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Öğe Comparison of C-reactive protein levels inpatients with coronary artery ectasia versus patients with obstructive coronary artery disease(Excerpta Medica Inc-Elsevier Science Inc, 2004) Turhan, H; Erbay, AR; Yasar, AS; Balci, M; Bicer, A; Yetkin, EThis study evaluated plasma C-reactive protein (CRP) levels, a specific marker of inflammation, in 32 patients with isolated coronary artery ectasia (CAE) and compared the results with those of 32 patients with obstrucfive coronary artery disease without coronary artery ectasia and 30 subjects with angiographically normal coronary arteries. CRP levels were found to be significandy higher in patients with isolated CAE (p < 0.001), suggesting that more severe inflammation may be involved in the pathogenesis of CAE. (C) 2004 by Excerpta Medica, Inc.Öğe Effects of long-term beta-blocker therapy on P-wave duration and dispersion in patients with rheumatic mitral stenosis(Elsevier Ireland Ltd, 2005) Erbay, AR; Turhan, H; Yasar, AS; Bicer, A; Senen, K; Sasmaz, H; Sabah, IBackground: P-wave dispersion (PWD), has been defined as the difference between maximum and minimum P-wave duration. Prolonged P-wave duration and increased PWD have been reported to be related with increased risk for atrial fibrillation (AF). AF is the most common sustained arrhythmia encountered in patients with rheumatic mitral stenosis (MS). Beta-blockers are the mainstay of therapy in patients with rheumatic MS to control ventricular rate both during sinus rhythm and AF. In the present study, we aimed to evaluate the effect of long-term beta-blocker therapy on P-wave duration and PWD in patients with rheumatic MS. Method: Study population includes 46 patients (group I, 8 men, 38 women, mean age=34 +/- 8 years) with newly diagnosed moderate-to-severe rheumatic MS who have not taken any medication before and prescribed oral beta-blocker therapy and 46 healthy control subjects without any cardiovascular disease (group II, 8 men, 38 women, mean age=35 +/- 7 years). Mitral valve area, maximum and mean diastolic mitral gradients, left atrial diameter, and systolic pulmonary artery pressure were evaluated by transthoracic echocardiography before initiation of beta blocker therapy and repeated at the end of the first month. Baseline maximum and minimum P-wave duration and PWD were determined on 12-lead electrocardiogram recorded for each patient and control subject and repeated at the end of the first month after initiation of beta-blocker therapy in patient group. Results: Maximum P-wave duration and PWD were found to be significantly higher in patients with MS than those in control subjects (Maximum P-wave duration: 128 +/- 7 ms vs. 104 +/- 4 ms and PWD: 52 +/- 6 ms vs. 27 +/- 3 ms, p < 0.001 for both). Both groups had comparable minimum P-wave duration (75 +/- 4 ms vs. 76 +/- 4 ms, p=0.093). Maximum P-wave duration and PWD were found to be significantly decreased by long-term beta blocker therapy (Maximum P-wave duration; 128 +/- 7 ms vs. 122 +/- 6 ms, p < 0.001, PWD; 52 +/- 6 ms vs. 47 5 ms, p < 0.001). However, there was no significant difference between the values of minimum P wave duration measured before and at the end of the first month of beta-blocker therapy (75 +/- 4 ms vs. 75 +/- 3 ms, p=0.678). Statistically significant decrease were detected on maximum and mean mitral gradient and systolic pulmonary artery pressure and resting heart rate at the end of the first month of beta-blocker therapy. However, only the change in resting heart rate was found to be significantly correlated with the decrease in maximum P-wave duration and PWD (Maximum P-wave duration: r=0.327, p=0.026, PWD: r=0.378, p=0.01). Conclusion: We have shown for the first time that long-term beta-blocker therapy causes a significant decrease in maximum P-wave duration and PWD in patients with rheumatic MS. (c) 2004 Elsevier Ireland Ltd. All rights resrved.Öğe High prevalence of metabolic syndrome among young women with premature coronary artery disease(Lippincott Williams & Wilkins, 2005) Turhan, H; Yasar, AS; Basar, N; Bicer, A; Erbay, AR; Yetkin, EBackground The metabolic syndrome is more prevalent with the use of the recently defined National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria and is associated with a greater risk of atherosclerotic cardiovascular disease than any of its individual components. This study evaluated the prevalence of metabolic syndrome in female and male patients with newly diagnosed premature coronary artery disease. Method The study population included 582 consecutive patients (496 men, 86 women) with newly diagnosed premature coronary