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Increased circulating soluble urokinase-type plasminogen activator receptor (suPAR) levels in patients with slow coronary flow

INTRODUCTION: Slow coronary flow (SCF) is an angiographic phenomenon characterized by delayed opacification of epicardial coronary arteries without an obstructive coronary disease. Serum soluble urokinase-type plasminogen activator receptor (suPAR) levels seem closely related to atherosclerosis due...

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Detalles Bibliográficos
Autores principales: Emrah, Acar, Akın, İzgi İbrahim, Servet, İzci, Muzaffer, Kahyaoğlu, Fatih, Yılmaz Mehmet, Yeliz, Güler, Çağan, Efe Süleyman, Ahmet, Güler, Alev, Kılıçgedik, Cevat, Kırma
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5421532/
https://www.ncbi.nlm.nih.gov/pubmed/28905020
http://dx.doi.org/10.5114/amsad.2016.60819
Descripción
Sumario:INTRODUCTION: Slow coronary flow (SCF) is an angiographic phenomenon characterized by delayed opacification of epicardial coronary arteries without an obstructive coronary disease. Serum soluble urokinase-type plasminogen activator receptor (suPAR) levels seem closely related to atherosclerosis due to increased inflammation and prothrombotic state. We studied whether circulating suPAR is related to SCF. MATERIAL AND METHODS: The present study was cross-sectional and observational. It included 75 individuals who underwent coronary angiography with suspected CAD and had angiographically normal coronary arteries of varying coronary flow rates. The relationship between suPAR, C-reactive protein (CRP) and SCF was investigated. Forty patients with isolated SCF (mean age: 46.0 ±4.14 years) and 35 age- and gender-matched control participants with normal coronary flow (NCF) and normal coronary arteries (NCA) (mean age: 46.0 ±5.7 years) were included in the study. We used logistic regression analysis to determine the predictors of SCF. RESULTS: The clinical characteristics were not statistically significantly different between SCF and NCA groups. Serum suPAR level was significantly higher in the SCF group than the control group (2.5–5.4 ng/ml vs. 0.1–1.4 ng/ml; p < 0.001). Also the serum CRP level was higher in the CSF group than the control group (1.57 ±0.43 mg/l vs. 0.53 ±0.23 mg/l; p < 0.001). CONCLUSIONS: This study revealed significantly increased serum suPAR levels in patients with SCF. Although we cannot draw conclusions on the underlying pathological process of SCF, we believe that these findings may be pioneering for further studies investigating the specific roles of circulating suPAR in the SCF phenomenon in the coronary vasculature.