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Öğe Assessment of ventricular repolarization in deaf-mute children(Springer, 2000) Tuncer, C; Çokkeser, Y; Komsuoglu, B; Ödemir, R; Güven, A; Pekdemir, H; Sezgin, ATThe long QT syndrome is a congenital disease with frequent familial transmission, characterized primarily by prolongation of the QT interval and by the occurrence of life-threatening arrhythmias. The syndrome may be familial, with or without congenital deafness, or it may be idiopathic. We attempted to assess ventricular repolarization and to identify patients with the Jervell and Lange-Nielsen syndrome among 132 deaf-mute school children. Five deaf-mute subjects had Jervell and Lange-Nielsen syndrome. The deaf-mute subjects were divided into two subgroups according to the length of their QT intervals: group 1 included 5 cases with the long QT interval (>440 msec), and group 2 included 127 subjects with the normal QT interval (less than or equal to 440 msec). Group 3 was composed of 96 control subjects. The mean QT, QTc, JT, and JTc intervals (418 +/- 70, 500 +/- 38, 302 +/- 65, and 389 +/- 36 msec, respectively) in group 1 were significantly longer than those of group 2 (344 +/- 23, 408 +/- 22, 249 +/- 34, and 291 +/- 28 msec, respectively) and group 3 (325 +/- Il, 383 +/- 26, 228 +/- 36, and 269 +/- 46 msec, respectively). The dispersion (d) values (QT-d, QTc-d, JT-d, and JTc-d; 63 +/- 10, 73 +/- 8, 60 +/- 8, and 62 +/- Il msec, respectively) of group 1 were significantly longer than those of group 2 (49 +/- 16, 43 +/- 11, 48 +/- 21, and 45 +/- 18 msec, respectively) and group 3 (33 +/- 13, 33 +/- 14, 28 +/- 16, and 27 +/- 14 msec, respectively) at similar mean RR intervals. Also, the mean QT, QTc, JT, and JTc intervals and the dispersion values (QT-d, QTc-d, JT-d, and JTc-d) in group 2 were significantly longer than those of group 3 at similar mean RR intervals. Consequently, in this study, we determined that the deaf-mute children who did not meet the criteria for Jervell and Lange-Nielsen syndrome still had evidence of subtle derepolarization abnormalities evidenced by intermediate prolongation of QTc, JTc, and the corresponding measures of dispersion, and we believe an electrocardiogram examination of deaf-mute subjects will reveal this potentially life-threatening syndrome.Öğe Effect of trimetazidine on late potentials after acute myocardial infarction(Springer, 1999) Özdemir, R; Tuncer, C; Aladag, M; Güven, A; Sezgin, AT; Pekdemir, H; Korkmaz, METhe purpose of this study was to evaluate the effect of trimetazidine on late potentials in patients with acute myocardial infarction. A total of 60 patients (52 males, mean age 55 +/- 2 years, and 8 females, mean age 54 +/- 1.8 years) with the diagnosis of acute myocardial infarction were included in this study. The study was designed as a randomized, double-blinded, and placebo-controlled trial. Signal-averaged electrocardiography and echocardiography were performed during the first 2 days of acute myocardial infarction and were repeated between days of 8 and 15 (mean 11). Patients were treated with trimetazidine (n = 30) or placebo (n = 30). In the placebo group, the total filtered QRS duration and low-amplitude terminal signal duration increased (from 102.7 +/- 1.8 ms to 113.3 +/- 1.8 ms, and from 32.2 +/- 0.9 ms to 38.3 +/- 1.1 ms; P < 0.001), the root mean square voltage of the terminal 40 ms of the QRS decreased (from 28.6 +/- 2.1 mu V to 21.4 +/- 1.3 mu V; P < 0.001), and the incidence of late potentials increased (from 30% to 46%; P < 0.01) significantly. In the trimetazidine group, these measurements were a decrease from 102.9 +/- 1.9 ms to 100 +/- 2.0 ms (NS), an increase from 31.6 +/- 0.9 ms to 32.5 +/- 0.9 ms (NS), a decrease 9.3 +/- 2.0 mu V to 27.3 +/- 1.8 mu V (P < 0.01), and a decrease from 33% to 30% (NS), respectively. The ejection fraction was 47.1 +/- 1.3% to 50.8 +/- 1.2% in the placebo group (P = 0.05), and 48.1 +/- 1.1% to 53.4 +/- 1.2% (P < 0.01) in the trimetazidine group. It is concluded that trimetazidine reduces late potentials after acute myocardial infarction without changing blood pressure and heart rate.