artery disease (aged less than or equal to 45 years). Besides classic major coronary risk factors, all patients were evaluated for the presence of metabolic syndrome based on the NCEP ATP III criteria. Results The majority of patients were male (85% versus 15%). The overall prevalence of metabolic syndrome was 37%. Women with premature coronary artery disease were found to have a higher prevalence of metabolic syndrome than men (73% versus 31% respectively, p < 0.001). Furthermore, the mean number of components of metabolic syndrome was significantly higher in women compared to men (2.81 +/- 1.09 versus 1.85 +/- 1.08 respectively, p < 0.001). In addition, metabolic syndrome was detected to be the most frequent coronary risk factor in women (73%). Besides, cigarette smoking was found to be significantly higher in males compared to females (70% versus 36% respectively, p < 0.001) and it was the most prevalent coronary risk factor in men with premature coronary artery disease. Conclusion We have shown for the first time a higher prevalence of metabolic syndrome in young females compared with young males with premature coronary artery disease. This data may be useful in directing primary and secondary preventive measures. (C) 2005 Lippincott Williams Wilkins.Öğe Impaired coronary blood flow in patients with metabolic syndrome: Documented by Thrombolysis in Myocardial Infarction (TIMI) frame count method(Mosby-Elsevier, 2004) Turhan, H; Erbay, AR; Yasar, AS; Bicer, A; Sasmaz, H; Yetkin, EBackground Endothelium plays an important role in regulating coronary vascular tone. In addition, several of cardiovascular risk factors that are associated metabolic syndrome have been reported to be associated with endothelial dysfunction. In the present study we aimed to evaluate the coronary blood flow in patients with metabolic syndrome by means of the Thrombolysis in Myocardial Infarction (TIMI) frame count. Method Forty-two patients with metabolic syndrome (group 1) and 42 control subjects without metabolic syndrome (group II) were included in the study. All subjects had angiographically proven normal coronary arteries. Diagnosis of metabolic syndrome was based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines published in 2001. Coronary flow rates of all subjects were documented by TIMI frame count method. Results TIMI frame counts for each of the major epicardial coronary arteries were found to be significantly higher in patients with metabolic syndrome compared with control subjects (corrected TIMI frame count for left anterior descending coronary artery: 35 +/- 7 vs 25 +/- 7, respectively; left circumflex coronary artery: 32 9 vs 25 7, respectively; right coronary artery: 31 +/- 9 vs 24 +/- 5, respectively; P <.001 for all). Statistically significant independent relationships were found between TIMI frame count and body mass index (R-2 = 0.480, P =.009), waist circumference (R-2 = 0.551, P = .001), and triglyceride level (R-2 = 0.434, P =.036). Conclusion We have shown for the first time that patients with metabolic syndrome and angiographically normal coronary arteries have higher TIMI frame counts for all 3 coronary vessels, indicating impaired coronary blood flow, compared to control subjects without metabolic syndrome.Öğe Plasma homocysteine levels in patients with isolated coronary artery ectasia(Elsevier Ireland Ltd, 2005) Turhan, H; Erbay, AR; Yasar, AS; Bicer, A; Sahin, O; Nurcan, B; Yetkin, EObjective: Hyperhomocysteinemia is recognized as an independent risk factor for arterial disease including coronary artery disease, cerebrovascular disease and peripheral vascular disease. Previously, an association between increased plasma homocysteine level and peripheral arterial aneurysms has been reported. However, the relationship between coronary artery ectasia (CAE) and plasma homocysteine level has not been investigated. Accordingly, this study was designed to investigate plasma homocysteine level in patients with isolated CAE. Methods: Thirty-two patients with isolated CAE without significant stenosis and 30 control subjects with angiographically normal coronary arteries were included in this study. Fasting plasma homocysteine concentrations were measured by Florescence Polarization Immunoassay method using homocysteine kids. Hyperhomocysteinemia is defined as plasma homocysteine levels above the 95th percentile of the control subjects (13.6 mu mol/l). Results: According to the definition of hyperhomocysteinemia, 19 (59%) of patients with isolated CAE had elevated levels of plasma hornocysteine compared to 2 (7%) in the control subjects with angiographically normal coronary arteries (p < 0.001). In addition, patients with isolated CAE had significantly higher levels of plasma homocysteine compared to control subjects (14.9 +/- 4.5 mu mol/l vs. 8.6 +/- 1.9 mu mol/l respectively, p < 0.001). Besides, we detected a significant positive correlation between the number of ectasic segment and plasma homocysteine level (r=0.537, p=0.002). Conclusion: We have shown for the first time an association between elevated plasma homocysteine level and isolated CAE. Larger prospective studies are needed to confirm the role of hyperhomocysteinemia in CAE and to evaluate the usefulness of homocysteine-lowering therapies. (c) 2005 Elsevier Ireland Ltd. All rights reserved.