Acute phase reactants in patients with coronary slow flow phenomenon

Abstract

Acute phase reactants in patients with coronary slow flow phenomenonKoroner yavaş akım fenomeni olan hastalarda akut faz reaktanları 416ABSTRACT Objective: In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP). Methods: A total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis.Results: Hs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p<0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p<0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels.

The Relationship between Ventricular Repolarization Indexes and Neutrophil to Lymphocyte Ratio in Patients with Slow Coronary Flow

“…During the pathogenesis of cardiac disease and arrhythmia, there is an increase in inflammatory activity [23][24][25] and in SCF patients inflammatory activity is further increased [6,26]. In our study, the inflammation level was evaluated by NLR and our results correlated with previous studies demonstrating that inflammation levels were higher in SCF patients compared to controls.…”

“…The etiopathogenesis of SCF is not fully understood. However, microvascular dysfunction [1], endothelial dysfunction [2], small vessel disease [3], diffuse atherosclerosis [4], vasomotor dysfunction [5], and increased inflammatory [6] and thrombotic [7] activities are potential causes. Thus, the frequency of cardiovascular complications is increased in SCF patients.…”

Echo-Tracking Technology Assessment of Carotid Artery Stiffness in Patients with Coronary Slow Flow

“…Atherosclerosis leads to increased arterial resistance through thickening and stiffening of the arterial wall. Because the increased aortic resistance acts to decrease the flow propagation speed within the arterial lumen, a similar decrease in aortic flow propagation with increased downstream resistance is logical (Madak et al 2010;Nakamura et al 2013). Simsek et al (2013) reported a relationship between the CSF phenomenon and endothelial dysfunction, atherosclerosis and inflammation.…”

Increased pentraxin-3 level in patients with slow coronary flow

“…Such endothelial dysfunction at microvascular level leads atherothrombosis or angina (14)(15). Demonstration of diffuse atherosclerosis and elevation of acute phase reactants, such as CRP, are significant findings in understanding the etiopathogenesis of SCF (16)(17). In the present study, while hs-CRP level in SCF group was found to increase significantly compared to the control group, there was no difference between CAD and SCF groups.…”