Affiliations: Department of Cardiology, Başkent University Faculty of Medicine, Ankara, Turkey | Department of Physiology and Hematology Research Laboratory, Başkent University Faculty of Medicine, Ankara, Turkey | Department of Hematology, Başkent University Faculty of Medicine, Ankara, Turkey | Department of Biochemistry, Başkent University Faculty of Medicine, Ankara, Turkey
Note: [] Corresponding author: Muhammet Bilgi, Başkent University, Faculty of Medicine, Department of Cardiology, Dadaloglu Mahallesi, 39. Sk. No. 6, 01250 Yuregir, Adana, Turkey. Tel.: +90 322 231 07 91; Fax: +90 322 327 12 98; E-mail: [email protected]
Abstract: Coronary slow flow (CSF) has been documented in 25% of patients evaluated for angina or angina-like chest pain, despite the presence of normal epicardial coronary arteries on angiography. The risk for the development of clinical events in patients with non-obstructive coronary artery disease (NOCAD) is higher than in patients with completely normal coronary arteries. The object of this study was to evaluate changes in blood and plasma viscosity in patients with CSF or NOCAD. The study included 147 subjects (CSF, n = 42, NOCAD, n = 42 and controls, n = 63). Blood and plasma viscosity, complete blood counts, fibrinogen, and high sensitivity C-reactive protein (hs CRP) levels were measured. There was no significant difference between the groups with respect to blood and plasma viscosity (p > 0.05). Hemoglobin, hematocrit, and erythrocyte counts were significantly higher in the CSF group compared to the NOCAD group (p = 0.017, p = 0.023 and p = 0.023 respectively) and the control group (p = 0.026, p = 0.02 and p = 0.02, respectively). High sensitivity CRP levels in the NOCAD group were higher than the CSF group and the control group (p = 0.001 and p = 0.018, respectively). In conclusion, no significant difference was observed in the blood and plasma viscosity in patients with CSF or NOCAD. Increases in hemoglobin and hematocrit values without an increase in viscosity may play a role in the pathophysiology of CSF.
