Inflammatory response to percutaneous coronary intervention in stable coronary artery disease

Abstract

Percutaneous coronary intervention (PCI) can be regarded as a model for mechanical induced plaque rupture. The objective of this study was to evaluate the inflammatory response to PCI in stable coronary artery disease (CAD) by analysing plasma levels of a wide range of inflammatory mediators. Consecutively, we included 36 patients with stable angina pectoris after successful revascularization by PCI with implantation of a bare metal stent (BMS) or a drug eluting stent (DES). Patients were followed for 7 days with serial measurements of inflammatory mediators in plasma. C-reactive protein (CRP) and Pentraxin 3 showed a statistical significant early increase after PCI peaking at 3 days and 3 h, respectively. Vascular cell adhesion molecule-1 (VCAM-1) increased significantly with a peak at 3 days, while E-selectin showed a statistical significant gradual decrease. Markers of platelet mediated inflammation showed increasing (CD40 ligand) and decreasing (P-selectin) levels after PCI. While monocyte chemoattractant protein, CCL21 and CXCL16 increased rapidly in response to PCI, Interleukin-8, CCL19 and RANTES decreased. Patients with DES had significantly lower levels of VCAM-1 and RANTES compared to those with BMS. A femoral access site was associated with higher CRP levels than a radial access site. The use of glycoprotein-IIb/IIIa-inhibitors was associated with significantly higher CD40L and RANTES levels. Our findings underscore the complex nature of the inflammatory responses during PCI in stable CAD, and suggest that simultaneous measurements of several markers may be needed to characterize these PCI-related responses. The responses were only in a minor degree influenced by stent type, access site and the use of glycoprotein-IIb/IIIa-inhibitors.

Microbial Carriage State of Peripheral Blood Dendritic Cells (DCs) in Chronic Periodontitis Influences DC Differentiation, Atherogenic Potential

“…The results support mfa-1-dependent secretion of MMP-9 by mDCs (Figure 3D). Other indicators of risk of plaque rupture, including C1q (49), HSP60/HSP70 (reviewed in (50), CCR2 (51) and CXCL16 (52) (53) were analyzed at the mRNA level (Figure 3E). Analysis of these transcripts indicates that C1q, HSP60, HSP-70, CCR2 and CXCL16 are upregulated in response to fimbriated Pg381, relative to untreated control.…”

Prognostic Value of Plasma Pentraxin-3 Levels in Patients with Stable Coronary Artery Disease after Drug-Eluting Stent Implantation

“…Kotooka et al [ 17 ] reported that the plasma PTX3 levels began to increase at 15 min after coronary stenting and reached a maximum at 24 h in the coronary sinus and peripheral blood. Other 2 studies also found PCI could mediate the increase of PTX3 [ 15 , 16 ].…”

Increased expression of monocyte tissue factor and soluble CD40 ligand at mid-term follow-up following percutaneous coronary intervention

“…This is followed by a statistically significant (P < 0.05) increase in the levels of sCD40 ligand from the pre-PCI time line to follow-up. An increase in sCD40L 7 days after PCI of stable coronary artery disease patients has recently been reported [5].…”