Relationship Between the Reciprocal Change in Inflammation-Related Biomarkers (Fibrinogen-to-Albumin and hsCRP-to-Albumin Ratios) and the Presence and Severity of Coronary Slow Flow

Abstract

Inflammation has been implicated in the pathogenesis of endothelial dysfunction, atherosclerosis, and microvascular coronary dysfunction. In this context, it is thought that fibrinogen, high-sensitive C-reactive protein (hsCRP), and albumin may be associated with the pathogenesis of coronary slow flow (CSF). We aimed to evaluate the ratios of fibrinogen-to-albumin and hsCRP-to-albumin in patients with CSF compared to patients with angiographically normal coronary arteries and stable coronary artery disease (CAD). In all, 65 patients with CSF, 65 patients with newly diagnosed stable CAD, and 65 control participants with angiographically normal coronary arteries were included. The coronary flow rates of all patients were determined by the Thrombolysis in Myocardial Infarction frame count method. Fibrinogen, hsCRP, and albumin levels were analyzed in all patients, and the fibrinogen-to-albumin and hsCRP-to-albumin ratios were calculated. The baseline characteristics of the 3 groups were similar. The plasma albumin level was significantly lower, whereas the fibrinogen and the hsCRP levels were significantly higher, in the CSF and CAD groups compared to the controls. The fibrinogen-to-albumin and hsCRP-to-albumin ratios were significantly higher in both the CSF and the CAD groups compared to the control group. The hsCRP-to-albumin ratio was positively correlated with the mean Thrombolysis in Myocardial Infarction frame count in the whole study population. According to the receiver–operating characteristic analysis, the efficacies of the fibrinogen-to-albumin and hsCRP-to-albumin ratios in predicting CSF were significant. The fibrinogen-to-albumin and hsCRP-to-albumin ratios, which were increased by a reciprocal change, suggest that inflammation may play a role in the pathogenesis of CSF.