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Öğe Comparison of P-wave duration and dispersion in patients aged ?65 years with those aged ?45 years(Churchill Livingstone Inc Medical Publishers, 2003) Turhan, H; Yetkin, E; Sahin, O; Yasar, AS; Senen, K; Atak, R; Sasmaz, HP-wave dispersion (PWD) is a Dew electrocardiographic marker that reflects discontinuous and inhomogeneous propagation of sinus impulses, which has been studied in some cardiac conditions as a useful predictor of paroxysmal atrial fibrillation (AF). The aim of the peresent study was to compare P-wave duration and PWD in patients less than or equal to45 versus greater than or equal to65 years of age. The study consisted of 2 groups. Group I included 118 patients aged greater than or equal to65 years (86 men, 32 women, mean age = 69 +/- 4 years). Group II included 72 patients aged less than or equal to45 years (53 men, 19 women, mean age = 41 +/- 4 years). All patients were selected from those who were undertaken coronary angiography in our hospital with a suspicion of coronary artery disease and detected as having angiographically normal coronary arteries. All patients were undertaken transthoracic echocardiography to evaluate the presence of any structural and functional cardiac abnormality. Maximum and minimum P-wave durations and PWD were calculated from 12-lead surface electrocardiogram. Maximum P-wave duration and PWD were significantly higher in group I patients than in group II patients (P <.00 1). However, there was no statistically significant difference between group I patients and group H patients regarding minimum P-wave duration (p =0.9). Left atrial diameter, left ventricular wall thicknesses, mitral A velocity, deceleration time and isovolumic relaxation time were significantly higher in group I patients than in group 11 patients. However, mitral E velocity were significantly lower in group I patients than in group II patients. A significant positive correlation was detected between PWD and age, left atrial diameter, mitral A velocity, deceleration time and isovolumic relaxation time. in addition, we found a significant negative correlation between PWD and mitral E velocity. PWD, indicating increased risk for paroxysmal AF, was found to be significantly higher in patients greater than or equal to65 years of age than in those less than or equal to45 years of age. Further prospective studies that include larger series and long term follow-up are needed to clarify the clinical utility of PWD as a predictor of increased risk for paroxysmal AF in old patients.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 Elevated level of plasma homocysteine in patients with slow coronary flow(Elsevier Ireland Ltd, 2005) Erbay, AR; Turhan, H; Yasar, AS; Ayaz, S; Sahin, O; Senen, K; Sasmaz, HBack-ground: Elevated plasma levels of homocysteine are currently considered a major, independent risk factor for cardiovascular diseases. Recently, several investigators have Suggested that even mild elevation in plasma homocysteine level can severely disturb vascular endothelial function and subsequently impair coronary blood flow. Accordingly, we investigated plasma homocysteine level in patients with slow coronary flow. Method: Study population included 53 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 21 females, 32 males, mean age=48 +/- 9 years), and 50 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 22 females, 28 males, mean age=50 +/- 8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviations above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. The mean TIMI frame Count for each patient and control subject was calculated by adding the TIMI frame counts for each major epicardial coronary artery and then dividing the obtained value into 3. Plasma homocysteine level was measured in all patients and control subjects using commercially available homocysteine kits. Results: There was no statistically significant difference between two groups in respect to age, gender, hypertension, diabetes mellitus, hyperlipidemia and cigarette smoking (p > 0.05). Plasma homocysteine level of patients with slow coronary flow were found to be significantly higher than those of control subjects (15.5 +/- 5.7 vs. 8.7 +/- 4.2 mu M/l, respectively, p < 0.001). Moreover, we found a significant positive correlation between plasma homocysteine level and mean TIMI frame count (r=0.660, p < 0.001). Conclusion: We have shown that patients with slow coronary flow have raised level of plasma homocysteme compared to control subjects with normal coronary flow. This data suggests that elevated level of plasma homocysteine may play a role in the pathogenesis of slow coronary flow. (c) 2004 Elsevier Ireland Ltd. All rights reserved.