title: 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.
authors.affiliation: Department of Cardiology, Stavanger University Hospital, Postbox 8100, 4068 Stavanger, Norway. munk@lyse.net
authors.forename: Peter S
authors.initials: PS
authors.lastname: Munk
authors.forename: Unni M
authors.initials: UM
authors.lastname: Breland
authors.forename: Pål
authors.initials: P
authors.lastname: Aukrust
authors.forename: Oyvind
authors.initials: O
authors.lastname: Skadberg
authors.forename: Thor
authors.initials: T
authors.lastname: Ueland
authors.forename: Alf I
authors.initials: AI
authors.lastname: Larsen
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000628:therapy; D017130:Angioplasty; D002097:C-Reactive Protein / Q000032:analysis; D023201:CD40 Ligand / Q000032:analysis; D003324:Coronary Artery Disease / Q000097:blood* / Q000628:therapy*; D016207:Cytokines / Q000097:blood; D054855:Drug-Eluting Stents; D019040:E-Selectin / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000628:therapy; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D000683:Serum Amyloid P-Component / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D000099153:Pentraxins
chemical_list: D002097:C-Reactive Protein; D023201:CD40 Ligand; D016207:Cytokines; D019040:E-Selectin; D018836:Inflammation Mediators; D019007:P-Selectin; D000683:Serum Amyloid P-Component; D019010:Vascular Cell Adhesion Molecule-1; D000099153:Pentraxins