title: Time course of systemic markers of inflammation in patients presenting with acute coronary syndromes.
abstract: Inflammation within coronary plaques may cause an acute coronary syndrome by promoting rupture and erosion. It was the aim of this study to examine whether markers of inflammation derive from a cardiac or extracardiac source and how their levels develop over time. Blood samples were taken from patients with acute coronary syndromes (ACS) with proven atherosclerotic lesion(s) of the left coronary artery (n=13) and from control patients without coronary artery disease (n=13). Blood was taken from the femoral vein and the coronary sinus vein before and after coronary angioplasty (day 0) and on days 1 and 120. Levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-1-receptor antagonist (IL-1 ra) and soluble CD40 ligand (sCD40L) were higher in ACS patients as compared to controls and remained elevated up to day 120. In the long-term time course these markers of inflammation and plaque remodeling slightly decreased in ACS patients. There were no statistically significant differences detectable in the levels of TNF-alpha, IL-6, IL-1 beta, IL-10, IL-1 ra, sCD40L and monocyte chemoattractant protein-1 (MCP-1) in the blood of ACS patients taken from a cardiac source as compared to an extracardiac source (coronary sinus vs. femoral vein). This study demonstrates the importance of a systemic inflammatory condition in patients with ACS, in whom markers of inflammation are increased as compared to controls. During long-term follow-up the pro-inflammatory activity remains elevated in ACS patients, supporting the concept of a systemic rather than a local vascular inflammation contributing to the development of atherosclerosis.
authors.affiliation: First Department of Medicine, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany. martina.brueckmann@med.ma.uni-heidelberg.de
authors.forename: Martina
authors.initials: M
authors.lastname: Brueckmann
authors.forename: Thomas
authors.initials: T
authors.lastname: Bertsch
authors.forename: Siegfried
authors.initials: S
authors.lastname: Lang
authors.forename: Tim
authors.initials: T
authors.lastname: Sueselbeck
authors.forename: Christian
authors.initials: C
authors.lastname: Wolpert
authors.forename: Jens J
authors.initials: JJ
authors.lastname: Kaden
authors.forename: Carlos
authors.initials: C
authors.lastname: Jaramillo
authors.forename: Guenter
authors.initials: G
authors.lastname: Huhle
authors.forename: Martin
authors.initials: M
authors.lastname: Borggrefe
authors.forename: Karl K
authors.initials: KK
authors.lastname: Haase
mesh_terms: D000210:Acute-Phase Reaction; D000368:Aged; D015415:Biomarkers / Q000097:blood*; D023201:CD40 Ligand / Q000097:blood / Q000378:metabolism; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D008024:Ligands; D008297:Male; D008875:Middle Aged; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors / Q000378:metabolism; D013223:Statistics as Topic; D013995:Time; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; D018932:Chemokine CCL2; D015850:Interleukin-6; D008024:Ligands; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D023201:CD40 Ligand