lipocalin (NGAL) levels in acute myocardial infarction (AMI) patients are markedly higher. In addition, plasma NGAL levels were increased in patients with acute and chronic heart failure as a complication of myocardial infarction. In this study, we investigated whether there is a difference between the prognostic use of plasma NGAL levels in ST-elevation myocardial infarction (STEMI) patients with preserved and reduced left ventricular ejection fraction (LVEF). METHODS: 235 consecutive STEMI patients were enrolled in the study. Patients were divided into groups according to LVEF. Plasma NGAL, troponin I, creatine kinase MB (CKMB), and C-reactive protein (CRP) were measured. Finally, the study population examined with 34 reduced LVEF and 34 preserved LVEF consisted of a total of 68 patients (12 females; mean age, 61.5 ± 14.7). All patients were followed up prospectively for 6 months. This study group was divided into two subgroups as the patients who died (n = 14) and survived (n = 34), and plasma NGAL levels of the groups were compared. RESULTS: The median of NGAL was 190.08 ng/ml. Age, troponin I, CKMB, CRP, glomerular filtration rate, and creatinine were higher in reduced LVEF groups. Plasma NGAL levels were also higher in reduced LVEF than in preserved LVEF, but statistically not significant (p=0.07). Plasma NGAL levels were significantly higher in death patients than in survived patients (p < 0.001). In ROC curve analysis, the level to detect isolated cardiovascular mortality with a sensitivity of 86% and a specificity of 77% was 190 ng/mL for NGAL. CONCLUSION: Plasma NGAL levels can be used to predict cardiovascular mortality in STEMI patients.

Total methylated arginine load as a risk parameter in subjects with masked hypertension.

Asymmetric dimethylarginine, symmetric dimethylarginine, and L-monomethylarginine are originated from the subsequent proteolytic catalysis of methylated arginine residues on different proteins and inhibit the endogenous nitric oxide generation. The changes in total methylarginine load (Asymmetric dimethylarginine plus symmetric dimethylarginine plus L-monomethylarginine) may contribute to hypertension. The aim of this study was to determine serum methylarginine concentrations in patients with masked hypertension and determine the association between these biomarkers and blood pressure measurements. Control group, masked hypertension and hypertension groups consisted of 40 subjects (11 males, 28 females, mean age 48.6 ± 13.1), 28 subjects (14 males, 14 females, mean age 50.9 ± 11.0) and 36 subjects (15 males, 21 females, mean age 54.4 ± 12.3 years), respectively (P= 0.149). Serum total methylarginine load was significantly higher in hypertension group (0.63 ± 0.23) compared to masked hypertension (0.49 ± 0.16) and control groups (0.38 ± 0.13) (P= 0.008 and P< 0.001). While there was no statistically significant difference between healthy control groups [0.147 (0.03-0.29)] and masked hypertension patients [0.144 (0.05-0.42)] for serum symmetric dimethylarginine levels (P= 0.970), it was markedly elevated in hypertension group [0.25 (0.07-0.54)] compared to masked hypertension group [0.14 (0.05-0.42)] (P= 0.001). Serum total methylarginine load was positively correlated with night-time SBP (r = 0.214, P= 0.029). Serum methylarginine levels might be a useful marker for determining the courses of clinical hypertension.

Comparative effects of atorvastatin 80 mg and rosuvastatin 40 mg on the levels of serum endocan, chemerin, and galectin-3 in patients with acute myocardial infarction.

