The profile of circulating Pentraxin 3 after PCI in patients with acute myocardial infarction or angina pectoris

Abstract

Background: Pentraxin 3 (PTX 3) is an acute phase protein in the same superfamily as C-reactive protein (CRP) and is synthesized and released by endothelial cells, macrophages and smooth muscle cells, and also by circulating neutrophils by different stimuli. High levels of PTX3 have been found in patients with acute myocardial infarction (AMI). Aim: We have investigated the time profile of PTX3 in patients with acute myocardial infarction (AMI) and in patients with stable angina pectoris (AP) undergoing percutaneous coronary intervention (PCI) and stent implantation, to 1) compare the groups 2) to elucidate any influence of the PCI procedure. Methods: Ten patients with stable AP and 20 patients with AMI, all treated with PCI and stent implantation in a central coronary artery, were included. Blood samples were drawn immediately before PCI (in the AP group only), and after 3 and 12 hours, days 1, 3, 5, 7, and 14 in both groups. EDTA plasma was used for analyses of PTX3, determined by an ELISA-method. Degree of myocardial necrosis was assessed by Troponin T (max) and infarct size in the AMI patients was determined by MRI (gadolinium late contrast enhancement technique) after 6 weeks. Results: PTX3 levels at 3 and 12 hours after the procedure were significantly higher in the AMI group compared to the AP group (median levels: 2.36 vs 1.36 ng/mL, p<0.001 and 1.52 vs 0.93 ng/mL, p=0.003) and borderline significantly higher after 3 days (p=0.058). In the AMI group, there was a significant overall change (Friedmans test p<0.001). A significant reduction from 3 to 12 hours was observed (2.36 to 1.52 ng/mL, p=0.001) with sustained reduced levels throughout the time periode (all p<0.001). Also in the AP group, a significant overall change was found (p< 0.001). From baseline (before PCI) to 3 hours after there was a significant increase (from 0.82 to 1.36 ng/mL, p=0.022), followed by a reduction after 12 hours (to 0.93 ng/mL), sustained reduced throughout (all p<0.05). There were no significant correlations between levels of PTX3 and degree of myocardial necrosis or infarct size at any time points (in the AMI group). Conclusion: The elevated levels of PTX3 at 3 and 12 hours after the PCI procedure in the AMI group compared to the stable AP group, is probably related to the myocardial infarction per se, although not related to infarct size or damaged myocardium in our population. The PCI procedure itself seems to influence the levels of PTX3 to a limited, although statistically significant extent.