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 Impaired coronary collateral vessel development in patients with metabolic syndrome(Lippincott Williams & Wilkins, 2005) Turhan, H; Yasar, AS; Erbay, AR; Yetkin, E; Sasmaz, H; Sabah, IBackground The development of coronary collateral vessels is the physiological response of myocardial tissue to hypoxia or ischemia, which results in an increase in blood supply to the tissue. However, a lack of collateral vessels or the presence of poor collateralization in some patients despite the presence of significant coronary stenosis or obstruction and evidence of myocardial ischemia suggest that some other factors may affect the development of collateral circulation. In the present study we aimed to evaluate coronary collateral circulation in patients with metabolic syndrome with advanced coronary artery disease and compare the results with those of patients without metabolic syndrome. Method The study population comprised 102 patients with metabolic syndrome and advanced coronary artery disease (-90% diameter stenosis in at least one major epicardial coronary artery) and 102 control participants without metabolic syndrome who also had >= 90% diameter stenosis in at least one major epicardial coronary artery. The diagnosis of metabolic syndrome was based on the National Cholesterol Education Program Adult Treatment Panel III clinical definition. Coronary collateral vessels were analysed according to the Cohen and Rentrop grading system. Both groups were also divided into two additional groups according to the Rentrop collateral score as patients with poor collateral circulation (Rentrop score 0-1) and good collateral circulation (Rentrop score 2-3). Results The mean Rentrop collateral score for patients with metabolic syndrome was significantly lower than for those without metabolic syndrome (1.38 +/- 0.79 compared with 1.99 +/- 1.08, respectively, P < 0.001). When two groups were compared with respect to poor and good collateral circulation, poor collateral circulation was found to be significantly higher in the metabolic syndrome group (70% compared with 32%, respectively, P < 0.001). Moreover, multivariate logistic regression analysis revealed a significant relationship between poor collateral circulation and metabolic syndrome (odds ratio=4.29, 95% confidence interval = 1.73-10.69, P = 0.002). Conclusion We have shown for the first time that the development of coronary collateral vessels is poorer in patients with metabolic syndrome with advanced ischemic heart disease than in control participants without metabolic syndrome. Thus, it can be suggested that metabolic syndrome is one of the significant factors affecting the development of coronary collateral vessels adversely.Öğe Increased levels of soluble adhesion molecules in patients with isolated coronary artery ectasia(W B Saunders Co Ltd, 2003) Turhan, H; Yetkin, E; Erbay, AR; Atak, R; Senen, K; Sasmaz, H; Cehreli, S[Abstract Not Available]Öğe Increased P-wave duration and P-wave dispersion in patients with aortic stenosis(Blackwell Futura Publishing, Inc, 2003) Turhan, H; Yetkin, E; Atak, R; Altinok, T; Senen, K; Ileri, M; Sasmaz, HBackground: P-wave dispersion (PWD), defined as the difference between the maximum and minimum P-wave duration, has been proposed as being useful for the prediction of paroxysmal atrial fibrillation (AF). AF is the most common arrhythmia and an important prognostic indicator for clinical deterioration in patients with aortic stenosis (AS). The,aim of the present study was to evaluate PWD in patients with AS. Methods: The study population consisted of two groups: Group I consisted of 98 patients with AS (76 men, 22 women; aged 63 8 years) and group II consisted of 98 healthy subjects (same age and sex) without any cardiovascular disease. A 12-lead electrocardiogram was recorded for each subject. The P-wave duration was calculated in all leads of the surface electrocardiogram. The difference between the maximum and minimum P-wave duration was calculated and was defined as the PWD. All patients and control subjects were also evaluated by echocardiography to measure the left atrial diameter, left ventricular ejection fraction, left ventricular wall thicknesses, and the maximum and mean aortic gradients. Patients were also evaluated for the presence of paroxysmal AF. Results: Maximum P-wave duration and PWD of group I were found to be significantly higher than those of group II. In addition, patients with paroxysmal AF had significantly higher PWD than those without paroxysmal AF. There was no significant difference between the two groups regarding minimum P-wave duration. In addition, there was no significant correlation between echocardiographic variables and PWD. Conclusion: PWD, indicating increased risk for paroxysmal AF, was found to be significantly higher in patients with AS than in those without it. Further assessment of the clinical utility of PWD for the prediction of paroxysmal AF in patients with severe AS will require longer prospective studies.Öğe Increased soluble adhesion molecules in patients with slow coronary flow(W B Saunders Co Ltd, 2003) Turhan, H; Yetkin, E; Erbay, AR; Atak, R; Senen, K; Sasmaz, H; Cehreli, S[Abstract Not Available]
