Atiye Çengel

Association between nonalcoholic fatty liver disease and coronary artery disease

AimsTo demonstrate whether there is a relationship between the presence of nonalcoholic fatty liver disease (NAFLD) and the presence and extent of coronary artery disease (CAD). Patients and methodsNinety-two consecutive patients who planned to undergo coronary angiographies (CAG) without known CAD, other than findings of acute coronary syndrome, were enrolled in this study. Abdominal ultrasonography was performed before the CAG to detect NAFLD. CAD was defined as a stenosis of at least 50% in at least one major coronary artery. The extent of CAD was measured according to the number of major coronary artery/arteries affected by CAD. All the risk factors for CAD were included in a binary logistic regression model. Forward, backward, or step-wise selections were not used. P<0.05 was accepted as being significant. ResultsSixty-five of the 92 patients (70.7%) were detected, by abdominal ultrasonography, to have fatty liver and 43 patients out of 92 (46.7%) were detected, by CAG, to have significant CAD. According to the results of logistic regression analysis, the presence of NAFLD independently increased the risk for CAD, as seen in CAG [odds ratio (OR), 95% confidence interval (CI): 6.73 (1.14–39.61); P=0.035]; this was despite factoring in the other risk factors for CAD and the components of metabolic syndrome. NAFLD was more commonly found in patients as the extent of CAD increased (P=0.001). ConclusionThe presence of NAFLD is independently associated with the presence and extent of CAD. Future studies are needed to explain the mechanisms of this relationship.

Coronary heart disease is associated with mean platelet volume in type 2 diabetic patients

Background: Mean platelet volume (MPV) is an indicator of platelet activation which is a central process in the pathophysiology of coronary heart disease (CHD). The aim of the study was twofold; first to determine whether MPV values is increased in patients with DM, and secondly to evaluate the relation between diabetic complications and MPV. Methods: The study population included 258 patients divided into two groups. Group A composed of 158 type 2 diabetic patients with coexistent coronary artery disease (stenotic lesions of 50%) (78 women, 80 men; mean age 53.9_10.8; mean diabetes duration 13.1_6.0). One hundred subjects (48 women, 52 men; mean age 53.9_11) without type 2 diabetes with normal coronary angiographies were taken as the control group (group B). To evaluate the extension of CHD, Gensini scoring system was used. Results: The MPV was significantly different in the patient group compared to the controls (9.79 ± 1.5 fl vs 8.3 ± 0.9 fl, P<0.001). The existence of CHD was associated with MPV with odds ratio (95% CI) of 2.31 (1.55–4.42, p50.001). Conclusion: We have found that diabetic patients with coronary heart disease have significantly higher MPV values compared to control subjects without diabetes and with angiographically normal coronary arteries.

Asymmetrical dimethylarginine level in atrial fibrillation

Objective — Atrial fibrillation (AF) is known to be related with increased risk of thromboembolic events. Asymmetrical dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthase (NOS), can cause endothelial dysfunction by decreasing nitric oxide (NO) and lead to increased risk of thrombosis. In the present study our aim was to compare plasma levels of ADMA in patients with acute onset (< 24 hours) and chronic AF (> 1 year) to determine the risk of thrombosis. Method — 17 patients with the first detected attack of AF within the first 24 hours of presentation (group I), 25 patients who had permanent chronic AF lasting at least 1 year or more (group II) and 18 healthy persons as the control group (group III) were included in the study. For each patient the plasma ADMA, L-arginine, symmetrical dimethylarginine (SDMA) concentrations were measured by high-performance liquid chromatography in venous blood samples collected before cardioversion. We compared the plasma ADMA, L-arginine and SDMA concentrations between the groups. Results — Plasma L-arginine (78.18 ± 28.29 vs. 73.14 ± 14.11 vs. 71.03 ± 21.31, P = 0.549) and plasma SDMA concentrations (0.38 ± 0.18 vs. 0.42 ± 0.21 vs. 0.32 ± 0.24, P = 0.224) were similar in all groups. There was a significant difference between plasma ADMA concentrations (0.76 ± 0.27 vs. 0.50 ± 0.26 vs. 0.36 ± 0.20, P < 0.001) among the groups.When we compared plasma ADMA levels between the subgroups, we also found a significant difference (P = 0.002 when comparing group I and group II, P < 0.001 when comparing of group I and group III, P = 0.042 when compareng of group II and group III). Conclusion — ADMA levels in patients with acute onset AF were significantly increased when compared with patients with chronic AF and the healthy control group indicating the presence of endothelial dysfunction and a prothrombotic state even in a very early phase of AF.

