Strong correlation between serum levels of inflammatory mediators and their distribution in infarct-related coronary artery

Abstract

Background: Little is known regarding the correlation between circulating levels of inflammatory mediators and their distribution within the infarct-related coronary artery (ICA). Methods and Results: Atherothrombotic tissue and blood were aspirated by export suction catheter from the ICA in 49 patients with an acute myocardial infarction (AMI) <6 h duration who underwent primary percutaneous coronary intervention (PCI). Blood samples were collected before PCI for levels of high-sensitivity (hs) C-reactive protein (CRP), soluble P-selectin (sP-selectin) and white blood cell (WBC) counts. Immunohistochemical staining was performed for localization of CRP within the ICA. Staining intensity was graded for macrophage and extracellular tissue (0: no staining; 1+: <30%, 2+: 30% to 60%, and 3+: >60%). The hs-CRP levels were markedly higher in grade 3+ compared with both grade 2+ and grade 1+ of macrophage and extracellular staining of CRP (all p values <0.0001), and in grade 2+ compared with grade 1+ (p<0.001). Additionally, the ICA had a significantly higher sP-selectin level and WBC count compared with the systemic circulation (p<0.0001). Furthermore, the ICA level of sP-selectin was noticeably higher in patients with a total atherothrombus volume ≥0.5 cm 3 than in patients with total volume <0.5 cm 3 (p<0.0001). Moreover, correlation analysis demonstrated that the increase in the ICA level of sP-selectin was significantly related to the increase in the WBC count in the artery (r=0.548, p<0.0001). Multiple analysis identified an increased circulating level of hs-CRP as the only independent predictor of ≥2+ in macrophage (p<0.0001) and ≥2+ in extracellular (p<0.0001) staining of CRP. Conclusions: Following AMI, the sP-selectin level and WBC count were markedly higher in the ICA than in the circulation. Moreover, the circulating level of hs-CRP was strongly associated with ICA localization of CRP.