Fatma Yigit
Başkent University
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Featured researches published by Fatma Yigit.
Blood Coagulation & Fibrinolysis | 2008
Yucel Colkesen; Tayfun Acil; Bahri Abayli; Fatma Yigit; Tuna Katircibasi; Tolga Kocum; Senol Demircan; Alpay Turan Sezgin; Bülent Özin; Haldun Muderrisoglu
Paroxysmal atrial fibrillation might be a risk factor for stroke such as chronic atrial fibrillation. We examined the relation between mean platelet volume and paroxysmal atrial fibrillation to determine the effect of paroxysmal atrial fibrillation on the thrombotic state via elevated mean platelet volume. Mean platelet volume is a marker of platelet size, function, and activation. Increased mean platelet volume reflects active and large platelets that release more thromboxane A2 than smaller ones. We hypothesized that mean platelet volume is elevated in patients with paroxysmal atrial fibrillation. The study population comprised 103 consecutive patients who were detected to have paroxysmal atrial fibrillation by 24-h Holter monitoring and 87 control individuals with normal Holter monitoring. Mean platelet volume and inflammatory parameters were measured. Comprehensive clinical and echocardiographic data were collected. Patients with aortic and mitral stenosis, hyperthyroidism, hypothyroidism, malignancy, infection, and pregnancy were excluded from the study. Mean age of the patients was 63 ± 11 vs. 45 ± 14 years (P < 0.001) in paroxysmal atrial fibrillation and control groups, respectively. Fifty-seven patients (55%) in paroxysmal atrial fibrillation and 19 (21%) (P < 0.001) patients in control group were men. Mean platelet volume was significantly higher in the paroxysmal atrial fibrillation group when compared with control group (10.0 ± 2.0 vs. 8.3 ± 1.5 fl, respectively; P < 0.001). C-reactive protein (18.5 ± 28 vs. 3.8 ± 2 mg/l, respectively; P = 0.004) and erythrocyte sedimentation rate (21 ± 21 vs. 12 ± 7 mm/h, respectively; P = 0.01) were also higher in the paroxysmal atrial fibrillation group. There was no difference in white blood cell and platelet counts between groups. In a multivariate analysis, elevated mean platelet volume was associated with the occurrence of paroxysmal atrial fibrillation before and after adjustment for age and sex. Our results indicate that inflammatory markers such as C-reactive protein and erythrocyte sedimentation rate and the marker of platelet size and activity mean platelet volume are elevated in patients with paroxysmal atrial fibrillation.
Angiology | 2004
Fatih Yalçin; Haldun Muderrisoglu; Mehmet Emin Korkmaz; Bülent Özin; Mehmet Baltali; Fatma Yigit
Basal septal hypertrophy (BSH), a cause of left ventricular outflow tract (LVOT) obstruction, is thought to occur by increased ventricular dynamics. The aim of the study was to evaluate the effect of pharmacologic stress on LVOT gradients in a group of hypertensive patients with BSH. Dobutamine stress was used in 24 hypertensive patients (mean age 56 ±8 years; 11 women) with BSH and 20 normal controls (mean age 54 ±9 years; 7 women). Ejection fraction and myocardial mass, basal septal dimension, and LVOT diameter were measured with 2-dimensional echocardiography. LVOT velocities and transmitral velocities before and at peak dobutamine infusion were determined by continuous wave Doppler and pulsed Doppler, respectively. There were no differences in mean ejection fraction and myocardial mass between BSH patients (58 ±3%, 204 ±24 g) and normals (56 ±4%, 201 ±32 g). The basal septum was thicker in patients (1.55 ±0.2 cm) than in normals (1.03 ±0.1 cm, p<0.001). Maximum LVOT velocities were similar in BSH (1.2 ±0.4 m/sec) and normals (1.1 ±0.2 m/sec) at rest. At peak stress, maximum LVOT velocities were higher in BSH (3.3 ±0.6 m/sec) than normals (1.7 ±0.4 m/sec, p<0.001). LV rate-pressure product at peak stress was higher in BSH (23,326 ±4,388) than normals (17,592 ±2,409, p<0.001). LV isovolumetric relaxation time was prolonged, and the E/A ratio was decreased in the patients at rest (130 ±14 msec and 0.72 ±0.18, respectively, p<0.001). At peak stress, diastolic function did not significantly change in two groups. The correlations between LVOT velocity change by stress and mean LVOT diameter (r =-0.668, p<0.001) and mean BS thickness (r =0.610; p<0.001) were significant in the whole group. High velocities appeared on LVOT at peak pharmacologic stress in the hypertensive patients with BSH compared with control group. This suggests dynamic ventricular ejection by stress may contribute to hypertrophy of the basal segment, which is the closest part of septum to increased afterload.