OBJECTIVE: Endocan, chemerin, and galectin-3 are discrete biomarkers associated with cardiovascular diseases and acting through different pathophysiological pathways. The aim of this study is to investigate and compare the effects of high doses of atorvastatin and rosuvastatin on serum endocan, chemerin, and galectin-3 levels in patients with acute myocardial infarction (AMI). METHODS: Sixty-three patients with AMI were randomized to receive atorvastatin (80 mg/day) or rosuvastatin (40 mg/day) after percutaneous revascularization. Serum levels of endocan, chemerin, and galectin-3 were evaluated at baseline and after 4-week therapy. RESULTS: Endocan levels were not decreased statistically significantly with atorvastatin 80 mg, but rosuvastatin 40 mg markedly decreased the levels of endocan according to baseline [from 110.27 (86.03-143.69) pg/mL to 99.22 (78.30-122.87) pg/mL with atorvastatin 80 mg and from 110.73 (77.28-165.22) pg/mL to 93.40 (70.48-115.13) pg/mL with rosuvastatin 40 mg, p=0.242 for atorvastatin 80 mg and p=0.014 for rosuvastatin 40 mg]. Chemerin levels significantly decreased in both groups according to baseline [from 264.90 (196.00-525.95) ng/mL to 135.00 (105.95-225.65) ng/mL with atorvastatin 80 mg and from 309.95 (168.87-701.27) ng/mL to 121.25 (86.60-212.65) ng/mL with rosuvastatin 40 mg, p<0.001, respectively, for both groups]. Galectin-3 levels did not change markedly with atorvastatin 80 mg, but they decreased with rosuvastatin 40 mg [from 17.00 (13.10-22.25) ng/mL to 19.30 (15.25-23.45) ng/mL with atorvastatin 80 mg, p=0.721, and from 18.25 (12.82-23.82) ng/mL to 16.60 (10.60-20.15) ng/mL with rosuvastatin 40 mg, p=0.074]. There were no significant between-group differences in terms of absolute and percentage changes of endocan, chemerin, and galectin-3 at 4 weeks. CONCLUSION: We reported that both statins similarly decreased the endocan levels, whereas rosuvastatin seems to have more prominent effects on the reduction of the chemerin and galectin-3 levels in patients with AMI.

Effects of Glycogen Synthase Kinase Inhibitor on Glioblastoma Multiforme Cell Line via Apoptosis and Cell Signaling Pathways.

AIM: To investigate the apoptotic and molecular effects of glycogen synthase kinase-3 (GSK-3) in glioblastoma multiforme (GBM). MATERIAL AND METHODS: Human primary glioblastoma cell line (U-87 MG) and the human fetal glial cell line (SVGp12) were used. The cells were exposed to the different doses of GSK inhibitor for 24, 48 and 72 hours. Induction of apoptosis was assessed by DNA fragmentation (TUNEL) assay. EGFR and NF-kB expression was evaluated by immunofluorescence analyses. RESULTS: GSK-3 inhibitor IX induced cytotoxicity and apoptosis in dose-dependent manner in GBM cells. Our results indicated that GSK-3 inhibitor IX induces apoptosis, resulting in a significant decrease in the expression of NF-kB and EGF. CONCLUSION: Inhibition through GSK-3 has been found promising in creating therapeutic management of GBM cells. Proliferation, differentiation, cell cycle regulation, and apoptosis are mechanisms that must be interpreted as a whole. Components associated with EGFR, NF-kB, and apoptosis affect the mechanism solely and collectively. Our collective data suggest that GSK-3 inhibitor IX inhibited cellular proliferation and induced apoptotic events by modulating EGFR and NF-kB expression in GBM cells. GSK-3 inhibition holds promise for the development of new approaches for the therapeutic management of GBM cells.

Comparative effects of high-dose atorvastatin versus rosuvastatin on lipid parameters, oxidized low-density lipoprotein, and proprotein convertase subtilisin kexin 9 in acute coronary syndrome.

AIM: Current guidelines recommend administration of high-dose statins in acute coronary syndrome (ACS). It has been reported that statins upregulate proprotein convertase subtilisin kexin 9 (PCSK9) mRNA expression and increase circulating PCSK9 levels. We aimed to compare the effects of high-dose atorvastatin and rosuvastatin on serum oxidized low-density lipoprotein (oxidized-LDL) and PCSK9 levels in statin-naive patients with ACS. PATIENTS AND METHODS: One hundred and six patients with ACS were enrolled in this study. The patients were assigned randomly to receive atorvastatin (80 mg/day) or rosuvastatin (40 mg/day) by using a ratio of 1 : 1 in randomization. The levels of total cholesterol (TC), triglyceride, high-density lipoprotein cholesterol, LDL-cholesterol, oxidized-LDL, and PCSK9 were compared between groups after a 4-week treatment. RESULTS: Our study population included 53 patients in the atorvastatin group (age: 58.13±11.30 years, 11.32% female) and 53 patients in the rosuvastatin group (age: 59.08±12.44 years, 15.09% female). In both groups, lipid parameters, oxidized-LDL, and PCSK9 values changed significantly according to the baseline following treatment. High-dose atorvastatin and rosuvastatin induced similar decreases in LDL-cholesterol, oxidized-LDL, and triglyceride levels and similarly increased in high-density lipoprotein cholesterol and PCSK9 levels (P>0.05). CONCLUSION: We showed that atorvastatin and rosuvastatin treatment regimens have comparable effects on lipid parameters and PCSK9 levels in ACS patients.

