Introduction: During inflammation, the in-flammatory glycoprotein of pentraxin-3 (PTX3) is synthesized by endothelial cells, macrophages and myelogenous cells. This inflammatory glycoprotein plays a fund-amental role in the process of atheros-clerosis and coronary artery disease (CAD). Moreover, this protein is predominantly re-marked in sclerotic lesions and may act as an independent prognostic factor in CAD compared with healthy subjects and its in-crease might bring about harsh conseq-uences for CAD. Materials & Methods: In the present res-earch, 30 patients with unstable CAD, 30 patients with stable CAD, and 30 healthy control subjects were studied based on ang-iographic findings. ELISA method was em-ployed to determine the plasma level of PTX3. The concentration of the high-sens-itivity C-reactive protein of plasma (hsC-RP) was assigned via a latex-enhanced im-munoturbidimetric method. Plasma leve-ls of HDL-cholesterol, LDL- chole-sterol, total cholesterol and triglycerides were also measured by enzymatic methods. The con-dition of other cardiovascular risk-factors was determined by referring to individuals’ medical history and questionnaires. Findings: Using ROC curve with high sens-itivity and specificity, the findings revealed that the levels of PTX3 and hsCRP were higher among patients with unstable CAD than patients with stable CAD (p <0.01). Furthermore, the levels of these two com-binations were more among patients with stable CAD than control subjects (p <0.01). Among the patient groups, PTX3 had a significant relationship with hsCRP as well as the occurrence of CAD (p <0.01). Discussion & Conclusion: Inflammatory processes play a central role in the form-ation of atherosclerotic plaques in athero-sclerosis from the primary phase of starting defects in endothelial cells to the formation of mature atherosclerotic plaques and their subsequent rupture. The inflammatory gly-coprotein of pentraxin-3 (PTX3) is bas-ically remarked in sclerotic lesions. Among the CAD patients, the rupture of the fibrous cap on atherosclerosis plaque leads to the direct exposure of underlying thrombosis (clot-causing) sections of atherosclerosis plaque to blood flow which starts the water-fall activation of blood coagulation via attachment, activation and aggregation of platelets. Among unstable CAD patients, pentraxin-3 is freed from activated neutr-ophils by platelets and it seems that it incre-ases at the end stage of heart failure but its level is lower in neutrophils of stable CAD and this factor is the agent cause of differ-rentiation between stable CAD and unstable CAD. Moreover, physiological concentrate-on of this biomarker in plasma is 2ng/ml and the control subjects are specified based on this level of concentration. In other words, the increase in the plasma level of PTX3 may well act as a positive predictor for the presence of CAD, discriminate between stable CAD patients, unstable CAD patients and the control subjects and have a diagnostic value.