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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Tate, Jillian R. / Tsongalis, Gregory J.

13 Issues per year


IMPACT FACTOR 2013: 2.955
Rank 5 out of 29 in category Medical Laboratory Technology in the 2013 Thomson Reuters Journal Citation Report/Science Edition

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Time course of systemic markers of inflammation in patients presenting with acute coronary syndromes

Martina Brueckmann1 / Thomas Bertsch2 / Siegfried Lang3 / Tim Sueselbeck4 / Christian Wolpert5 / Jens J. Kaden6 / Carlos Jaramillo7 / Guenter Huhle8 / Martin Borggrefe9 / Karl K. Haase10

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Corresponding author. Martina Brueckmann, MD, First Department of Medicine, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Phone/Fax: +49-621-383-2875, E-mail:

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 42, Issue 10, Pages 1132–1139, ISSN (Print) 1434-6621, DOI: 10.1515/CCLM.2004.232, June 2005

Publication History

Received:
May 28, 2004
Accepted:
August 23, 2004
Published Online:
2005-06-01

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-α (TNF-α), 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-α, IL-6, IL-1 β, 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.

Keywords: acute coronary syndrome; coronary sinus; inflammation; time course

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