Journal of Human Hypertension | 2006
Yalçin F; Fatma Yigit; Tansel Erol; Mehmet Baltali; Mehmet Emin Korkmaz; Haldun Muderrisoglu
Left ventricular outflow tract (LVOT) obstruction has been classically observed in hypertrophic cardiomyopathy in which the LVOT obstruction is associated with asymmetric septal hypertrophy producing a systolic pressure gradient across the LVOT. Basal septal hypertrophy (BSH) with hypertension may result in dynamic LVOT obstruction as well. It was suggested that regional hypertrophy may be related to enhanced ventricular dynamics.
Clinical and Experimental Hypertension | 2012
Dilek Torun; Ruya Ozelsancak; Fatma Yigit; Hasan Micozkadioglu
The aim of this study was to investigate whether inflammatory markers are associated with hypertensive end organ damage or obesity in patients with hypertension. Seventy newly diagnosed essential hypertensive patients (29 men and 41 women aged 49.6 ± 9.5 y) and 25 age–sex-matched normotensive subjects (12 men and 13 women aged 45.8 ± 7.3 y) were asked about their family history of hypertension and smoking habits, and body mass index (BMI) was recorded and blood samples were taken to measure fibrinogen, C-reactive protein (CRP), and homocysteine levels. In hypertensive patients, creatinine clearance, urinary albumin extraction, and left ventricular mass index were determined. Hypertensive patients had significantly higher BMIs and inflammatory markers when compared with normotensive healthy controls. The CRP was positively associated with BMI (P < .05), diastolic blood pressure (P < .05), fibrinogen (P < .01), urinary albumin extraction (P < .01), and left ventricular mass index (P < .05). The BMI and serum fibrinogen level were independently associated with CRP. The effect of inflammation on the development of hypertensive end organ damage may be associated with obesity, so that control of obesity may eliminate the inflammatory state in hypertensive patients and also hypertensive end organ damage.
International Journal of Dermatology | 2010
Aydolu Eryılmaz; Murat Durdu; Mete Baba; Nebil Bal; Fatma Yigit
Background Cutaneous leishmaniasis is a parasitic disease caused by a Protozoan. Clinically and histopathologically, it can be confused with various dermatologic diseases.
Saudi Journal of Kidney Diseases and Transplantation | 2016
Dilek Torun; Ismail Yildiz; Hasan Micozkadioglu; Gül Nihal Nursal; Fatma Yigit; Ruya Ozelsancak
The aim of this study was to investigate the effects of cinacalcet therapy on anemia parameters, bone mineral metabolism, left ventricular mass index (LVMI) and parathyroid gland volume in hemodialysis (HD) patients with secondary hyperparathyroidism. Twenty-five HD patients (M/F: 11/14, mean age: 45.2±17.9 years, mean HD duration: 96.4±32.7 months) were included in this prospective pilot study. The indication to start calcimimetic therapy was persistent serum levels of parathyroid hormone (PTH)>1000 pg/mL, refractory to intravenous (i.v.) vitamin D and phosphate-binding therapy. The initial and one-year results of adjusted serum calcium (Ca+2), phosphate (P), Ca×P product, PTH, hemoglobin (Hb) and ferritin levels, transferrin saturation index (TSAT), median weekly erythropoietin (EPO) dose, LVMI, and parathyroid volume by parathyroid ultrasonography were determined. There were no differences between pre- and post-treatment levels of serum Ca+2 (P=0.853), P (P=0.447), Ca×P product (P=0.587), PTH (P=0.273), ferritin (P=0.153) and TSAT (P=0.104). After 1 year of calcimimetic therapy, the Hb levels were significantly higher than the initial levels (P=0.048). The weekly dose of EPO decreased with no statistical significance. The dose of cinacalcet was increased from 32.4±12.0 to 60.0±24.4 mg/day (P=0.01). There were no differences between the pre- and post-treatment results regarding weekly vitamin D dose, parenteral iron dose, LVMI and parathyroid volume. The results of our study suggest that cinacalcet therapy might have an additional benefit in the control anemia in HD patients.