Lack of Association Between Matrix Metalloproteinase-9 and Endothelial Nitric Oxide Synthase Gene Polymorphisms and Coronary Artery Disease in Turkish Population

Polymorphic variants of genes encoding proteins involved in vascular remodeling may genetically diverge among different populations and play a role in the susceptibility to the coronary artery disease (CAD). MMP-9-1562 C/T (rs3918242), eNOS T-786C (rs2070744), and Glu298Asp (rs1799983) are among the most studied of these polymorphisms. The aim of this study was to determine the relationship between CAD and these polymorphisms in the Turkish population. The analysis included 146 CAD+ and 122 CAD- individuals. Genomic DNA was isolated from whole blood and genotyping was performed by the PCR-RFLP method. No significant associations were found between -1562 C/T (p = 0.557), Glu298Asp (p = 0.432), and -786 T/C (p = 0.055) polymorphisms and CAD. The distribution of each haplotype also did not differ between CAD+ and the CAD- samples (p > 0.05). The present investigation is the first to study an association between -1562 C/T polymorphism and CAD in the Turkish population. In conclusion, no appreciable differences between CAD+ and CAD- samples were found in terms of polymorphisms mentioned above.

Use of long-term combined therapy with inhaled iloprost and oral sildenafil in an adult patient with eisenmenger syndrome.

Eisenmenger syndrome is characterized by elevated pulmonary vascular resistance and right-to-left shunting of blood through a systemic to pulmonary circulation connection. Treatment requires either lung transplantation with intracardiac repair or heart–lung transplantation. There are inadequate data regarding treatment alternatives when the patient is not a candidate for surgery. In this article, we report on the case of a 68-year-old woman with Eisenmenger syndrome related to congenital heart disease who was treated with inhaled iloprost and oral sildenafil for 2 years.

Serum uric acid levels as a predictor of in-hospital death in patients hospitalized for decompensated heart failure

Objectives — The aim of this study was to determine the value of serum uric acid levels in predicting in-hospital mortality of chronic heart failure patients hospitalized for decompensation in spite of appropriate medical therapy. Methods and results — This study was conducted in patients who were admitted to our clinic between January 2003 and April 2004 due to decompensated heart failure. Only patients who had a functional capacity of class IV and who already received loop diuretic and ACE inhibitor therapy before their admission were included. Patients with recurrent admissions during this period were excluded. Eighty-five patients fulfilled these criteria: group I consisted of 25 patients who died during hospitalization whereas group II consisted of 60 patients who were discharged alive after treatment. Age, sex, left ventricular ejection fraction derived from 2-D echocardiography, serum sodium (Na), gamma-glutamyl transpeptidase (GGT), creatinine, uric acid levels, white blood cell counts and drugs used on admission were the selected parameters as predictors of in-hospital mortality in these patients.When stepwise logistic regression analysis was used, female sex and serum uric acid levels at admission appear to be the only predictors of death during that hospitalization independent of other variables. Conclusions — Serum uric acid levels may be used as a predictor of death in hospitalized heart failure patients with class IV symptoms.

Carotid intima–media thickness in patients with cardiac syndrome X and its association with high circulating levels of asymmetric dimethylarginine

BACKGROUND The cause of myocardial ischemia and chest pain in patients with cardiac syndrome X (CSX) has been explained by mechanisms including endothelial dysfunction. CSX patients have higher levels of asymmetric dimethylarginine (ADMA) and increased mean common carotid intima-media thickness (C-IMT). Accordingly, this study was designed to examine C-IMT with its association serum endothelial function parameters in patients with CSX. METHODS The study population consisted of 30 enrolled consecutive patients with diagnosis of CSX. As a control group, 30 individuals with the complaint of anginal chest pain without any ischemia on myocardial perfusion scintigraphy and with normal coronary angiographies were selected. C-IMT was measured by recording ultrasonographic images of both the left and the right common carotid artery. Plasma levels of L-arginine, ADMA, and nitrate/nitrite (NO(x)) were measured from blood samples. RESULTS Both C-IMT (mm) and carotid atherosclerotic plaques were significantly higher in patients with CSX than in control group. Also, the plasma level of NO(x), L-arginine, and L-arginine/ADMA ratio were lower in patients with CSX than they were in the control group subjects. Plasma ADMA level increased in the CSX patients group. Correlation analysis showed significant positive correlation with C-IMT and plasma ADMA levels and showed significant negative correlation with plasma NO(x) and L-arginine levels. L-arginine/ADMA ratio and C-IMT was also showed significant negative correlation with the same analysis. CONCLUSIONS CSX patients had higher plasma ADMA levels and C-IMT values than the controls, reflecting the presence of subclinical atherosclerosis. These findings suggest that, besides endothelial dysfunction, presence of atherosclerosis may also contribute to the etiopathogenesis of the CSX phenomenon.

