Objective: Obesity is an important risk factor of atherosclerosis and its prevalence in humans is increasing. Recent studies suggest that the leptin and adiponectin play important roles in obesity, and they are associated with complications of obesity. However, the mechanism of effects has not been outstandingly established. In this study, we studied leptin and adiponectin levels according to body mass index (BMI) and their relationship with oxidative parameters. Methods: A total of 87 healthy individuals with BMI >35 kg/m2 (n=29, Group 1), BMI=25-35 kg/m2 (n=29, Group 2) and BMI <25 kg/m2 (n=29, Group 3) were included in the cross-sectional observational study. Leptin, adiponectin levels, total antioxidant capacity (TAC) and total oxidant status (TOS) were measured. Oxidative stress index (OSI) was calculated using TAC and TOS values. Statistical analyses were performed using Chi-Square, Mann-Whitney U, one-way ANOVA, Kruskal-Wallis, Pearson correlation and multiple regression analyses tests. Results: Age and gender ratio were similar in the groups. The TAC level was the lowest in group 3 and the highest in group 1. The TOS level was higher in groups 2 and 3 than in group 1 (p <0.05 for both). OSI levels were similar in groups 2 and 3, and it was significantly different from the group 1 (p<0.05). The trend for leptin levels was decreasing and for antiponectin levels was increasing from group 1 to group 3. Except for other parameters, levels of leptin were independently related to the TOS (b=-1.123, 95% CI=-12.734-0.255, p=0.040), OSI (b=1.689, 95% CI=1.105-12.481, p=0.018) and waist circumference (b=-0.592, 95% CI= -0.630-0.134, p=0.003). Adiponectin had no significant relation with these parameters. Conclusion: Findings of the present study reveal that leptin decreased and adiponectin increased with BMI in healthy people. These data support that these changes may be responsible in the increased TOS and OSI levels.

Objective: In this study, we evaluated the possibility that, levels of circulating adhesion molecules following direct stent implantation may be a marker of restenosis. Methods: This prospective, observational study investigated levels of circulating intercellular (ICAM-1), and vascular cell (VCAM-1) adhesion molecules in 15 patients with stable angina pectoris before and after coronary stent implantation for single vessel-single lesion disease in proximal left anterior descending artery. All patients received bare-metal stents. Patients underwent repeat coronary angiography for detection of restenosis at 6 month. Continuous data between patients with and without restenosis were compared using Mann-Whitney U test. Repeated measurements were compared using Wilcoxon T test. Categorical data were compared using Chi-square statistics. Results: Baseline ICAM-1 and VCAM-1 concentrations before percutaneous coronary intervention (PCI) were 4.89±2.28 and 46.35±22.96 ng/ml respectively. Levels of ICAM and VCAM increased nonsignificantly 24 hours after PCI (5.01±2.35 ng/ml and 52.57±19.40 ng/ml, respectively). Six patients (40%) developed restenosis within 6 months. Mean stent length, mean stent diameter, and mean dilatation pressure were comparable in patient groups with and without restenosis. Levels of plasma VCAM-1 measured before and after PCI did not change significantly in patients without restenosis. However, these levels increased significantly in the group of restenosis. At 6 months, patients who developed restenosis, had higher VCAM-1 levels, as compared to baseline values (from 45.1±21.0 to 57.2±14.3 ng/ml, p<0.05). Plasma levels of pre and post PCI ICAM-1 did not differ significantly between groups with and without restenosis. Conclusion: These results suggest a more dominant role for VCAM-1, but not for ICAM-1 in development of restenosis following coronary stent implantation.

Objective: Elevated homocysteine levels induce a hypercoagulable state and make the clot more resistant to fibrinolysis. In this prospective observational study, we investigated the influence of homocysteine levels on infarct-related artery (IRA) patency and flow as determined with regard to thrombolysis in myocardial infraction (TIMI) flow grade and corrected TIMI frame count (CTFC). Methods: Sixty-one patients who received fibrinolytic therapy for a first ST elevation myocardial infarction (STEMI) within 12 hours of chest pain were included. Coronary angiography was performed according to the Judkins technique within 72 hours after fibrinolytic therapy. Total plasma homocysteine level was determined by the high-performance liquid chromatography method with fluorescence detection. Statistical analysis was performed using Chi-square, Student’s t and Pearson correlation tests. Logistic regression analysis was used to determine the predictors of IRA occlusion. Results: Of the 61 patients, 22 (36.1%) had an occluded IRA (group 1), 39 (63.9%) had a patent IRA (group 2). Mean plasma homocysteine levels were found to be significantly higher in the group 1 compared to the group 2 (18.5±9.6 µmol/L vs 14.3±5 µmol/L, p=0.04). In addition, we found a significant positive correlation between CTFC and plasma homocysteine levels (r=0.415; p<0.01). In multiple logistic regression analysis, high levels of plasma homocysteine (OR=1.2; 95% CI 1.1-1.25; p=0.03) and being a non-smoker (OR=5.9; 95% CI 1.1-31.6; p=0.03) were found to be significant independent predictors of having an occluded IRA. Conclusion: There is an inverse relation between plasma homocysteine levels and IRA patency and flow in patients receiving fibrinolytic therapy for STEMI.

