title: The influence of low-grade inflammation on platelets in patients with stable coronary artery disease.
abstract: Inflammation is likely to be involved in all stages of atherosclerosis. Numerous inflammatory biomarkers are currently being studied, and even subtle increases in inflammatory biomarkers have been associated with increased risk of cardiovascular events in patients with coronary artery disease (CAD). Low-grade inflammation may influence both platelet production and platelet activation potentially leading to enhanced platelet aggregation. Thrombopoietin is considered the primary regulator of platelet production, but it likely acts in conjunction with numerous cytokines, of which many have altered levels in CAD. Previous studies have shown that high-sensitive C-reactive protein (CRP) independently predicts increased platelet aggregation in stable CAD patients. Increased levels of CRP, fibrinogen, interleukin-6, stromal cell-derived factor-1, CXC motif ligand 16, macrophage migration inhibitory factor, RANTES, calprotectin, and copeptin have been associated with increased risk of cardiovascular events in CAD patients. Additionally, some of these inflammatory markers have been associated with enhanced platelet activation and aggregation. However, CRP and other inflammatory markers provide only limited additional predictive value to classical risk factors such as smoking, blood pressure, and cholesterol levels. Existing data do not clarify whether inflammation simply accompanies CAD and increased production and aggregation of platelets, or whether a causal relationship exists. In this review, we provide a comprehensive overview of inflammatory markers in stable CAD with particular emphasis on platelet production, activation, and aggregation in CAD patients.
authors.forename: Sanne Bøjet
authors.initials: SB
authors.lastname: Larsen
authors.forename: Erik Lerkevang
authors.initials: EL
authors.lastname: Grove
authors.forename: Morten
authors.initials: M
authors.lastname: Würtz
authors.forename: Søs
authors.initials: S
authors.lastname: Neergaard-Petersen
authors.forename: Anne-Mette
authors.initials: AM
authors.lastname: Hvas
authors.affiliation: Steen Dalby Kristensen, MD, DMSc, FESC, Professor, consultant cardiologist, Department of Cardiology, Aarhus University Hospital, DK - 8200 Aarhus, Denmark, Tel.: +45 78452030, Fax: +45 78452260, E-mail: steendk@dadlnet.dk.
authors.forename: Steen Dalby
authors.initials: SD
authors.lastname: Kristensen
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood; D015539:Platelet Activation; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D015398:Signal Transduction
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D018836:Inflammation Mediators; D010975:Platelet Aggregation Inhibitors
keywords: Inflammation; antiplatelet therapy; coronary artery disease; platelet aggregation; platelet production