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    Endothelial nitric oxide synthase levels and their response to exercise in patients with slow coronary flow
    (Clinics Cardive Publ Pty Ltd, 2013) Tasolar, Hakan; Eyyupkoca, Ferhat; Akturk, Erdal; Karakus, Yasin; Cansel, Mehmet; Yagmur, Julide; Ozyalin, Fatma
    Background: Endothelial dysfunction plays a key role in the aetiopathogenesis of slow coronary flow (SCF) even if there is no obstructive epicardial lesion. Reduced plasma levels of endothelial nitric oxide synthase (eNOS) are an important indicator of endothelial dysfunction. We aimed to determine plasma levels of eNOS and their relationship with exercise in patients with SCF. Methods: Twenty-two patients with SCF in at least one coronary artery and 17 healthy individuals were included in this study. The TIMI frame count method was used to determine SCF. Plasma levels of eNOS before and after effort were determined in the patient and control groups. Results: Basal eNOS levels in the patient group were lower than in the control group (p = 0.040), and plasma eNOS levels after exercise decreased more significantly in the patient group compared to the control group (p = 0.002). Median decreases of eNOS in response to exercise were higher in the SCF group than in the control group (p < 0.001), and the decrease observed in the control group was not statistically significant (p = 0.35). There were significantly negative correlations between TIMI frame count and plasma levels of eNOS at baseline and after exercise (r = -0.51, p = 0.015, r = -0.58, p = 0.005, respectively). Moreover, there was also a positive correlation between the rate-pressure product and plasma levels of eNOS after exercise in patients with SCF (r = 0.494, p = 0.019). Conclusion: Our findings indicate an important pathophysiological relationship between the severity of SCF in which endothelial dysfunction plays a role in its pathogenesis and the level of circulating plasma levels of eNOS.
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    The Relationship between Extracellular Volume Compartments and Matrix Metalloproteinases-2 in Left Ventricular Remodeling after Myocardial Infarction
    (Arquivos Brasileiros Cardiologia, 2022) Eyyupkoca, Ferhat; Eyerci, Nilnur; Altintas, Mehmet Sait; Felekoglu, Mehmet Ali; Biter, Halil Ibrahim; Hidayet, Siho; Sivri, Serkan
    Background: Matrix metalloproteinases (MMPs) can affect myocardial extracellular volume (ECV) and its compartments, and this can provide more detailed information about the mechanism of adverse left ventricular (LV) remodeling (AR) after acute myocardial infarction (MI).Objectives: To investigate the role of changes (Delta) in ECV compartments (matrix volume (MVi) and cell volume (CVi)) in the development of AR after MI, and their relationship with MMP-2 expressions.Methods: Ninety-two first MI patients who underwent 3 Tesla cardiovascular magnetic resonance imaging performed 2 weeks (baseline) and 6 months post-MI. We measured T1 mapping with MOLLI sequences. ECV was performed post-gadolinium enhancement. ECV and LV mass were used to calculate MVi and CVi. AR was defined as an increase of >= 12% in LV end-diastolic volume in 6 months. MMPs were measured using a bead-based multiplex immunoassay system at first day (baseline) and 2 weeks post-MI. P <0.05 was accepted as statistically significant.Results: Mean ECV and mean MVi baseline levels were higher in AR group compared to without AR group (42.9 +/- 6.4 vs 39.3 +/- 8.2%, p= 0.037; 65.2 +/- 13.7 vs 56.7 +/- 14.7 mL/m2, p=0.010; respectively). CVi levels was similar between groups. A positive correlation was found between baseline levels of MMP-2 and baseline levels of ECV (r=0.535, p<0.001) and MVi (r=0.549, p<0.001). Increased Delta MVi levels was independently predictor of AR (OR=1.03, p=0.010). Delta MVi had superior diagnostic performance compared to Delta ECV in predicting AR (Delta AUC: 0.215 +/- 0.07, p<0.001).Conclusion: High MVi levels are associated with AR, and Delta MVi was independently predictor of AR. This may be associated with MMP-2 release due to increased inflammatory response.