Öğe Heparin-induced exfoliative dermatitis in a patient on haemodialysis(Adis International Ltd, 1999) Sevinc, A; Pekdemir, H; Harputluoglu, M; Sari, R; Buyukberber, S; Senol, M[Abstract Not Available]Öğe Impact of hemodialysis on comprehensive ventricular repolarization(Acta Cardiologica, 1997) Tuncer, C; Kulan, K; Komsuoglu, B; Ozdemir, R; Guven, A; Pekdemir, H; Sezgin, ATImpact of hemodialysis on comprehensive ventricular repolarization - Cardiac arrhythmia are one of the most important problems in haemodialysis patients. An important cause of the arrhythmias is inhomogenous myocardial repolarization. In this study, the ventricular repolarization parameters (QT, QTc, JT and JTc) and dispersions (d) of the parameters (QT-d, QTc-d, JT-d and JTc-d) were evaluated. Also, were recorded the right-sided lends (RV3-6) and posterior leads (V7-9) in addition to the standard 12 lead ECG to assess comprehensive ventricular repolarization. The leads were divided in three groups: Group A (Standard ECG leads), Group B (Right-sided leads) and Group C (All of the leads). Among the above mentioned parameters, only JT and JTc intervals decreased significantly in all groups. There was no significant difference between the groups in evaluation of the parameters. It was concluded that in assessment of ventricular repolarization, the most important ECG intervals may be JT and JTc intervals, and the standard 12 lead ECG record is sufficient in evaluation of ventricular repolarization in hemodialysis patients.Öğe Impaired cardiac autonomic functions in patients with environmental asbestos exposure: A study of time domain heart rate variability(Churchill Livingstone Inc Medical Publishers, 2003) Pekdemir, H; Camsari, A; Akkus, MN; Cicek, D; Tuncer, C; Yildirim, ZEnvironmental asbestos exposure is related to diffuse pleural disease (thickening and calcification) and restrictive pulmonary disease. To assess cardiac autonomic system, we investigated the time domain heart rate variability (HRV) by Holter monitoring and their correlation with pulmonary function tests in patients with pleural disease caused by environmental asbestos exposure. We studied 45 patients (26 men, 19 women, aged 62.67 +/- 10.1 years) and 35 healthy patients who had similar sex and age profile to the patients (24 men, 11 women, aged 59.31 +/- 8.4 years). The asbestosis group was divided into 3 subgroups according to the severity of forced vital capacity (FVC) severe (group 1) (n = 12): FVC less than 50% of expected, moderate (group 2) (n = 16): FVC 64%-51% of expected and mild (group 3) (n = 17): FVC 65%-80% of expected. HRV parameters were significantly different among all groups (P < .0001). Comparing the 4 groups (subgroups and control group), group 1 had the lowest mean HRV values and controls had the highest mean HRV values (P < .0001). Severity of autonomic dysfunction was correlated with the severity of FVC and arterial oxygen pressure. Right ventricular end-diastolic internal diameter (RVEDID) and right ventricular end-systolic internal diameter (RVESID) values were significantly increased in patients ( P < .0001, P < 0.0001, respectively). Pulmonary acceleration time (AcT) values were shorter in all patient groups than control group (P < .0001). It was shortest in group 1. Group 2 and 3 had shorter AcT values than control group. HRV parameters were correlated positively with AcT values and negatively with RVEDID and RVESID values. In conclusion, patients with restrictive pulmonary disease due to environmental asbestos exposure had autonomic dysfunction, which was correlated with the severity of restriction. This was thought to be the result of chronic hypoxia, pulmonary hypertension, and right ventricular enlargement.