Objective: In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP). Methods: A total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis. Results: Hs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p<0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p<0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels. Conclusion: Hs-CRP and NT proBNP are significantly higher in patients with coronary slow flow compared with normal control group. Their increased levels are positively correlated with TIMI frame count.

Objective: We aimed to assess the relationship between C-reactive protein (CRP) and the severity and diffusion of coronary artery lesions in patients with unstable angina pectoris (UAP) and the independent association of CRP with this clinical situation. Methods: This cross-sectional, observational study included 50 patients. Classification by Braunwald was used for UAP. The severity and diffusion of angiographic coronary disease were graded according to Reardon’s modified scoring system. Plasma CRP levels were quantified by immunoturbidimetry. Nonparametric tests were used for comparison of CRP and other risk factors, and logistic regression analysis for evaluation of independent association between CRP and unstable angina pectoris. Results: The severity score was 46±18 points in class IIB1 UAP, 36±20 points in class IIB2 and 53±18 points in class IIIB2 (p=0.017, class IIIB2 vs IIB2). Respectively, CRP levels were 6.6 mg/L, 3.8 mg/L and 4.8 mg/L (p=0.371, class IIB1 vs IIB2 vs IIIB2). Lesions with diffusion score 4 revealed higher CRP values than lesions with diffusion score 1 (11.1 mg/L vs 3.1 mg/L, p=0.048). Adjusting age, sex and smoking, assessment of partial correlation analysis showed a positive, moderately powerful and significant association between CRP levels and the severity and diffusion scores of the coronary lesions (r=0.30; p=0.034 and r=0.31; p=0.030, respectively) in the whole study group. Multiple logistic regression analysis showed no appreciable independent association between CRP and UAP (OR: 1.63, 95%CI: 0.90-5.63, p=0.093). Conclusion: Although, CRP was correlated with the severity and diffusion of angiographic coronary disease in patients with UAP, there was no independent association between CRP and clinical severity of UAP.

Objective: Strong evidence has suggested that there is a circadian periodicity of acute coronary event. Beta-blockers, aspirin and angiotensin-converting enzyme inhibitors decrease the rate of acute myocardial infarction (AMI) and blunt the peak incidence in the morning. However, such effect has not been evaluated for statins. Accordingly, the present study aimed to evaluate the influence of statin therapy on circadian variation of AMI. Methods: This retrospective study consisted of 451 consecutive patients with acute ST segment elevation AMI. The patients were divided into two group based on prior statin usage. In statistical analysis t test, Chi-square test and Mann Whitney U test were used for comparison of groups. We used harmonic regression models to evaluate the circadian variation of onset of MI symptoms in patients receiving statin and patients not receiving statin. Results: In all study participants, the highest incidence of AMI was between 6.00 and 12.00; the odds ratio was 1.34 (95% CI 1.20 to 1.46, p<0.001). In the non-statin group, the highest incidence of AMI occurred between 0: 00 A.M. and 06.00. There was still a peak incidence between 6.00 A.M. and noon in the statin therapy receiving group; the odds ratio was 1.61 (95% CI 1.34 to 1.80, p<0.001). Accordingly, there was no statistical difference between the statin and non-statin groups regarding circadian variation of AMI. Prior usage of statin did not blunt the peak incidence of AMI in the morning. Conclusion: Prior usage of statin does not seem to play a role in the circadian periodicity of AMI.

Objective: To determine the diagnostic accuracy of D-dimer testing for detection of acute aortic dissection. Methods: This study is a retrospective chart review of patients who had been evaluated with suspicion of acute aortic dissection. All patients’ D-dimer levels were determined prior to their further work up in the emergency department. The study was conducted in a tertiary care center between February 2006-August 2008. The D-dimer assay used was the immunoturbidimetric assay, with a normal range up to 0.246 µg/ml. Statistical analysis was accomplished using Chi-square test, Student’s t-test and a receiver-operating characteristics (ROC) curve analysis. Results: Ninety-nine patients were included in the study, 30 patients were diagnosed as having acute aortic dissection and 69 patients were evaluated in non-acute aortic dissection group. In comparison of the two groups, positive D-dimer results were found to be significantly higher in acute aortic dissection group than in non-acute aortic dissection group (p<0.001). Sensitivity of the D-dimer test in detection of acute aortic dissection was found as 96.6% and the negative predictive value of the test was 97.3%. Specificity and positive predictive value of the D-dimer test were 52.2% and 46.8%, respectively. The area under the ROC curve yielded an acceptable certainty for excluding acute aortic dissection on base of negative results (AUC: 0.764; CI 95%: 0.674-0.855; p<0.001). Conclusion: D-dimer testing is helpful for emergency physicians in detection of patients with suspected acute aortic dissection in the emergency department.

