Yazar "Baspinar, Osman" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim Yok
    Öğe
    Closure of Patent Ductus Arteriosus in Children, Small Infants, and Premature Babies with Amplatzer Duct Occluder II Additional Sizes: Multicenter Study
    (Wiley-Blackwell, 2013) Sungur, Metin; Karakurt, Cemsit; Ozbarlas, Nazan; Baspinar, Osman
    ObjectivesTo evaluate safety and efficacy of closure of patent ductus arteriosus (PDA) with Amplatzer duct occluder II Additional Sizes (ADO II AS) and to report early and midterm results of the device in children and very young symptomatic infants. MethodsRetrospective analysis of angiographic data of 60 children from four pediatric cardiology centers. ResultsThe median patient age and weight were 6.5 (0.5-168) months and 6.8 (1.19-57) kg, respectively. In the study, 26 children had a body weight of 6 kg. Of these 26 children, 9 had a body weight of 3 kg. The median narrowest diameter of PDA was 2 (1.2-4) mm. Ductal anatomy was Type A in 29, Type B in 2, Type C in 11, Type D in 1, and Type E in 16 patients, and a residual PDA after surgery in 1 patient. Closure with ADO II AS was achieved in 58 (96.6%) of 60 attempted cases. In two infants, the device was not released because of significant residual shunt. ADO II was used in one, and the other was sent to surgery. Complete closure was observed in all ADO II AS deployed children by the next day on echocardiography. Median follow-up was 12 (1-18) months. Neither death nor any major complications occurred. ConclusionsOur study shows that closure of medium and small sized PDA by using ADO II AS device is effective and safe in children. The use of the device will expand the field of application of PDA closure in small infants. (c) 2013 Wiley Periodicals, Inc.
  • Küçük Resim Yok
    Öğe
    Serum Pentraxin 3 and hs-CRP Levels in Children with Severe Pulmonary Hypertension
    (Galenos Publ House, 2014) Karakurt, Cemsit; Baspinar, Osman; Celik, Fazli Serkan; Taskapan, Cagatay; Sahin, Aydin Derya; Yologlu, Saim
    Background: Pulmonary arterial hypertension secondary to untreated left-to-right shunt defects leads to increased pulmonary blood flow, endothelial dysfunction, increased pulmonary vascular resistance, vascular remodelling, neointimal and plexiform lesions. Some recent studies have shown that inflammation has an important role in the pathophysiology of pulmonary arterial hypertension. Aims: The aim of this study is to evaluate serum pentraxin 3 and high sensitive (hs)-C reactive protein (hs-CRP) levels in children with severe pulmonary arterial hypertension (PAH) secondary to untreated congenital heart defects and evaluate the role of inflammation in pulmonary hypertension. Study Design: Cross sectional study. Methods: After ethics committee approval and receiving consent from parents, there were 31 children were selected for the study with severe PAH, mostly with a left-to-right shunt, who had been assessed by cardiac catheterisation and were taking specific pulmonary vasodilators. The control group consisted of 39 age and gender matched healthy children. After recording data about all the patients including age, gender, weight, haemodynamic studies and vasodilator testing, a physical examination was done for all subjects. Blood was taken from patients and the control group using peripheral veins to analyse serum Pentraxin 3, N-terminal pro-Brain Natriuretic Pep-tide (NT-ProBNP) and hs-CRP levels. Serum Pentraxin-3 levels were measured by enzyme linked immunosorbent assay (ELISA) and expressed as ng/mL. Serum hs-CRP levels were measured with an immunonephelometric method and expressed as mg/dL. The serum concentration of NT-proBNP was determined by a chemiluminescent immunumetric assay and expressed as pg/mL. Results: Serum Pentraxin-3 levels were determined to be 1.28 +/- 2.12 (0.12-11.43) in the PAH group (group 1) and 0.40 +/- 0.72 (0.07-3.45) in group 2. There was a statistically significant difference between the two groups (p<0.01). Serum hs-CRP levels were measured as 2.92 +/- 2.12 (0.32-14.7) mg/dL in group 1 and 0.35 +/- 0.16 (0.07-3.45) mg/dL in group 2. The hs-CRP level was increased in the PAH group to a significant degree (p<0.01). Conclusion: Our study showed that pentraxin 3 and hs-CRP levels were increased significantly in the PAH group. We consider that inflammation plays an important role in severe pulmonary hypertension and progressive pulmonary arterial hypertension in children with PAH.