An Association Between Inflammatory State and Left Ventricular Hypertrophy in Hemodialysis Patients

This study was performed to investigate the potential relationship between left ventricular hypertrophy (LVH) and proinflammatory cytokines in hemodialysis (HD) patients and the effect of HD on cytokine production. Serum interleukin 1 beta (IL-1 β), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) measurements and echocardiographic studies were performed in 35 stable HD patients. A variety of probable risk factors for LVH including age, HD duration, blood pressure (BP), body mass index, lipid profile, hemoglobin, albumin, parathormone and homocysteine levels were also investigated. Additionally, the effect of HD procedure on cytokine levels was evaluated. Predialysis serum levels of IL-1β, IL-6, TNF-α, and homocysteine in HD patients were compared with 12 healthy subjects. Left ventricular hypertrophy was demonstrated in 20 (57%) of HD patients by echocardiography. Left ventricular mass index (LVMI) was correlated positively with systolic BP (r = 0.556, p = 0.001), diastolic BP (r = 0.474, p = 0.004), and serum levels of TNF-α (r = 0.446, p = 0.009).Multiple regression analysis showed that systolic BP and TNF-α levels were significant independent predictors of LVH. No relationship was observed between LVH and other parameters. The mean predialysis serum level of IL-6 was significantly higher in HD patients compared to healthy controls (15.7 ± 8.7 vs. 7.3 ± 0.7 pg/mL, p = 0.001). Predialysis serum levels of TNF-α in HD patients were higher when compared to healthy subjects, but the difference was not statistically significant (8.3 ± 3 vs. 7 ± 1.45 pg/mL, respectively, p > 0.05). However, serum levels of IL-6 and TNF-α significantly elevated after HD, when compared to predialysis levels (from 15.7 ± 8.7 to 17.8 ± 9.5 pg/mL, p = 0.001 and from 8.3 ± 3.0 to 9.9 ± 3.5 pg/mL p = 0.004, respectively). As a conclusion, in addition to BP, proinflammatory cytokines, TNF-α in particular, seem to be associated with LVH in ESRD patients.

B-type natriuretic peptide and extent of lesion on coronary angiography in stable coronary artery disease.

ObjectiveAlthough it is well established that plasma B-type natriuretic peptide (BNP) levels are higher in patients with acute coronary syndromes, the relationship between plasma BNP level and stable coronary artery disease is not clear. The aim of this study was to examine the relationship between plasma BNP levels and the extent of obstructive lesions on coronary angiography in stable coronary artery patients. MethodsPlasma BNP concentrations were measured in 62 patients with a diagnosis of stable angina pectoris who had a left ventricular ejection fraction (LVEF) ≥45% on echocardiographic evaluation. Coronary angiography was performed for all patients, who were than divided into two groups according to the results of the angiography. Group I consisted of the patients who had a lesion leading to an obstruction of the lumen in any coronary artery by less than 50% or those who had normal coronary arteries. All other patients constituted group II. ResultsIn group I (n=26), the mean plasma BNP level was 64.8±29.5 pg/ml. In group II (n=36), it was 99.7±55.4 pg/ml. BNP was significantly higher in group II (P=0.007) than group I. The BNP concentration of the patients with one-vessel disease (n=12), two-vessel disease (n=16), and three-vessel disease (n=8) were 77.9±34.9 pg/ml, 109.3±67.9 pg/ml, 113.3±48.1 pg/ml consecutively. In this respect, the plasma BNP was significantly higher in the groups with more extended vessel disease (P=0.02). When we compared the patients according to involvement of left anterior descending artery (LAD), BNP levels were significantly higher in this group, (116.1±55.8 pg/ml versus 64.1±30.2 pg/ml; P=0.001). ConclusionPlasma levels of BNP were higher in patients who have stable coronary artery disease with preserved left ventricular systolic function. The level of increase in plasma BNP concentration was positively correlated with the extent of lesion and LAD involvement on coronary angiography.

Independent relationship of serum uric acid levels with leukocytes and coronary atherosclerotic burden.

BACKGROUND AND AIM Epidemiological studies have shown that increased serum uric acid (SUA) level is associated with coronary artery disease (CAD). Leukocytes have been shown to play an important role in the atherosclerotic process. The aim of the study was to investigate whether there is any relationship among SUA, leukocyte counts and coronary atherosclerotic burden in patients who are suspected of having CAD. METHOD AND RESULTS We enrolled 690 eligible patients who had undergone coronary angiography between October 2005 and June 2006 in a consecutive manner. The relationship of SUA with total and differential leukocyte counts and CAD was investigated. Serum uric acid levels (5.57+/-1.64 vs 4.63+/-1.27 mg/dl, p<0.001) and leukocytes were higher in patients with CAD than those with normal coronary arteries (NCA). When we divided the patients into four groups according to the quartiles of SUA, we found that the monocyte count was prominently related with SUA (478+/-165, 553+/-177, 565+/-199 and 607+/-229 mm(-)(3), Q1-Q4, p<0.001). In multivariate analysis, SUA was an independent predictor of CAD (OR, 1.270; 95% CI, 1.087-1.484, p=0.003). When we performed multiple linear regression analyses to determine the independent predictors of inflammatory cells in blood, we found a strong, positive and independent relationship between SUA with neutrophils (beta+/-SE: 206+/-60, p=0.001) and monocytes (beta+/-SE: 35+/-7, p<0.001). CONCLUSION Our study results demonstrated that neutrophils and monocytes which play an important role in inflammation and atherosclerosis were independently related with SUA. This finding suggests an important epidemiologic relation and may provide a possible causative mechanism of SUA in atherosclerotic process.