Objective: Congenital heart disease (CHD) associated with thyroid disease has been reported in Down syndrome (DS). The purpose of this work was to assess abnormalities of the thyroid in relation to the frequency and type of CHD on admission among children with DS. Methods: This retrospective study included 187 children with DS between August 1993- December 2005. Karyotype analysis, thyroid function tests and echocardiographic studies were performed in patients all children with DS. If necessary, hemodynamic study by catheterization was carried out. Thyrotropin releasing hormone (TRH) stimulation test was performed in having elevated thyroid stimulating hormone (TSH) level. Statistical analyses were performed using Chi-square, “t” test for independent samples or Mann-Whitney U test. Results: It was found that 136 (72.73%) patients with DS had CHD. The age difference at the time of admission was statistically significant for these two groups (p<0.001) in children with /without CHD. There were 12 (11.88%) patients with congenital hypothyroidism and DS, of whom 11 had CHD. There were statistically significant differences in the levels of TSH and total thyroxine (tT4) between congenital and subclinical hypothyroid and euthyroid groups (p<0.001 for TSH and p< 0.001 for tT4). But there was no significant relationship between having any kind of CHD and levels of TSH and tT4. Conclusion: Our data suggest that all patients with DS should be evaluated with careful physical and echocardiographic examination on admission. In addition, congenital or subclinical hypothyroidism should also be kept in mind in children with DS and monitored accordingly.

Objective: Atrial fibrillation (AF) is a common complication of cardiovascular surgery and its mechanisms are not well understood. The aim of our study was a prospective investigation of the relationship between AF development and tissue or blood magnesium levels. Methods: This prospective observational study evaluated 20 patients undergoing elective initial coronary artery bypass graft (CABG) surgery. Right atrial appendage and skeletal muscle samples were obtained for tissue magnesium level analysis before, during (at 60th minute) and 30 minutes after cardiopulmonary bypass (CPB) with simultaneous blood samples. Daily measurements of blood Mg levels and continuous monitoring for AF were performed for 7 postoperative days. Statistical analyses were performed using ANOVA, independent samples t and Chi-square tests. Results: AF developed in 5 out of 20 patients during postoperative period (25%). Patients with or without AF did not differ in terms of tissue and blood magnesium levels during and early after CPB and during 7 days after the operation. Blood magnesium levels were significantly higher in the whole study population on postoperative days 3 through 7 (day 3 - 1.13±0.11 mmol/L; day 4-, 1.18±0.07 mmol/L; day 5-1.15±0.10 mmol/L; day 6-1.17±0.08 mmol/L; and day 7, 1.22±0.08 mmol/L) compared to day 1 and day 2 (day 1-0.96±0.13 mmol/L and day 2-1.02±0.12 mmol/L; p<0.002 for all comparisons). Conclusion: Although patients with and without AF did not significantly differ with regard to blood and tissue magnesium levels, the coincidence of an early postoperative reduction in magnesium levels in all patients and occurrence of all AF incidences at this time period suggests a potential association deserving further investigation.

Objective: Our objective was to evaluate the degree of change in left ventricular mass index (LVMI) regression after aortic valve replacement (AVR) using three different valves. Methods: Group 1 (n=17) included patients with bioprosthesis (Medtronic Hancock 2), Group 2 (n=21) included patients with mono-leaflet mechanical valve (Medtronic Hall), and Group 3 (n=17) included patients with bi-leaflet mechanical valve (St Jude). The mean ages of Group 1, 2 and 3 patients were 70.8±9.1, 61.6±13.7 and 56.2±18.3 years, respectively. In this observational study, patients were followed-up after surgery and left ventricular wall thickness and valvular functions were evaluated with echocardiography. The findings were compared with preoperative values. Statistical analyses were performed using one-way variance analysis (ANOVA), Kruskal Wallis, and Chi-square tests. Results: Statistically significant difference was observed among the three groups with respect to age (p=0.015). LVMI regressed in all groups; Group 1 from 232.74±53.36 g/m2 (preoperative) to 174.64±46.33 g/m2 (postoperative) (p=0.0001), Group 2-from 198.49±40.53 g/m2 to 167.04±33.9 g/m2 (p=0.0001), and Group 3-228.77±47.87 g/m2 to 185.44±37.76 g/m2 (p=0.0001). No statistically significant difference was observed among the groups with respect to LVMI regression (p=0.054, p=0.363). Conclusion: Mid-term results of AVR with three different aortic valve prosthesis revealed that all groups showed a similar regression of left ventricular mass. However, we advocate that long-term results of an increased number of patients should be evaluated for assessment in depth.