Repression of the Notch pathway prevents liver damage in streptozotocin-induced diabetic mice.

INTRODUCTION: Sunitinib is an oral inhibitor of vascular endothelial growth factor that is used to treat a variety of cancer. There are limited data regarding the effect of sunitinib on diabetes. In the liver, Notch signaling plays an important role in liver tissue development and homeostasis and its dysfunction is associated with liver pathol-ogies. The aim of the present study is to investigate the effects of sunitinib on streptozotocin (STZ)-induced diabetic liver in mice models. MATERIAL AND METHODS: An experimental diabetes mellitus (DM) model was created in 28 male CD-1 mice. Twenty-eight male CD-1 mice divided in four groups (n = 7 each) were used; control mice (C), control mice treated with sunitinib (C + S), diabetic mice (DM), and diabetic mice treated with sunitinib (DM + S) for four weeks. The histopathological changes in the liver were examined by histochemistry and immunohistochemistry. Immunoreactivity of Notch1, Jagged1, DLL-1 and VEGF were evaluated in control and diabetic mice after sunitinib treatment. RESULTS: The significant morphological changes in the liver were mostly seen in hepatocytes that were hyper-trophied in the DM mice, with an increased amount of eosinophilic granules; moreover, some hepatocytes contained empty vacuole-like structures. The livers of the DM mice revealed increased deposition of collagen fibers. After sunitinib treatment the hepatocytes and hepatic lobules had almost similar morphology to control mice. The immunoreactivities of Notch1, Jagged1, DLL-1 and VEGF in hepatocytes were significantly lower in the DM group when compared with the C, DM + S and C + S group treated with sunitinib. CONCLUSIONS: These results suggest that sunitinib effectively protects the liver from diabetes-induced damage through the inhibition of the Notch pathway.

Impact of a Type D Personality on Clinical and Psychometric Properties in a Sample of Turkish Patients With a First Myocardial Infarction.

BACKGROUND: Recent studies have shown that a Type D personality is associated with an increased risk of cardiac mortality. OBJECTIVE: This study aimed to examine the impact of a Type D personality on clinical and psychometric properties in a sample of Turkish patients with a first myocardial infarction (MI). METHOD: The study included 131 patients who were admitted to the coronary care unit of a hospital. All of the patients underwent a psychiatric assessment within 2 to 6 months after their MI. Psychiatric interviews were conducted using the Structured Clinical Interview for DSM-IV (SCID-I). Patients also completed the Beck Depression Inventory, the Spielberger State-Trait Anxiety Inventory, the Health Anxiety Inventory, and the Type D personality scale. RESULTS: The patients were divided into 2 groups on the basis of the presence or absence of Type D personality. There was a 38.2% prevalence of Type D personality in the patients with a first MI. Those with this type of personality had a significantly higher frequency of hypertension and stressful life events. The Type D patients also had more psychiatric disorders, including depressive and anxiety disorders, than the non-Type D patients. CONCLUSIONS: Our findings suggest that Type D personality traits may increase the risk of hypertension and the risk of psychiatric morbidity in patients with a first MI. We suggest that this type of personality is a contributor to depression and anxiety disorders. These findings emphasize the importance of screening for Type D personality as both a cardiovascular and psychiatric risk marker in patients who have had an MI.

Effects of flavopiridol on critical regulation pathways of CD133high/CD44high lung cancer stem cells.

