Objective: To evaluate the acute phase (pre- and in-hospital) antithrombotic management patterns (AMPs) and in-hospital outcomes for patients hospitalized with an acute coronary syndrome (ACS).
Methods: In total, 1034 patients [514 patients with ST-segment elevation myocardial infarction (STEMI) and 520 with unstable angina/non-STEMI (UA/NSTEMI)] hospitalized for ACS within 24 h of symptom onset were included in this multicenter prospective registry study conducted at 34 hospitals across Turkey. Patient characteristics, index event description, pre- and in-hospital AMPs, and clinical outcomes were evaluated.
Results: Majority (89.1%) of patients did not receive pre-hospital treatment. Overall 87.9% patients with STEMI and 55.6% patients with NSTEMI underwent percutaneous coronary intervention and dual antiplatelet therapy (DAPT) was based mainly on acetylsalicylic acid (ASA) and clopidogrel during hospitalization (99.8% and 98.2%, respectively). DAPT use at discharge was 98.4% and 86.8%, respectively. The percentage of patients with STEMI who received pre-hospital care, in-hospital cardiac catheterization, and pre and/or in-hospital triple antiplatelet therapy was higher than that of patients with UA/NSTEMI. In addition, higher rate of in-hospital hemorrhagic (2.3% vs. 0.8%) and cardiac ischemic (1.2% vs. 0.4% for MI and 1.6% vs. 0.8% for recurrent ischemia) complications and earlier induction of pre and/or in-hospital antiplatelet therapy and cardiac catheterization were also noted in patients with STEMI than in those with UA/NSTEMI.
Conclusion: Our findings revealed in-hospital and at-discharge management to be mainly based on DAPT in patients with ACS. Interventional strategies were used in the majority of patients with STEMI, while the usage and timing of immediate pre-hospital ECG from symptom onset should be improved in these patients. (Anatol J Cardiol 2016; 16: 900-15)

Objective: Cardiac uptake of fructose is thought to be mediated by glucose transporter 5 (GLUT5), whereas the uptake of glycerol is facilitated by aquaporin 7 (AQP7). We aimed to investigate the effect of a high-fructose diet (HFD) on GLUT5 and AQP7 levels in the rat heart subjected to exercise.
Methods: Male Sprague–Dawley rats were allocated to control (C; n=11), exercise (E; n=10), HFD (n=12), and HFD plus exercise (HFD-E; n=12) groups. HFD was started 28 days before euthanasia. From day 24 to 27, rats were subjected to moderate exercise, followed by vigorous exercise on day 28 (groups E and HFD-E). Cardiac GLUT5 and AQP7 mRNA levels were determined using RT-PCR. The protein contents of GLUT5 and AQP7 were immunohistochemically assessed. Paired-t, ANOVA with Bonferroni, Kruskal–Wallis, and Bonferroni-corrected Mann–Whitney U tests were used for statistical analysis.
Results: GLUT5 mRNA expression and protein content did not differ between the groups. AQP7 mRNA levels significantly increased (4.8-fold) in group E compared with in group C (p<0.001). Compared with group C, no significant change was observed in AQP7 mRNA levels in groups HFD and HFD-E. The AQP7 staining score in group E was significantly higher than that in groups C (p<0.001), E (p<0.001), and HFD-E (p<0.001).
Conclusion: Our study indicates that exercise enhances cardiac AQP7 mRNA expression and protein content. However, HFD prevents the exercise-induced increase in cardiac AQP7 expression. This inhibitory effect may be related to the competition between fructose and glycerol as energy substrates in the rat heart subjected to 5 days of physical exercise. (Anatol J Cardiol 2016; 16: 916-22)

Objective: Viscum album L. has favorable cardiovascular effects including antihypertensive and vasorelaxant activity, and the nitric oxide (NO) pathway upregulation has been proposed to be the underlying mechanism. NO also plays an important role in the pathophysiology of heart failure. However, its effects on cardiac systolic function are unclear.
Methods: A total of 30 male Wistar albino rats at 12 weeks of age were randomly divided into three groups: control, isoproterenol-induced heart failure group (ISO), and isoproterenol-induced heart failure + V. album treatment group (VA) groups (n=10 in each group). V. album was orally given at a dose of 250 mg/kg/day by gavage. Parameters of heart failure were compared among the groups. Tamhane’s T2 test, paired sample t-test, and Bonferroni methods were used for statistical analysis.
Results: V. album resulted in an improvement in all parameters of heart failure including left ventricular diameters (6.34±0.23 mm, 6.98±0.35 mm, and 6.71±0.10 mm for left ventricular end-diastolic diameter in control, ISO, and VA groups, respectively, p<0.05), ejection fraction (73.3±3.1%, 56.7±2.6%, and 65.2±1.5% for control, ISO, and VA groups, respectively, p<0.05), serum NT-proBNP levels, and histopathological changes. V. album treatment resulted in a statistically significant attenuation of increased levels of NO and iNOS (p<0.0001). The levels of hs-CRP were also found to be lower in the VA group compared with the controls and ISO groups (p<0.01).
Conclusion: V. album exerted favorable effects on left ventricular function in isoproterenol-induced heart failure rats. Upregulation of the NO pathway seems to be the possible pathophysiological mechanism. Favorable vascular outcomes can also be speculated considering the reduction in serum hs-CRP levels. (Anatol J Cardiol 2016; 16: 923-30)

