Abstract
Background : Resistin is an adipokine that mediates insulin resistance in obese mice. In human, however, circulating resistin levels are not associated with obesity or insulin resistance. Although the function of human resistin is enigmatic, it has recently been reported that human resistin plays a role in hepatocyte low-density lipoprotein (LDL) receptor suppression. Objectives : Aim of this study was to determine if serum levels of resistin are associated with the response to lipid-lowering therapy and the prognosis in coronary artery disease (CAD). Methods : One hundred and eighty two patients without diabetes who underwent percutaneous coronary intervention for CAD participated in this study. We measured pre-procedural serum resistin levels. After procedures, we treated the patients with atorvastatin 20mg and evaluated response to the statin therapy at 6-month follow-up. We also performed 6-month follow-up coronary angiography (CAG) in all patients and quantitative coronary angiographic analysis was conducted. Results : After adjusting age, sex, BMI, hypertension and smoking, serum levels of resistin had positive correlation with total cholesterol (Pearson’s partial correlation coefficient (r)=0.170, p =0.015) and LDL (r=0.159, p =0.023) at baseline. However, there was no correlation between baseline serum levels of resistin and the decrement of LDL after statin therapy (r= 0.07, p =0.36). Although, serum resistin (odds ratio 1.714, 95%CI 1.266-2.319) and hypertension (odds ratio 4.617, 95%CI 1.535-13.887) were independent predictors of coronary artery disease in multivariate logistic regression analysis, we found no relationship between baseline serum levels of resistin and decrement in minimal lumen diameter of target vessel at follow-up CAG (r=0.003, p =0.96). Conclusions : Higher baseline serum resistin levels and the positive correlation between serum resistin and baseline LDL in CAD patients suggest that resistin may affect coronary atherosclerosis via lipid metabolism pathway. However, serum resistin is not associated with the response to lipid-lowering therapy and the prognosis in CAD. The different mechanism of restenosis after DES implantation might explain the irrelevance of resistin level and restenosis.
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