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    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, I
    Background: 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.
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    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, I
    Background 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.