Dursun Atilgan
Istanbul University
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Featured researches published by Dursun Atilgan.
American Journal of Cardiology | 2000
Tufan Tükek; Vakur Akkaya; Şeref Demirel; Ahmet Bilge Sözen; Hasan Kudat; Dursun Atilgan; Mustafa Özcan; Özen Güven; Ferruh Korkut
The purpose of this study was to investigate the effect of the Valsalva maneuver on P-wave durations and dispersion. After the Valsalva maneuver, we found that maximum P-wave duration increased, minimum P-wave duration decreased, and P-wave dispersion increased in controls, whereas the opposite was true for unselected patients with paroxysmal AF. It was concluded that patients with paroxysmal AF performing the Valsalva maneuver normalized their P-wave dispersion, thereby correcting the inhomogeneous intra-atrial conduction.
Journal of International Medical Research | 2006
Hasan Kudat; Vakur Akkaya; Ahmet Bilge Sözen; S Salman; Seref Demirel; Mustafa Özcan; Dursun Atilgan; Mt Yilmaz; Özen Güven
Diabetes mellitus can cause cardiovascular autonomic neuropathy and is associated with increased cardiovascular deaths. We investigated cardiovascular autonomic neuropathy in diabetics and healthy controls by analysis of heart rate variability. Thirty-one diabetics and 30 age- and sex-matched controls were included. In the time domain we measured the mean R-R interval (NN), the standard deviation of the R-R interval index (SDNN), the standard deviation of the 5-min R - R interval mean (SDANN), the root mean square of successive R - R interval differences (RMSSD) and the percentage of beats with a consecutive R - R interval difference > 50 ms (pNN50). In the frequency domain we measured high-frequency power (HF), low-frequency power (LF) and the LF/HF ratio. Diabetes patients had lower values for time-domain and frequency-domain parameters than controls. Most heart rate variability parameters were lower in diabetes patients with chronic complications than in those without chronic complications.
International Journal of Cardiology | 2003
Tufan Tükek; Pinar Yildiz; Dursun Atilgan; Volkan Tuzcu; Mehmet Eren; Osman Erk; Şeref Demirel; Vakur Akkaya; Murat Dilmener; Ferruh Korkut
We examined the possible effect of diurnal variability of heart rate on the development of arrhythmias in patients with chronic obstructive pulmonary disease (COPD). Forty-one COPD patients (M/F: 39/2, mean age: 59+/-8.5 years) and 32 (M/F: 27/5, mean age: 57+/-11 years) healthy controls were included. Twenty-four hour ECG recordings were analyzed for atrial fibrillation (AF) or ventricular premature beats (VPB), and circadian changes in heart rate variability (HRV) were assessed by dividing the 24-h period into day-time (08:00-24:00 h) and night-time (24:00-08:00 h) periods. Night-time total (TP), low frequency (LF) and high frequency (HF) powers were similarly lower from day-time parameters in AF(-) COPD patients (HF 3.91+/-1 vs. 4.43+/-1.04 ms(2), P=0.001) and controls (HF 3.95+/-0.72 vs. 4.82+/-0.66 ms(2), P<0.001). The LF/HF ratios were also significantly reduced in the same patient groups (AF(-) COPD 1.35+/-0.21 vs. 1.27+/-0.19, P=0.04, controls 1.43+/-0.14 vs. 1.24+/-0.09, P<0.001). Night-time TP and LF were increased, HF unchanged and LF/HF significantly increased (1.11+/-0.25 vs. 1.19+/-0.27, P<0.05) in AF(+) COPD patients. Frequency of VPB was correlated with corrected QT dispersion (QTc(d)) (r=0.52, P=0.001) and the day-time/night-time HF ratio (r=0.43, P=0.02). Patients with QTc(d)>or=60 ms did not have the expected increase in night-time HF and had a statistically insignificant increase in LF/HF ratio. In COPD patients with QTc(d)<60 ms, circadian changes in HRV parameters were parallel with the controls. We concluded that COPD patients with arrhythmia had circadian HRV disturbances such as unchanged night-time parasympathetic tone and disturbed sympatho-vagal balance in favor of the sympathetic system all day long, which may explain the increased frequency of arrhythmia.