Objective: Atherosclerotic coronary artery disease (CAD) appears to be a multifactorial process caused by the interaction of environmental risk factors with multiple predisposing genes. Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk.
Methods: A case-control study was conducted on 59 individuals who had undergone coronary angiographic evaluation. Of these, 29 were patients diagnosed with CAD (mean age =61.5±10.3) and 30 were controls examined for reasons other than suspected CAD and who had angiographically documented normal coronary arteries (mean age =60.4±11.6). Basal DNA damage as well as pyrimidine and purine base damage were evaluated in peripheral blood lymphocytes using the modified comet assay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based assay was used for genotyping.
Results: Basal DNA damage levels in patients [9.16 (3.26)] were significantly higher than those in controls [7.59 (3.23); p=0.017], and basal DNA and pyrimidine base damage levels were significantly correlated with disease severity based on Gensini scoring (r=0.352, p=0.006; r=0.318, p=0.014, respectively). However, no significant differences were observed in terms of oxidized DNA bases between patients and controls. The frequencies of studied genotypes (GSTM1, GSTT1, and hOGG1) were similar between groups.
Conclusion: The results of this study pointed out the role of DNA damage in CAD and its severity. However, GSTM1, GSTT1, and hOGG1 gene polymorphisms seemed to have no effect on individual susceptibility for disease progression. (Anatol J Cardiol 2016; 16: 931-8)

Objective: Bioactive roles of adipokines in coronary atherosclerosis and acute coronary syndromes have been demonstrated previously. Ho-
wever, there is a lack of data regarding the relationship between serum adipokines and periprocedural myocardial injury (PMI) following elective percutaneous coronary intervention (PCI). Therefore, we aimed to investigate the association between serum adipokines and PMI related to elective PCI.
Methods: In total, 153 consecutive patients (aged 60.6±8.2 years, 98 men) with stable angina pectoris undergoing elective PCI were enrolled in this observational cross-sectional study. Serum resistin, leptin, adiponectin, and high-sensitive Troponin T (hscTnT) levels were measured immediately before PCI and after 12-h PCI. The no-injury, PMI, and type 4a myocardial infarction (type 4a MI) groups were defined as groups consisting patients with post-procedural hscTnT concentrations <14 ng/L, between 14–70 ng/L, and >70 ng/L, respectively.
Results: Serum hscTnT, resistin, and leptin concentrations significantly (p<0.001) increased while serum adiponectin levels decreased (p<0.001) after 12-h elective PCI. However, no correlation was found between post-procedural hscTnT concentrations and resistin, leptin, and adiponectin levels. The no-injury group consisted of 65 patients (42.4%), whereas PMI and type 4a MI were observed in 70 (45.8%) and 18 (11.8%) patients, respectively. The average pre-procedural and post-procedural resistin, leptin, and adiponectin levels did not show any significant difference in the no-injury, PMI, and type 4a MI groups.
Conclusion: There is no correlation between serum adipokine levels and post-procedural troponin elevations reflecting PMI or type 4a MI. However, serum resistin and leptin levels increase, whereas adiponectin levels decrease significantly after elective PCI.
(Anatol J Cardiol 2016; 16: 940-6)

