The role of urotensin II and atherosclerotic risk factors in patients with slow coronary flow ÖMER ¸ SATIRO ˘ GLU*, MURTAZA EMRE DURAKO ˘ GLUGIL, MUSTAFA ÇETIN, YÜKSEL ÇIÇEK, TURAN ERDO ˘ GAN, HAKAN DUMAN Department of Cardiology, Faculty of Medicine, Recep Tayyip Erdo ˘ gan University, Rize, Turkey *Corresponding author: Ömer ¸ Satıro ˘ glu; Kardiyoloji bölümü, Tip Fakültesi, Recep Tayyip Erdogan Üniversitesi, 53100 Rize, Turkey; Phone: +90 464 212 30 00, +90 538 276 33 57; Fax: +90 464 212 30 15; E-mail: omersatiroglu@yahoo.com (Received: March 27, 2016; Revised manuscript received: August 7, 2016; Second revised manuscript received: September 15, 2016; Accepted: September 20, 2016) Abstract: Background: Slow coronary flow (SCF) is an angiographic finding characterized with delayed opacification of epicardial coronary arteries without obstructive coronary disease. Urotensin II (UII) is an important vascular peptide, which has an important role in hypertension, coronary artery disease, and vascular remodeling in addition to potent vasoconstrictor effect. Objectives: We investigated UII levels, hypertension, and other atherosclerotic risk factors in patients with SCF, a variety of coronary artery disease. Methods: We enrolled 14 patients with SCF and 29 subjects with normal coronary arteries without SCF. We compared the UII levels and the atherosclerotic risk factors between patients with SCF and control subjects with normal coronary flow. Results: UII concentrations were significantly higher in patients with SCF compared to controls (711.0 ± 19.4 vs. 701.5 ± 27.2 ng/mL, p = 0.006). We detected a positive correlation between SCF and age (r = 0.476, p = 0.001), BMI (r = 0.404, p = .002), UII concentrations (r = 0.422, p = 0.006), and hypertension (r = 0.594, p = 0.001). Conclusion: We identified increased UII levels in patients with SCF. We think that UII concentrations may be informative on SCF pathogenesis due to relationship with inflammation, atherosclerosis, and vascular remodeling. Keywords: slow coronary flow, urotensin II, atherosclerosis, atherosclerotic risk factors, CRP Introduction Slow coronary flow (SCF) is an angiographic finding characterized with delayed opacification of epicardial cor- onary arteries without obstructive coronary disease [1]. SCF is a relatively common angiographic finding with a reported incidence of 1% in patients undergoing coronary angiography for the suspicion of coronary artery disease (CAD) [2]. Since the first description in 1972 by Tambe et al. [1], only a limited number of studies have focused on SCF; therefore, the precise pathophysiological mechanisms and the clinical importance of SCF are not fully understood at the moment. Several mechanisms have been proposed for SCF phenomenon including small vessel disease, microvascular vasomotor dysfunction, dif- fuse atherosclerosis, and endothelial dysfunction [3–6]. Occlusive disease of the small coronary arteries, which may be a form of early phase atherosclerosis, has also been suggested as a cause [7]. Moreover, SCF may cause transient myocardial hypoperfusion in patients with angina and normal coronary arteries, and these patients have higher probability of significant CAD and an appar- ently worse prognosis [8]. Urotensin II (UII), an undecapeptide cleaved from a precursor protein, promotes vasoconstriction and vascular smooth muscle cell proliferation [9, 10]. UII is one of the most important and the most studied peptide involved in vascular remodeling. UII, a potent vascular constrictor, is up-regulated in patients with hypertension, and athero- sclerosis in addition to relevant receptors [11–13]. Even though, the pathophysiological impact of UII in atherosclerosis and coronary artery disease has been This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited. Interventional Medicine & Applied Science, Vol. 8 (4), pp. 158–163 (2016) ORIGINAL PAPER DOI: 10.1556/1646.8.2016.4.1 158 ISSN 2061-1617 © 2016 The Author(s)