Surgery Today | 2001
Ertan Onursal; Türkan Tansel Elmacı; Emin Tireli; Aygün Dindar; Dursun Atilgan; Mustafa Özcan
Abstract Cardiac involvement of hydatid disease is uncommon, and establishing a diagnosis is difficult because the presenting symptoms are variable. Between 1985 and 1997, eight patients ranging in age from 8 to 56 years underwent surgical excision of cardiac hydatid cysts, located in the interventricular septum in two, the right atrium in one, and the intrapericardium in five. There was one hospital death due to septic shock, but the other seven patients recovered uneventfully.
International Journal of Immunogenetics | 2006
Hasan Kudat; G. Telci; Ahmet Bilge Sözen; Fatma Oguz; Vakur Akkaya; Mustafa Özcan; Dursun Atilgan; M. Carin; Özen Güven
Only a small fraction of the streptococcal pharyngitis progress to rheumatic carditis, which implies that environmental, host and microbial factors interact to cause an aberrant immune response against the antigens of the microorganism that cross‐react with cardiac tissues. Although there are numerous studies and a general consensus on the relation between human leucocyte antigen (HLA) class II antigens and rheumatic heart disease (RHD), the details and the culprit antigens are still controversial. The study was undertaken to examine 100 patients with chronic RHD and 100 controls for HLA class I and class II antigens for differences in prevalence. All samples were typed at the HLA‐DRB1/3/4/5 and DQB1 loci by the sequence‐specific primer (PCR‐SSP) method at low resolution. For HLA class I antigens, HLA‐B13 frequency was marginally increased in patients with RHD compared to controls without reaching statistical significance. For class II antigens, RHD patients had higher frequencies for HLA‐DRB1*01 (RHD 24%, controls 10%), DRB1*04 (RHD 35%, controls 26%), DRB1*07 (RHD 18%, controls 11%) and HLA‐DQB1*02 (RHD 32%, controls 17%) without reaching statistical significance, and significantly lower frequencies for DRB1*13 (Pc < 0.003, OR: 5.69), DRB5* (Pc < 0.003, OR: 33) and DRB3* (Pc = 0.03, OR: 2.66) compared to controls. It was concluded that host, microbial and environmental factors collude to create acute rheumatic fever (RF) and chronic rheumatic valve disease. The HLA‐DRB1*13, DRB5* and DRB3* were protective against the development of rheumatic valve damage.
International Journal of Clinical Practice | 2005
Ahmet Kaya Bilge; Dursun Atilgan; Tufan Tükek; Mustafa Özcan; B. Özben; Nevres Koylan; Mehmet Meriç
The differences between long‐acting dihydropyridines and angiotensin‐converting enzyme inhibitors with regard to their long‐term effects on 24‐h heart rate variability (HRV) and left ventricular (LV) mass are less clear in mild‐to‐moderate essential hypertension. We studied the long‐term effects of amlodipine and fosinopril on 24‐h HRV and LV mass in mild‐to‐moderate essential hypertension.
International Journal of Cardiology | 2001
Tufan Tükek; Dursun Atilgan; Vakur Akkaya; Hasan Kudat; Seref Demirel; Mustafa Özcan; Ferruh Korkut
We evaluated left atrial appendage function and its relationship to pulmonary venous flow in 53 patients divided into four groups. Group 1 consisted of 10 normal subjects. Group 2 included 15 patients with significant pure mitral stenosis in sinus rhythm. In group 3, there were 13 patients with pure significant mitral stenosis and atrial fibrillation. Group 4 consisted of 15 patients with normal mitral valve and atrial fibrilltion. We found significant decrease in left atrial appendage ejection fraction and maximum emptying flow velocity, velocity time integral of systolic pulmonary venous flow in Groups 2, 3 and 4 in comparison with normal subjects. Systolic pulmonary venous flow velocity was significantly decreased in Groups 3 and 4. There was significant correlation between left atrial appendage ejection fraction and peak emptying flow velocity (r = 0.62, P < 0,001). Systolic peak pulmonary venous flow velocity was significantly correlated with left atrial appendage ejection fraction and maximum emptying flow velocity (r = 0.67, P = 0,01; r = 0.58, P < 0,001, respectively). There was also significant correlation between systolic pulmonary venous flow velocity time integral and left atrial appendage ejection fraction (r = 0.66, P = 0.001). When normals were excluded from analysis, all the correlations were still significant. We concluded that left atrial appendage is a contractile structure, and that systolic pulmonary venous flow velocity is influenced by left atrial appendage dysfunction. Therefore left atrial appendage function needs to be considered when interpreting Doppler transmitral and systolic pulmonary venous flow patterns.
