Increased serum resistin levels in patients with coronary slow-flow phenomenon

Abstract

Background. Slow coronary flow (SCF) is an angiographic finding characterized by delayed opacification of the epicardial coronary arteries without obstructive coronary disease. Resistin, an adipocytokine, plays a major role besides low-grade inflammation in atherosclerotic vascular processes and may be of importance in other coronary pathologies such as SCF. Methods. The present study was cross-sectional and observational, consisting of 70 individuals who underwent coronary angiography and had angiographically normal coronary arteries of varying coronary flow rates. The study included 50 patients with isolated SCF and 20 control participants with normal coronary flow (NCF). Results. There were no statistically significant differences between the SCF and NCF groups with respect to age, gender, presence of hypertension or diabetes mellitus, and smoking habit, except for increased creatinine levels (p=0.014). The serum resistin level was significantly higher in the SCF group than in the NCF group (8.4±7.2 vs. 5.4±2.6 ng/ml, p=0.014). Ln-transformed resistin levels correlated positively with left anterior descending (LAD) coronary artery TIMI frame count (TFC) (r=0.408, p<0.001) as well as with glucose (r=0.340, p=0.004), creatinine (r=0.248, p=0.044), and C-reactive protein (CRP; r=0.283, p=0.023) levels, and negatively with LAD coronary flow velocity (r=-0.314, p=0.009). When multivariate analyses were performed, in linear regression analysis, ln-resistin was associated with a longer TFC [beta (standardized regression coefficient): 0.404, p=0.001] and lower coronary flow velocity (beta: -0.280, p=0.035); in logistic regression analysis, ln-resistin was an independent predictor of the presence of SCF (OR: 6.692, 65%CI: 1.117-40.1, p=0.037). Conclusion. We demonstrated, for the first time, a significant increase in serum resistin levels in patients with SCF compared to subjects with NCF. We believe that further studies are needed to clarify the role of resistin in patients with SCF. © Urban & Vogel 2013.