Differing Behavior of Plasma Pentraxin3 and High-Sensitive CRP at the Very Onset of Myocardial Infarction with ST-segment Elevation

Tetsuo Yamasaki

doi:10.4172/2329-9495.1000108

Abstract

Although pentraxin3 (PTX3) has been reported as marker of more directly reflect the vascular inflammatory status than short pentraxin including high-sensitive CRP (hs-CRP), detailed difference in blood levels between PTX3 and hs-CRP at the onset of ST-segment elevation myocardial infarction (STEMI) are not fully investigated. Blood levels of pentraxins (PTX3 and hs-CRP) in 20 patients with early arrival of STEMI (2.9 ± 2.2 hours after onset) were measured at baseline, 24, 48, 72 and 120 hours after primary percutaneous coronary intervention (PCI). Also, the blood levels in infarct-related artery (IRA) were measured by thrombus aspiration during PCI. Samples of control (not myocardial infarction) with normal coronary artery (n=10) were drawn from both coronary and peripheral arteries during diagnostic coronary angiography. At baseline, the levels of PTX3 in both femoral and coronary artery in STEMI were significantly higher than those in control, but the hs-CRP did not different between STEMI and control. The level of both PTX3 and hs-CRP did not different between femoral artery and IRA in STEMI patients at baseline. Systemic level of PTX3 peaked 24 hours (p=0.01) followed by the hs-CRP that peaked 48 hours (p<0.01) after the PCI. PTX3 had appeared earlier than hs-CRP in the systemic circulation in the STEMI patients, but they may not be locally released from the IRA.

Highlights

PTX3 is a prototypic long pentraxin produced mainly by dendritic cells, macrophages, and endothelial cells in response to primary proinflammatory signals [1]
PTX3 is in the same family with CRP, its expression pattern is more tissue specific, especially in light of the fact that it is expressed in cells of atherosclerotic plaque itself, and reflects active atherosclerosis [7,8]
Given the similarities and differences between PTX3 and CRP, and due to the fact that PTX3 is produced from vascular endothelial cells and macrophages, instead of from the liver, it is important to assess the usefulness of PTX3 as a diagnostic tool for vascular inflammation, vulnerable coronary plaque which will rupture followed by acute myocardial infarction

Summary

Introduction

PTX3 is a prototypic long pentraxin produced mainly by dendritic cells, macrophages, and endothelial cells in response to primary proinflammatory signals [1]. CRP is an acute phase protein produced in the liver in response to inflammatory mediators and is referred to as a classical short pentraxin. PTX3 is in the same family with CRP, its expression pattern is more tissue specific, especially in light of the fact that it is expressed in cells of atherosclerotic plaque itself, and reflects active atherosclerosis [7,8]. Given the similarities and differences between PTX3 and CRP, and due to the fact that PTX3 is produced from vascular endothelial cells and macrophages, instead of from the liver, it is important to assess the usefulness of PTX3 as a diagnostic tool for vascular inflammation, vulnerable coronary plaque which will rupture followed by acute myocardial infarction. We investigate the plasma level of PTX3 and high sensitive CRP (hs-CRP) at the very onset of myocardial infarction with ST-segment elevation (STEMI) and hypothesize that profiles in blood levels of PTX3 and hs-CRP are different in those patients

Methods

Results

Conclusion