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    Effects of atrial electromechanical delay and ventriculoatrial conduction over the atrial functions in patients with frequent extrasystole and preserved ejection fraction
    (Wiley, 2019) Gurbuz, Ahmet Seyfeddin; Ozturk, Semi; Kilicgedik, Alev; Akgun, Taylan; Kalkan, Mehmet Emin; Demir, Serdar; Efe, Suleyman Cagan
    Background The deterioration of left atrial and ventricular functions was demonstrated in patients with frequent ventricular extrasystole (fVES). The exact pathophysiology of left atrial dysfunction in patients with fVES is unclear. Retrograde ventriculoatrial conduction (VAC) often accompanies fVES, which may contribute to atrial dysfunction. We investigated whether atrial electromechanical delay and VAC are related to these atrial functions in patients with frequent right ventricular outflow tract (RVOT) VES and preserved ejection fraction (pEF). Methods This study included 21 patients with pEF (eight males, 48 +/- 11 years), who had experienced more than 10 000 RVOT-VES during 24-h Holter monitoring and had undergone electrophysiological study/ablation. The study also included 20 healthy age- and sex-matched control subjects. Transthoracic echocardiography was performed on all of the subjects. Atrial conduction time was obtained by using tissue Doppler imaging. Strain analysis was performed with two-dimensional speckle tracking echocardiography. Results The peak atrial longitudinal strain was significantly impaired in patients with fVES (P = 0.01). In addition, although the interatrial and left atrial conduction delay times were significantly different between each group (P < 0.001, P < 0.001), the right atrial conduction delay times were similar. When patients with fVES were divided into groups depending on the existence of retrograde VAC, atrial deformation parameters and conduction delay time did not significantly differ between either group. Conclusion Frequent RVOT-VES causes left atrial dysfunction. This information is obtained through strain analyses and recordings of left atrial conduction times in patients with pEF. Regardless, retrograde VAC is not related to atrial dysfunction.
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    Heparanase is a predictive marker for high thrombus burden in patients with ST-segment elevation myocardial infarction
    (Taylor & Francis Ltd, 2019) Gurbuz, Ahmet Seyfeddin; Ozturk, Semi; Efe, Suleyman Cagan; Yilmaz, Mehmet Fatih; Yanik, Raziye Ecem; Yaman, Ali; Kirma, Cevat
    Objective: Heparanase (HPA) is an endo-beta-D-glucuronidase capable of degrading heparin sulphate (HS) and heparin side chains. HPA plays a role in tumour growth, angiogenesis, cell invasion and in activation of the coagulation system. We aimed to investigate the relationship between HPA and thrombus burden (TB) in patients with ST-Segment Elevation Myocardial Infarction (STEMI). Methods: This prospective study enrolled 187 patients with STEMI who were treated with primary percutaneous coronary intervention (pPCI). Blood samples were taken to determine serum HPA levels prior to coronary angiography and heparin administration. Serum HPA analysis was performed with a commercially available Human Elisa kit. Results: Patients were divided into two groups: high TB (n:58) and low TB (n:129) group. Serum HPA levels were significantly higher in patients with high TB than low TB [250.1 (188.5-338.1) vs. 173.6 (134.3-219.8) pg/mL] (p < 0.001). Serum HPA levels were higher in patients with no-reflow phenomenon compared with others [(409.3 (375.6-512.5) pg/mL vs. 186.2 (144.2-247.4) pg/mL, p < 0.001]. In multiple logistic regression analysis HPA was a predictor of high TB. Conclusion: Elevated HPA level in patients with STEMI is related to high TB. Furthermore, increased HPA level may be associated with thrombotic complications such as no-reflow phenomenon in patients with STEMI.
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    QTc nterval is prolonged in Wilson's disease with neurologic nvolvement
    (Taylor & Francis Ltd, 2018) Ozturk, Semi; Gurbuz, Ahmet Seyfeddin; Efe, Suleyman Cagan; Iliaz, Raim; Banzragch, Mutse; Demir, Kadir
    Background Neurologic and liver involvement in Wilson's disease (WD) is well-documented, however, few reports demonstrated cardiac involvement. Tpe and Tpe/QT are new measures of ventricular repolarization which were recently suggested as predictor of arrythmogenesis. We aimed to evaluate ventricular depolarization and repolarization parameters including QT, QTc, Tpe intervals, Tpe/QT, Tpe/QTc ratios, and QT dispersion (QTd) in patients with WD.Materials and methods Thirty-five patients with WD and 30 healthy controls were included in the study. Patients were evaluated by a neurologist in addition to MR imaging. Twenty-one of 35 patients were diagnosed as neuroWilson (NW), whereas 14 patients as non-NW. ECG recordings were obtained using a 12-lead commercial device (Cardiac Science, Burdick s500,USA). All patients underwent standard echocardiographic evaluation. These two groups of patients and healthy controls were compared.Results There were no difference between patients with WD and healthy controls in terms of age sex, BMI, liver, and kidney functions where as patients with WD were anemic and thrombocytopenic. Left atrial, ventricular dimensions, left ventricular systolic, and diastolic functions were similar between patients and healthy control. QT interval was prolonged in patient group, however, QTc, Tpe intervals, Tpe/QT, and Tpe/QTc ratios and QTd did not differ between groups. When patients with NW and non-NW were compared, both QT and QTc intervals were significantly longer in patients with NW, however, Tpe interval, Tpe/QT and Tpe/QTc ratios, and QTd did not differ.Conclusion QT and QTc intervals are prolonged in patients with Wilson's disease and neurologic involvement.
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    Serum Heparanase Level Is Decreased in Stable Coronary Artery Disease
    (Karger, 2019) Gurbuz, Ahmet Seyfeddin; Ozturk, Semi; Efe, Suleyman Cagan; Yilmaz, Mehmet Fatih; Yanik, Raziye Ecem; Yaman, Ali; Kirma, Cevat
    Objective: Heparanase (HPA), mammalian endo-beta-D-glu-cu-ronidase, separates heparan sulfate chains of proteoglycans and changes the structure of the extracellular matrix. We investigated whether serum levels of HPA differ in patients with stable coronary artery disease (SCAD) and subjects with normal coronary arteries. Methods: This study enrolled 92 patients with SCAD and 34 controls with normal coronary arteries. Levels of HPA were measured by a commercially available human HPA enzyme-linked immunosorbent assay kit. Results: Serum HPA levels were significantly lower in the SCAD group (137.5 [104.1-178.9] vs. 198.8 [178.2-244.9] pg/mL; p < 0.001). Serum HPA levels were significantly higher in subjects with diabetes mellitus (DM) compared to those without DM (p = 0.008). Levels of HPA were lower in the SCAD group, both in the diabetic and nondiabetic subgroups, as compared to controls (p < 0.001 for both subgroups). Levels of HPA positively correlated with fasting blood glucose (FBG) (r: 0.42; p < 0.001). In multiple logistic regression analysis, serum HPA level (odds ratio [OR]: 0.975; 95% confidence interval [CI]: 0.966, 0.985; p < 0.001) and FBG (OR: 1.028; 95% CI: 1.010, 1.047; p = 0.002) were independently associated with SCAD. The receiver operating characteristic curve showed that HPA levels less than 160.6 pg/mL predicted SCAD with 65% sensitivity and 97% specificity (AUC: 0.80; 95% CI: 0.728, 0.878; p < 0.001). Conclusion: Diabetes and FBG levels were closely associated with serum levels of HPA. Low serum levels of HPA may predict SCAD in both diabetic and nondiabetic populations.