Abstract
Objective. To investigate the changes in serum Myeloid-Related Protein 8/14 (MRP8/14) and Eosinophil Cationic Protein (ECP) levels in patients with different types of coronary artery diseases (CAD) and assess the value of MRP8/14 and ECP detection in predicting CAD. Methods. 178 patients were divided into CAD group including unstable angina pectoris (UAP), acute myocardial infarction (AMI), and stable angina pectoris (SAP). Thirty-six individuals with normal coronary artery served as the control group. Serum MRP8/14 and ECP were measured by ELISA. The severity of coronary artery stenosis was assessed by the numbers of involved coronary artery branches and the sum of Gensini scores. Results. The MRP8/14 levels were significantly higher in AMI and UAP group than SAP and control group (P < 0.05). The levels of MRP8/14 in AMI group were also obviously higher than UAP group (P < 0.05). The ECP levels were obviously increased in AMI group, but there was no difference between SAP and UAP group (P > 0.05). The ECP was significantly increased in three impaired coronary arteries and obviously correlated with Gensini score (P < 0.01), whereas the MRP8/14 was obviously positively correlated with CRP (P < 0.01). Conclusions. Increased MRP8/14 levels suggest the instability of the atherosclerotic plaque. ECP reflects the severity of coronary arteries stenosis, predicting atherosclerosis burden. They may become the new biomarkers of CAD.
Highlights
Coronary artery disease (CAD) is rapidly increasing in prevalence across the world
There were no statistical differences between age and gender, smoking, body mass index (BMI), hypertension, HbA1c, TG, total cholesterol (TC), CHOL, CREA, blood urea nitrogen (BUN), and URIC (P > 0.05)
The levels of white blood cell (WBC) and erythrocyte sedimentation rate (ESR) were higher in patients with CAD than the controls (P < 0.05) and were the highest in acute myocardial infarction (AMI) patients (P < 0.05)
Summary
Coronary artery disease (CAD) is rapidly increasing in prevalence across the world. The pathological basis of CAD is atherosclerosis (AS). Inflammation plays a key role in atherosclerotic plaque progression, vulnerability, and thrombogenicity [1]. Finding new biomarkers to reveal the atherosclerotic burden and the vulnerability of plaque are of great significance. Myeloid-Related Protein 8/14 (MRP8/14), a heterodimer of two calcium binding proteins, has been implicated in the pathobiology of inflammatory disorders, such as inflammatory bowel disease, ankylosing spondylitis, and transplant rejection [2]. MRP8/14 broadly regulates vascular inflammation and contributes to the biological response to vascular injury by promoting leukocyte recruitment [3]. The correlation of MRP8/14 and CAD is unclear
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