Öğe Plasma soluble adhesion molecules; intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin levels in patients with isolated coronary artery ectasia(Lippincott Williams & Wilkins, 2005) Turhan, H; Erbay, AR; Yasar, AS; Aksoy, Y; Bicer, A; Yetkin, G; Yetkin, EPlasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM)-1, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin leves of patients with isolated coronary artery ectasia (CAE), patients with obstructive coronary artery disease without CAE and subjects with angiographically normal coronary arteries were evaluated. Patients with isolated CAE were detected to have significantly higher levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive coronary artery disease without CAE OCAM, 673 153 versus 381 +/- 106, respectively, P < 0.001; VCAM-1, 2366 +/- 925 versus 1136 +/- 208, respectively, P < 0.001; E-selectin, 74 +/- 21 versus 61 +/- 18, respectively, P = 0.01) and subjects with normal coronary arteries (ICAM-1, 673 +/- 153 versus 303 +/- 131, respectively, P < 0.001; VCAM-1, 2366 925 versus 729 231, respectively, P < 0.001; E-selectin, 74 +/- 21 versus 49 +/- 9, respectively, P < 0.001), suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in patients with isolated CAE. \ Background The common coexistence of coronary artery ectasia (CAE) with coronary artery disease (CAD) suggests that it may be a variant of CAD. However, it is not clear why some patients with obstructive CAD develop CAE whereas most do not. inflammation has been reported to be a major contributing factor to both obstructive and aneurysmatic vascular disorders and therefore, in the present study, the plasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin levels in isolated CAE were investigated. Methods The study population consisted of three groups: the first consisted of 32 patients with isolated CAE without stenotic lesion; the second of 32 patients with obstructive CAD without CAE; and the third group of 30 control subjects with normal coronary arteries. Coronary diameters were measured as the maximum diameter of the ectasic segment by use of a computerized quantitative coronary angiography analysis system. According to the angiographic definition used in the Coronary Artery Surgery Study, a vessel is considered to be ectasic when its diameter is greater than or equal to 1.5 times that of the adjacent normal segment in segmental ectasia. Plasma soluble ICAM-1, VCAM-1 and E-selectin levels were measured in all patients and control subjects using commercially available enzyme-linked immunosorbent assay kits. Results Patients with isolated CAE were found to have significantly higher levels of plasma soluble ICAM-1, VCAM-1, and E-selectin in comparison with patients with obstructive CAD without CAE (ICAM, 673 +/- 153 versus 381 +/- 106, respectively; P < 0.001; VCAM-1, 2366 +/- 925 versus 1136 +/- 208, respectively; P < 0.001; E-selectin, 74 +/- 21 versus 61 +/- 18, respectively; P = 0.01) and control subjects with normal coronary arteries (ICAM-1, 673 +/- 153 versus 303 +/- 131, respectively;, P < 0.001; VCAM-1, 2366 +/- 925 versus 729 +/- 231, respectively; P < 0.001; E-selectin, 74 +/- 21 versus 49 +/- 9, respectively; P < 0.001). In addition, we detected statistically significant positive correlation between the total length of ectasic segments and the levels of plasma soluble ICAM-1 (r=0.625; P < 0.001), VCAM-1 (r= 0.548; P= 0.001) and E-selectin (r=0.390; P=0.027). Multivariate logistic regression analysis revealed a significant independent relation between isolated CAE and ICAM-1 [odds ratio (OR)= 1.023; 95% confidence interval (CI) = 1.0048-1.0414; P= 0.0129] and VCAM-1 (OR = 1.0057; 95% Cl = 1.0007-1.0106; P= 0.0240). Conclusions We have shown that patients with isolated CAE have raised levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive CAD without CAE and control subjects with normal coronary arteries, suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in these patients. (C) 2005 Lippincott Williams Wilkins.