BACKGROUND: Flavopiridol a semisynthetic flavone that inhibits cyclin-dependent kinases (CDKs) and has growth-inhibitory activity and induces a blockade of cell-cycle progression at G1-phase and apoptosis in numerous human tumor cell lines and is currently under investigation in phase II clinical trials. Cancer stem cells (CSCs) are comprised of subpopulation of cells in tumors that have been proposed to be responsible for recurrence and resistance to chemotherapy. The aim of the present study was to investigate the effects of flavopiridol in cancer stem cell cytoskeleton, cell adhesion, and epithelial to mesenchymal transition in CSCs. METHODS: The cells were treated with flavopiridol to determine the inhibitory effect. Cell viability and proliferation were determined by using the WST-1 assay. Caspase activity and immunofluorescence analyses were performed for the evaluation of apoptosis, cell cytoskeleton, and epithelial-mesenchymal transition (EMT) markers. The effects of flavopiridol on the cell cycle were also evaluated. Flow cytometric analysis was used to detect the percentages of CSCs subpopulation. We analyzed the gene expression patterns to predict cell cycle and cell cytoskeleton in CSCs by RT-PCR. RESULTS: Flavopiridol-induced cytotoxicity and apoptosis at the IC50 dose, resulting in a significant increase expression of caspases activity. Cell cycle analyses revealed that flavopiridol induces G1 phase cell cycle arrest. Flavopiridol significantly decreased the mRNA expressions of the genes that regulate the cell cytoskeleton and cell cycle components and cell motility in CSCs. CONCLUSION: Our results suggest that Flavopiridol has activity against lung CSCs and may be effective chemotherapeutic molecule for lung cancer treatment.

Comparison of cell cycle components, apoptosis and cytoskeleton-related molecules and therapeutic effects of flavopiridol and geldanamycin on the mouse fibroblast, lung cancer and embryonic stem cells.

Similarities and differences in the cell cycle components, apoptosis and cytoskeleton-related molecules among mouse skin fibroblast cells (MSFs), mouse squamous cell lung carcinomas (SqCLCs) and mouse embryonic stem cells (mESCs) are important determinants of the behaviour and differentiation capacity of these cells. To reveal apoptotic pathways and to examine the distribution and the role of cell cycle-cell skeleton comparatively would necessitate tumour biology and stem cell biology to be assessed together in terms of oncogenesis and embryogenesis. The primary objectives of this study are to investigate the effects of flavopiridol, a cell cycle inhibitor, and geldanamycin, a heat shock protein inhibitor on mouse somatic, tumour and embryonic stem cells, by specifically focusing on alterations in cytoskeletal proteins, cell polarity and motility as well as cell cycle regulators. To meet these objectives, expression of several genes, cell cycle analysis and immunofluorescence staining of intracellular cytoskeletal molecules were performed in untreated and flavopiridol- or geldanamycin-treated cell lines. Cytotoxicity assays showed that SqCLCs are more sensitive to flavopiridol than MSFs and mESCs. Keratin-9 and keratin-2 expressions increased dramatically whereas cell cycle regulatory genes decreased significantly in the flavopiridol-treated MSFs. Flavopiridol-treated SqCLCs displayed a slight increase in several cell cytoskeleton regulatory genes as well as cell cycle regulatory genes. However, gene expression profiles of mESCs were not affected after flavopiridol treatment except the Cdc2a. Cytotoxic concentrations of geldanamycin were close to each other for all cell lines. Cdkn1a was the most increased gene in the geldanamycin-treated MSFs. However, expression levels of cell cytoskeleton-associated genes were increased dramatically in the geldanamycin-treated SqCLCs. Our results revealing differences in molecular mechanisms between embryogenesis and carcinogenesis may prove crucial in developing novel therapeutics that specifically target cancer cells.

Diagnostic accuracy and effective radiation dose of high pitch dual source multidetector computed tomography in evaluation of coronary artery bypass graft patency.

