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Purpose: Vasovagal syncope is a common and challenging problem that may result in injury and causes susbstantial anxiety among patients and their relatives. However, treatment of vasovagal syncope with standard pharmacologic approaches is not satisfactory. The aim of this study is to investigate the effect of amitriptyline, a tricyclic antidepressant drug, by using its anticholinergic effects in preventing syncopal episodes in patients with vasovagal syncope. Methods: In this study, 74 patients (mean age 24 ± 1.9 years, 26 male) with a history of recurrent syncope and baseline positive head-up tilt table test (syncope or presyncope) were included. Oral amitriptyline treatment was given to all patients, with a starting dose of 10 mg once a day. Head-up tilt table test was performed in all patients 4 weeks after the treatment started. Patients were followed up clinically for 6 months. Results: After 4 weeks, during head-up tilt table test in 69 patients (93%), syncope or presyncope was not seen and test was assumed as negative. At the end of the 6th month, 67 patients (91%) were free of symptoms. Only two patients (0.3%) did not tolerate amitriptyline due to side effects. Conclusions: Oral amitriptyline can be used in the prevention of recurrent episodes of vasovagal syncope safely. However, randomized controlled studies are essential to assess the real effectiveness of this therapy.

Background: Reduced heart rate recovery (HRR) in coronary artery disease (CAD) is predictive of increased cardiovascular mortality and is related to reduced parasympathetic tonus. Objective: To investigate HRR and heart rate variability (HRV) measured at steady state condition and the relationship between these two parameters in CAD. Materials and Methods: In our study, we enrolled 33 (28 males, mean age 52.4 ± 9.6 years) patients with CAD who did not have heart failure, atrial fibrillation, pacemaker, and any disease state that could affect the autonomic functions and 38 age-matched healthy subjects (21 males, mean age 48.3 ± 7.8 years). All the patients underwent submaximal treadmill exercise testing (Bruce protocol). HRR was calculated by subtracting the heart rate values at the 1st, 2nd, and 3rd minutes of the recovery phase from the peak heart rate (HRR1, HRR 2, HRR3). Before exercise testing, short-term steady state HRV analyses of all subjects were obtained with the time- and frequency-domain methods and were correlated to HRR. For frequency-domain analysis, low-frequency HRV (LF, 0.004-0.15 Hz), high-frequency HRV (HF, 0.15-0.5 Hz), and LF/HF ratio were measured for 5 minutes in the morning. For time-domain analysis, standard deviation of the normal-to-normal NN intervals (SDNN), square root of the mean squared differences of successive N-N intervals (RMSSD), and proportion derived by dividing the number of interval differences of successive N-N intervals greater than 50 ms by the total number of N-N intervals (pNN50) were obtained. Only HRR3 was used for the correlation analysis. Results: In CAD groups, the HF, an indicator of parasympathetic activation, was significantly reduced, whereas the LF and LF/HF values, which are indicators of sympathetic activity, were increased (P = 0.0001 for each parameter). The time-domain parameters SDNN, RMSSD, and pNN50 were significantly reduced in the patient group (P = 0.0001, P = 0.009, and P = 0.0001, respectively). Similar to the HRV parameters, the HRR1, HRR2, and HRR3 values were significantly reduced in the patient group (P = 0.0001 for each parameter). We observed a significant negative correlation between HRR3 and LF (r =-0.67, P = 0.0001) and between HRR3 and LF/HF (r =-0.62, P < 0.0001), while there was a significant positive correlation between HRR 3 and HF, SDNN, RMSSD, and pNN50 (r = 0.69, P = 0.0001; r = 0.41, P = 0.0001; r = 0.31, P = 0.008; and r = 0.44, P = 0.0001). Conclusions: HRR and HRV are significantly reduced in CAD. The reduction in HRR is parallel to the changes in HRV parameters. HRR, which can be measured easily in the recovery phase of exercise testing, can be used to detect the depression of parasympathetic tonus and to evaluate the basal autonomic balance in this patient group. ©2006, Copyright the Authors.

