PMID- 15552272
OWN - NLM
STAT- MEDLINE
DCOM- 20050405
LR  - 20161018
IS  - 1434-6621 (Print)
IS  - 1434-6621 (Linking)
VI  - 42
IP  - 10
DP  - 2004
TI  - Time course of systemic markers of inflammation in patients presenting with acute 
      coronary syndromes.
PG  - 1132-9
AB  - 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.
FAU - Brueckmann, Martina
AU  - Brueckmann M
AD  - First Department of Medicine, Faculty of Clinical Medicine Mannheim, University 
      of Heidelberg, Mannheim, Germany. martina.brueckmann@med.ma.uni-heidelberg.de
FAU - Bertsch, Thomas
AU  - Bertsch T
FAU - Lang, Siegfried
AU  - Lang S
FAU - Sueselbeck, Tim
AU  - Sueselbeck T
FAU - Wolpert, Christian
AU  - Wolpert C
FAU - Kaden, Jens J
AU  - Kaden JJ
FAU - Jaramillo, Carlos
AU  - Jaramillo C
FAU - Huhle, Guenter
AU  - Huhle G
FAU - Borggrefe, Martin
AU  - Borggrefe M
FAU - Haase, Karl K
AU  - Haase KK
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Clin Chem Lab Med
JT  - Clinical chemistry and laboratory medicine
JID - 9806306
RN  - 0 (Biomarkers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Ligands)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 147205-72-9 (CD40 Ligand)
SB  - IM
MH  - Acute-Phase Reaction
MH  - Aged
MH  - Biomarkers/*blood
MH  - CD40 Ligand/blood/metabolism
MH  - Case-Control Studies
MH  - Chemokine CCL2/blood/metabolism
MH  - Coronary Artery Disease/blood/*metabolism
MH  - Humans
MH  - Inflammation
MH  - Interleukin-6/blood/metabolism
MH  - Ligands
MH  - Male
MH  - Middle Aged
MH  - Receptors, Interleukin-1/antagonists & inhibitors/metabolism
MH  - Statistics as Topic
MH  - Time
MH  - Tumor Necrosis Factor-alpha/analysis/metabolism
EDAT- 2004/11/24 09:00
MHDA- 2005/04/06 09:00
CRDT- 2004/11/24 09:00
PHST- 2004/11/24 09:00 [pubmed]
PHST- 2005/04/06 09:00 [medline]
PHST- 2004/11/24 09:00 [entrez]
AID - 10.1515/CCLM.2004.232 [doi]
PST - ppublish
SO  - Clin Chem Lab Med. 2004;42(10):1132-9. doi: 10.1515/CCLM.2004.232.