OBJECTIVE: The aim of the study was to evaluate the diagnostic accuracy and effective radiation dose (ERD) of high pitch dual source multidetector computed tomography (MDCT) for coronary artery bypass graft (CABG) patency. MATERIALS AND METHODS: Fourty-five patients who underwent 128 × 2­slice MDCT angiography with a prospective electrocardiogram-triggering, low-dose, high pitch, dual source, flash spiral acquisition mode after CABG surgery were included in the study. The interobserver agreement of the image quality was evaluated with Cohen κ value. The image quality was compared to the heart rates (HRs) using Mann-Whitney U test and to the graft segments using χ(2) test. The findings for the CABG patency on MDCT were compared to those determined on catheter coronary angiography. Dose-length product (DLP) and ERD were compared to the gender, HRs, and body mass index (BMI) of the patients using Kruskall Wallis and Mann-Whitney U tests. RESULTS: A total of 110 grafts and 330 vessel segments were evaluated with a good interobserver agreement (κ = 0.80). The image quality was better in proximal and middle graft segments (p < 0.05), as well as in the patients with low HRs (p < 0.05). High pitch MDCT had the following sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy for evaluation of graft patency: 92.8, 99.3, 92.8, 99.3 and 98.8 %, respectively. ERD was correlated to the HRs and BMI. CONCLUSIONS: High pitch 128 × 2­slice dual source CT angiography is a noninvasive imaging modality, and it can be safely and effectively used in evaluation of CABG patency with lower radiation dose.

Assessment of atrial electromechanical delay and P-wave dispersion in patients with type 2 diabetes mellitus.

OBJECTIVES: Diabetes mellitus is an independent and strong risk factor for development of atrial fibrillation (AF). Electrophysiologic and electromechanical abnormalities are associated with a higher risk of AF. In this study we aimed to determine the correlation of atrial conduction abnormalities between the surface electrocardiographic and tissue Doppler echocardiographic measurements in type 2 diabetes mellitus (T2DM) patients. METHODS: A total of 88 consecutive T2DM patients and 49 age-, gender-, and body mass index-matched healthy volunteers were included in the present study. Baseline characteristics were recorded and 24-hour ambulatory blood pressure monitoring, transthoracic echocardiography, and 12-lead surface electrocardiography were performed for all study participants. Atrial electromechanical delay (EMD) intervals were measured. RESULTS: Maximum P-wave duration and P-wave dispersion (Pd) were significantly higher in patients with T2DM (105.7±10.2ms vs. 102.2±7.5ms, p=0.02; 40.6±7.6ms vs. 33.6±5.9ms, p<0.001, respectively). Interatrial, intraatrial, and intraleft atrial EMD were significantly higher in the T2DM patients when compared with the controls (16.5±7.8ms vs.11.2±4.4ms, p<0.001; 9.0±7.3ms vs. 6.0±3.8ms, p=0.002, and 7.4±5.2ms vs. 5.1±3.2ms, p=0.002 respectively). Correlation analysis showed a positive correlation between interatrial EMD and Pd (r=0.429, p<0.001) and left atrial volume (r=0.428, p<0.001). CONCLUSIONS: In this study, there was significant EMD and Pd in patients with T2DM as compared with healthy volunteers. Additionally, interatrial EMD was correlated with Pd and left atrial volume index.

Clinical Characteristics and Outcome of Cardiovascular Implantable Electronic Device Infections in Turkey.

Infection is one of the most devastating outcomes of cardiovascular implantable electronic device (CIED) implantation and is related to significant morbidity and mortality. In our country, there is no evaluation about CIED infection. Therefore, our aim was to investigate clinical characteristics and outcome of patients who had infection related to CIED implantation or replacement. The study included 144 consecutive patients with CIED infection treated at 11 major hospitals in Turkey from 2005 to 2014 retrospectively. We analyzed the medical files of all patients hospitalized with the diagnosis of CIED infection. Inclusion criteria were definite infection related to CIED implantation, replacement, or revision. Generator pocket infection, with or without bacteremia, was the most common clinical presentation, followed by CIED-related endocarditis. Coagulase-negative staphylococci and Staphylococcus aureus were the leading causative agents of CIED infection. Multivariate analysis showed that infective endocarditis and ejection fraction were the strongest predictors of in-hospital mortality.