Background: Several studies demonstrated that P wave dispersion (PWD) increased after coronary occlusion. The effect of primary percutaneous coronary intervention (PCI) on PWD needs to be elucidated. Methods: The study consisted of 125 patients with acute myocardial infarction (110 men, mean age 59.8 ′ 7.8 years) undergoing primary PCI. The patients were divided into three groups according to thrombolysis in myocardial infarction myocardial perfusion grade (TMPC) after successful PCI. Groups 1 (n = 12), 2 (n = 9), and 3 (n = 104) included the patients with TMPC 0/1, 2, 3, respectively. Electrocardiograms were obtained before and approximately 66 ′ 18 minutes after PCI. Results: PWD and P m a x i m u m after PCI were significantly lower than the preintervention values (P < 0.001 for both). When PWD and P m a x i m u m values after PCI were compared among groups, PWD and P m a x i m u m in groups 1 and 2 were found to be higher than those of group 3 (P < 0.001 for PWD and P m a x i m u m ). Atrial fibrillation (AF) occurred in 14 patients. P m a x i m u m and PWD in patients with AF were higher compared to those of the patients without AF (P < 0.001 for both P wave parameters). Also more frequent AF attacks were observed in group 1 compared to group 3 (P < 0.001). Conclusions: PWD and P m a x i m u m after primary PCI were lower compared to the preintervention values. Prolonged PWD in patients with poor myocardial perfusion can contribute to increased mortality, and also it can can be combined with ST segment resolution to predict clinical reperfusion and might help in predicting AF.

Background: Atrial fibrillation is a frequent arrhythmia in patients undergoing hemodialysis. The consequences of hemodialysis on P wave durations and P wave dispersion have not been fully understood. The objective of this study was to study the effect of dialysis on P wave maximum (P m a x ), P wave minimum (P m i n ), and P wave dispersion (P d ). Methods: We studied P m a x , P m i n , and P d in 32 patients (17 men and 15 women, mean age 54 ′ 18 years) with chronic renal failure undergoing hemodialysis. The difference between maximum and minimum P wave duration was calculated and defined as P wave dispersion (P d = P m a x - P m i n ). Results: There was a significant increase in P m a x at the end of dialysis compared to the beginning (98 ′ 13 ms vs. 125 ′ 12 ms, P < 0.001). P m i n did not show any significant change (71 ′ 11 ms vs. 73 ′ 10 ms, P = 0.42). P d was significantly increased at the end of dialysis (27 ′ 9 ms vs. 52 ′ 11 ms, P < 0.001). There was a negative correlation between serum potassium, magnesium, phosphate, blood urea nitrogen, and creatinin at the end of dialysis and P m a x and P d respectively (P < 0.05). A weak positive correlation was found between serum calcium, bicarbonate at the end of dialysis and P m a x and P d (P < 0.05). Conclusion: Hemodialysis ends with significant increase in P wave maximum duration and P wave dispersion, which might be responsible for the increased occurrence of atrial fibrillation in these groups of patients.

Background: There are few data related to the seasonal influences on the QT dispersion. Methods: We analyzed the effects of seasons on QT dispersion in a large group of healthy young males. We studied the seasonal variability of QT dispersion in 523 healthy male subjects aged 22 ± 4 years (ranging from 20 to 26). Four seasonal 12-lead resting electrocardiograms (ECGs) recorded at double amplitude were performed at 25 mm/s at intervals of 3 months. Subsequent ECGs were recorded within 1 hour of the reference winter recording. QT dispersion was defined as the difference between the longest and the shortest mean QT intervals. Results: There was a significant seasonal variation in QT dispersion (P = 0.001), with the largest QT dispersion in winter (71 ± 18 ms) and the smallest one in spring (43 ± 19). Conclusion: There exists a significant seasonal variation in QT dispersion of healthy subjects and such variability should be taken into consideration in the evaluation process of QT dispersion.