The Anatolian journal of cardiology | 2010
Dursun Atilgan; Ahmet Kaya Bilge; Imran Onur; Burak Pamukcu; Mustafa Özcan; Kamil Adalet
OBJECTIVE Standard echocardiographic methods reflect chamber dynamics and do not provide a direct measure of myocardial fiber shortening. Therefore we evaluated longitudinal left ventricular myocardial function by tissue Doppler echocardiography; strain (S), strain rate (SR), tissue Doppler velocity (TDV) in newly diagnosed mild to moderate hypertensive patients. METHODS Our cross-sectional and observational study population consisted of 57 patients and 48 normotensive control subjects. Patients with obesity, diabetes mellitus, regional wall motion abnormality, secondary hypertension and a history or clinical evidence of cardiovascular disease, arrhythmias or conduction abnormalities were excluded from the study. Ejection fraction, endocardial fractional shortening (eFS), meridional end-systolic stress (mESS), stress-adjusted eFS (observed /predicted eFS) were measured by M-mode echocardiography. Relationship between the left ventricular mass index and mESS was assessed by Pearsons linear regression model. RESULTS Hypertensive patients had significantly decreased longitudinal myocardial function compared to control subjects determined by septal (-1.25+/-0.30 vs. -1.02+/-0.33, p<0.001) and lateral (-1.20+/-0.28 vs. 1.02+/-0.41, p<0.01) SR (1/s) measurements. However, there was no significant correlation between the mESS and strain-strain rate measurements in both normal and hypertensive subjects. CONCLUSIONS Early impairment in longitudinal left ventricular systolic function can be expected despite normal endocardial left ventricular function indicated by M-mode echocardiography in patients with newly diagnosed and never treated mild to moderate hypertension.
Nephrology | 2002
Tufan Tükek; Alaattin Yildiz; Vakur Akkaya; Bilal Görçtin; Mehmet Sukru Sever; Dursun Atilgan; Ferruh Korkut
SUMMARY: In this controlled study, systolic time intervals (STI) and diastolic functions were investigated in haemodialysis patients (HDp) with ejection fraction (EF) within normal limits. Echocardiographic findings in 86 HDp (M:F, 47:39, mean age 36 ± 13 years) and 51 healthy controls (M:F, 22:29, mean age 37±10 years) were compared for STI parameters (projection period (PEP), left ventricular ejection time (LVET) and STI index (PEP/LVET)) and diastolic dysfunction (isovolumetric relaxation time (IVRT) and E/A ratio and deceleration time). the pre‐ejection period (114±21 vs 94±4 msec, P < 0.001) and STI index (0.41 ±0.11 vs 0.34 ±0.02, P < 0.001) were higher in the HDp compared with controls. Increased STI index and prolonged PEP in HDp were independent of left ventricular (LV) hypertrophy and hypertension. Diastolic dysfunction was present in 61% of the patients. the IVRT were also found to be longer in HDp compared with controls (97±16 vs 75±16 msec, P < 0.001), independent of the presence of LV hypertrophy or hypertension. Diastolic dysfunction indicated by IVRT >100 msec and latent systolic dysfunction (STI index >0.4) were randomly distributed, with nearly half (48%) of the patients with prolonged IVRT having an STI index within the normal limits and the other half of the patients with deteriorated STI index having a normal IVRT. the combined systolic and diastolic dysfunction was observed in 30% of the patients. It was concluded that STI indexes deteriorate before an overt systolic dysfunction (normal EF), and that systolic and/or diastolic dysfunction of the myocardium may appear singly or simultaneously because of a common pathogenetic mechanism of myocardial fibrosis.
Clinical Cardiology | 2001
Tufan Tüukek; Vakur Akkaya; Dursun Atilgan; Şsleref Demirel; Mustafa Özcan; Özen Güuven; Ferruh Korkut