Relationship between resistin level in serum and acute coronary syndrome or stable angina pectoris

Objective： To investigate the relationship between serum resistin level and acute coronary syndrome （ACS） or stable angina pectoris （SAP）. Methods： Sixty-five patients, with coronary artery disease, were enrolled and divided into three subgroups： acute myocardial infarction （AMI）, unstable angina pectoris （UAP） and SAP, and 26 healthy people were recruited as controls in the cross-sectional study. Serum resistin levels were determined by ELISA （enzyme-linked immunosorbent assay）, and WBC （white blood cell count）, hsCRP （high sensitive C-reaction protein）, CKmax （maximum of creatinkinase）, CK-MBmax （maximum of isozyme of creatinkinase） and cTnImax （maximum of troponin） were measured by standard laboratory methods. Results： The serum resistin levels were 4 folds higher in AMI patients, 2.43 folds in UAP patients and I. 12 folds in SAP patients than in the healthy controls （P〈0.05）. The resistin levels were also significantly different between AMI [（8.16±0.79） ng/ml], UAP [（5.59±0.75） ng/ml] and SAP [（3.45±0.56） ng/ml] groups （P〈0.01）; WBC, hsCRP, CK CK-MBmax and cTnlmax were significantly increased in AMI patients over UAP and SAP patients. Spearman analysis showed that serum resistin levels were positively correlated with WBC （r=0.412, P=0.046）, hsCRP （r=0.427,p=0.037）, CK CK-MBmax and cTnImax （r=0.731, 0.678, 0.656; P〈0.01）. Conclusion： Serum resistin levels increased with inflammatory factors and myocardial impairment. The results suggest that human resistin might play an important role in the pathogenesis of atherosclerosis and AMI as an inflammatory factor.

Objective: To investigate the relationship between serum resistin level and acute coronary syndrome (ACS) or stable angina pectoris (SAP). Methods: Sixty-five patients, with coronary artery disease, were enrolled and divided into three subgroups: acute myocardial infarction (AMI), unstable angina pectoris (UAP) and SAP, and 26 healthy people were recruited as controls in the cross-sectional study. Serum resistin levels were determined by ELISA (enzyme-linked immunosorbent assay), and WBC (white blood cell count), hsCRP (high sensitive C-reaction protein), CKmax (maximum of creatinkinase), CK-MBmax (maximum of isozyme of creatinkinase) and cTnImax (maximum of troponin) were measured by standard laboratory methods. Results: The serum resistin levels were 4 folds higher in AMI patients, 2.43 folds in UAP patients and 1.12 folds in SAP patients than in the healthy controls (P<0.05). The resistin levels were also significantly different between AMI [(8.16±0.79) ng/ml], UAP [(5.59±0.75) ng/ml] and SAP [(3.45±0.56) ng/ml] groups (P<0.01); WBC, hsCRP, CKmax, CK-MBmax and cTnImax were significantly increased in AMI patients over UAP and SAP patients. Spearman analysis showed that serum resistin levels were positively correlated with WBC (r=0.412, P=0.046), hsCRP (r=0.427, P=0.037), CKmax, CK-MBmax and cTnImax (r=0.731, 0.678, 0.656; P<0.01). Conclusion: Serum resistin levels increased with inflammatory factors and myocardial impairment. The results suggest that human resistin might play an important role in the pathogenesis of atherosclerosis and AMI as an inflammatory factor.