Objective: Serum levels of nitric oxide (NO) are decreased in patients with atherosclerosis and also are a risk factor for the development of atherosclerosis. Endothelial dysfunction and diffuse atherosclerosis have been proposed for the etiology of coronary artery ectasia (CAE). The purpose of this clinical trial was to determine the relationship between CAE and serum NO levels.
Methods: This prospective controlled study was conducted between January 2008 and March 2012. Serum levels of NO were compared in 40 patients with CAE (mean age 60.1±7.3 years) and 40 patients with normal coronary arteries (mean age 57.6±5 years) as a control group. CAE was diagnosed when a segment of coronary artery was more than 1.5 times the diameter of the adjacent healthy segment. Patients with stenotic atherosclerotic plaques, slow coronary flow, previous history of revascularization, acute coronary syndromes, left ventricular dysfunction, valvular heart disease, and systemic diseases were not included in the study. The effect of NO on the outcome was studied by constructing a receiver operating characteristic (ROC) curve with CAE as the primary variable. Effects of different variables on CAE were calculated using binary logistics regression analysis.
Results: Serum NO concentrations were significantly lower in patients with CAE than in the control group (42.1±20.1 μmol/L vs. 77.3±15.7 μmol/L, p<0.001). According to the results of the multivariate regression analysis, LDL and NO levels were identified as independent factors associated with CAE (OR=1.02, 95% CI 1–1.04, p=0.02 and OR=0.88, 95% CI 0.83–0.93, p=0.001, respectively). ROC analysis revealed that using a cut-off point of 63.3, NO level predicts CAE with a sensitivity of 87.5% and specificity of 90%.
Conclusion: Our study indicates that decreased levels of NO are present in patients with CAE compared to patients with normal coronary arteries, supporting the hypothesis that decreased levels of NO might be associated with CAE development. (Anatol J Cardiol 2016; 16: 947-52)

Objective: Metabolic syndrome (MS) is defined by a cluster of interdependent physiological, biochemical, and clinical risk factors and linked to a state of chronic inflammation. YKL-40 is known as an inflammatory glycoprotein, which is secreted by various cell lines during inflammation. Thus, we aimed to assess the association of serum YKL-40 levels with the presence and severity of MS.
Methods: In this prospective cross-sectional study, a total of 177 consecutive patients [n=114 MS present and n=63 MS absent] were enrolled. MS was defined according to National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) criteria. Serum YKL-40 and hs-CRP levels were measured for all participants.
Results: Serum YKL-40, hs-CRP and white blood cell count (WBC) were significantly higher in the MS present group (p<0.05). There was a graded relationship between increasing number of MS components and serum YKL-40 level (p<0.05). In addition, serum YKL-40 level was positively correlated with hs-CRP level (r=0.467, p<0.001) and WBC count (r=0.251, p=0.001). In multivariable regression analysis, serum YKL-40 [1.022 (1.011–1.033), p<0.001] and hs-CRP [1.346 (1.111–1.632), p=0.002] were remained as independent predictors for the presence of MS. In the ROC curve analysis, using a cut-off level of 147.0, YKL-40 well predicted the presence of MS with a sensitivity of 73.7% and specificity of 69.8% (AUC: 0.785; 95% CI: 0.718–0.853, p<0.001).
Conclusion: In this study, we demonstrated that serum YKL-40 level was significantly associated with the presence of MS. According to these findings, we concluded that serum YKL-40 may be a novel and useful indicator for MS. (Anatol J Cardiol 2016; 16: 953-8)

Objective: Vitamin D deficiency is associated with coronary artery disease, hypertension, heart failure, endothelial dysfunction, and metabolic syndrome. The pathophysiology of cardiac syndrome X (CSX) involves many pathways that are influenced by vitamin D levels. This study aimed to investigate the relationship between vitamin D deficiency and abnormal blood pressure response to exercise in patients with CSX.
Methods: This was a cross-sectional and observational study. Fifty females with normal epicardial coronary arteries who presented with typical symptoms of rest or effort angina and 41 healthy age-matched female controls, were included. Patients with cardiomyopathy, severe valvular disease, congenital heart disease, and left ventricular hypertrophy were excluded. All patients underwent stress electrocardiography examination and 25-hydroxy (OH) vitamin D level measurements.
Results: Levels of 25-OH vitamin D were significantly lower in CSX patients (9.8±7.3 ng/mL vs. 18.1±7.9 ng/mL; p<0.001). Systolic blood pressure (SBP) (188±15 mm Hg vs. 179±17 mm Hg; p=0.013) and diastolic blood pressure (DBP) (98±9 mm Hg vs. 88±9 mm Hg; p<0.001) during peak exercise were higher in CSX patients. Levels of 25-OH vitamin D were negatively correlated with peak SBP (r=–0.310, p=0.004) and peak DBP (r=–0.535, p<0.001) during exercise. To discard the multicollinearity problem, two different models were used for multivariate analyses. In the first model, metabolic equivalents (METs) (p=0.003) and 25-OH vitamin D levels (p=0.001) were independent predictors. METs (p=0.007), 25-OH vitamin D levels (p=0.008), and peak DBP were determined as independent predictors in the second multivariate model.
Conclusion: In patients with CSX, 25-OH vitamin D levels were lower than those in controls; moreover, 25-OH vitamin D deficiency was also associated with higher levels of peak DBP during exercise. (Anatol J Cardiol 2016; 16: 961-6)