Renal Failure | 2008
Fatma Ulku Adam; Dilek Torun; Fatma Yigit; Ruya Ozelsancak; Siren Sezer; Fatma Nurhan Ozdemir; Mehmet Haberal
Aim. It has been shown that Hepatitis C virus (HCV) seropositivity and carotis artery plaque formation are independently correlated in the general population. Insulin resistance is also a risk factor for atherosclerosis. The association between HCV and type 2 diabetes mellitus is known. Determination of the impact of HCV on insulin resistance and arterial stiffness in hemodialysis patients would help to prevent related cardiovascular complications. Methods. Thirty-seven HCV(+) and 30 HCV(-) HD patients were enrolled in this study. All patients were non-diabetic. Insulin resistance was assessed by “HOMA-IR.” Arterial stiffness was measured by “stiffness index b” and “elastic modulus.”Results. In the HCV(+) group, there were 20 males and 17 females, while the HCV(-) group had 19 males and 11 females. The mean age was 43.4 ± 16.7 years and 44.5 ± 16.8 years, respectively. The HOMA-IR was 1.50 in HCV(+) group and 1.31 in HCV(-) group (p > 0.05). Stiffness index b and elastic modulus measurements revealed no difference between groups. In the HCV(+) group, arterial stiffness parameters were correlated with age, white blood cell, thrombocyte, total and LDL cholesterol, uric acid, mean arterial pressure, diastolic blood pressure, and HOMA-IR. There was no association between arterial stiffness and the above-mentioned parameters in the HCV(-) group.Conclusion. We found that there was no association of arterial stiffness in HCV(+) patients with insulin resistance. Further studies with larger patient groups and more sensitive methods of detecting HCV are needed. This study is the first in literature on this issue.
The American Journal of Gastroenterology | 2000
Yücel Üstündağ; Sedat Boyacioglu; Arif Ertürk; Fatma Yigit; Bülent Özin; Haldun Muderrisoglu
Are myocardial functional abnormalities biventricular in nonalcoholic cirrhotics with or without ascites?
Angiology | 2007
Senol Demircan; Alpay Turan Sezgin; Mehmet Baltali; Öner Gülcan; Semra Topcu; Fatma Yigit; Tansel Erol; Rıza Türköz; Haldun Muderrisoglu; Bülent Özin
The aim of the study was to determine carotid artery intima-media thickness (IMT) in patients with rheumatic mitral stenosis (RMS). Between January 2001 and December 2003, 112 consecutive patients who had been diagnosed with RMS were screened. Patients with known cerebrovascular disease, coronary artery disease, diabetes, hypertension, left ventricular hypertrophy, hyperlipidemia, abnormal laboratory results, smoking, or age over 50 years were excluded. Forty-eight patients (43 women, 5 men, mean age 39.7 ±8.3 years) with RMS without risk factors were enrolled in the study. Age- and sex-matched healthy individuals (n = 48; 43 women, 5 men, mean age 39.6 ±8.6 years) with normal echocardiographic findings constituted the control group. Carotid IMT was determined by using a high-resolution ultrasound system equipped with a 7-MHz imaging probe (Acuson 128 XP CI) with a computer measurement software. The mean common carotid artery IMT thicknesses both in the right (0.604 ±0.112 mm vs 0.521 ±0.072 mm) and in the left side (0.581 ±0.097 mm vs 0.516 ±0.065 mm) were significantly higher in patients with RMS than in the control group (p < 0.001). Backward stepwise logistic regression analysis identified RMS as independent predictors of increased IMT (OR, 17.25 (CI, 3.99 to 76.28), p <0.001). The present study demonstrated that RMS is associated with increased IMT. The findings indicate that in patients with RMS not only valvular but also systemic endothelium is damaged.
International Heart Journal | 2005
Dilek Torun; Siren Sezer; Z. Arat; Aysel Pelit; Fatma Yigit; Fatma Nurhan Ozdemir