Objective: This study attempted to fill the gaps in evidence related to response to clopidogrel treatment in the Turkish population. The study aimed to determine the prevalence, associated risk factors, and clinical outcomes of high on-treatment platelet reactivity (HTPR) of clopidogrel in patients undergoing percutaneous coronary intervention (PCI) in a tertiary cardiovascular hospital in Turkey.
Methods: In this prospective studied a total of 1.238 patients undergoing PCI were included in the present study. Blood samples were analyzed using a Multiplate analyzer. All patients were examined in the outpatient clinics at the end of the first and sixth months for recording drug therapy compliance and study endpoints.
Results: Among the study population, 324 (30.2%) patients were found to have HTPR (mean age 58.03±11.88 years, 71.7% men). The incidence of HTPR was higher amongst females than amongst males (38.3% vs. 27%, p=0.010). Hypertension and diabetes mellitus were more frequently observed in the HTPR group (57.7% vs. 48.7%, p=0.004; 35% vs. 29.1%, p=0.040, respectively). When the recorded data were analyzed using multinomial regression analysis, hypertension, hemoglobin level, platelet, lymphocyte, and eosinophil count were independently associated with HTPR.
Conclusion: On the basis of the results obtained from our study, we conclude that 30.2% of the Turkish population has HTPR. Our results also led us to believe that hypertension is an associated risk factor and decreased hemoglobin level as well as increased platelet counts are laboratory parameters that are strongly associated with the presence of HTPR. However, no differences were observed with regard to cardiovascular mortality and stent thrombosis. (Anatol J Cardiol 2016; 16: 967-73)

Objective: Nonalcoholic fatty liver disease is the most common cause of liver dysfunction in Western countries and an independent risk factor for atherosclerotic heart disease. Appropriate noninvasive parameters are lacking for optimal risk stratification of cardiovascular disease in these patients. We evaluated several recently discovered noninvasive parameters for atherosclerosis in patients with nonalcoholic fatty liver disease: epicardial fat thickness, aortic flow propagation velocity, and osteoprotegerin level.
Methods: Forty-one patients (27 men and 14 women; mean age, 37.9±8.9 years) with nonalcoholic fatty liver disease and 37 control subjects (17 men and 20 women; mean age, 34.5±8.6 years) were enrolled in this observational case-control study. Patients with nonalcoholic fatty liver disease diagnosed at a gastroenterology outpatient clinic were included. Patients with cardiac pathology other than hypertension were excluded. Epicardial fat thickness and aortic flow propagation velocity were measured by echocardiography. The serum concentration of osteoprotegerin was measured using a commercial enzyme-linked immunosorbent assay kit.
Results: Nonalcoholic fatty liver disease patients exhibited a significantly lower aortic flow propagation velocity (155.17±30.00 vs. 179.00±18.14 cm/s, p=0.000) and significantly higher epicardial fat thickness (0.51±0.25 vs. 0.29±0.09 cm, p=0.000) than control subjects. Osteoprotegerin levels were higher, but not significant, in patients with nonalcoholic fatty liver disease (28.0±13.0 vs. 25.2±10.8 pg/mL, p=0.244). Binary logistic regression analysis showed that aortic flow propagation velocity (OR, –0.973; 95% CI, 0.947–0.999) and waist circumference (OR, –1.191; 95% CI, 1.088–1.303) were independent predictors of nonalcoholic fatty liver disease.
Conclusion: In this study, epicardial fat thickness and osteoprotegerin level were higher and aortic flow propagation velocity was lower in patients with nonalcoholic fatty liver disease. Early detection of abnormal epicardial fat thickness and aortic flow propagation velocity may warrant a search for undetected cardiovascular disease in patients with nonalcoholic fatty liver disease. (Anatol J Cardiol 2016; 16: 974-9)

Prosthetic valve thrombosis is one of the major causes of primary valve failure, which can be life-threatening. Multimodality imaging is neces- sary for determination of leaflet immobilization, cause of underlying pathology (thrombus versus pannus or both), and whether thrombolytic therapy attempt in the patient would be successful or surgery is needed. Current guidelines for the management of prosthetic valve thrombosis lack definitive class I recommendations due to lack of randomized controlled trials, and usually leave the choice of treatment to the clinician’s experience. In this review, we aimed to summarize the pathogenesis, diagnosis, and management of mechanical prosthetic valve thrombosis. (Anatol J Cardiol 2016; 16: 980-9)