PMID- 19477372
OWN - NLM
STAT- MEDLINE
DCOM- 20110216
LR  - 20220410
IS  - 1876-4738 (Electronic)
IS  - 0914-5087 (Linking)
VI  - 53
IP  - 3
DP  - 2009 Jun
TI  - Inflammatory biomarkers in coronary artery disease.
PG  - 317-33
LID - 10.1016/j.jjcc.2008.12.007 [doi]
AB  - Current evidence supports that inflammation is a major driving force underlying 
      the initiation of coronary plaques, their unstable progression, and eventual 
      disruption; patients with a more pronounced vascular inflammatory response have a 
      poorer outcome. Biomarkers are generally considered to be proteins or enzymes - 
      measured in serum, plasma, or blood - that provide independent diagnostic and 
      prognostic value by reflecting an underlying disease state. In the case of 
      coronary artery disease (CAD), inflammatory biomarkers, have been extensively 
      investigated; more evidence exists for C-reactive protein (CRP). Using high 
      sensitivity (hs) assays, epidemiologic data demonstrate an association between 
      hs-CRP and risk for future cardiovascular morbidity and mortality among those at 
      high risk or with documented CAD. Moreover, a series of prospective studies 
      provide consistent data documenting that mild elevation of baseline levels of 
      hs-CRP among apparently healthy individuals is associated with higher long-term 
      risk for cardiovascular events. Yet, the predictive value of hs-CRP is found to 
      be independent of traditional cardiovascular risk factors. Recent studies suggest 
      that, besides CRP, other inflammatory biomarkers such as cytokines [interleukin 
      (IL)-1, IL-6, IL-8, monocyte chemoattractant protein-1 (MCP-1)], soluble CD40 
      ligand, serum amyloid A (SAA), selectins (E-selectin, P-selectin), 
      myeloperoxidase (MPO), matrix metalloproteinases (MMPs), cellular adhesion 
      molecules [intercellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule 
      1 (VCAM-1)], placental growth factor (PlGF) and A(2) phospholipases may have a 
      potential role for the prediction of risk for developing CAD and may correlate 
      with severity of CAD. Finally, indications suggest that the increased risk 
      associated with inflammation may be modified with certain preventive therapies 
      and biomarkers may help to identify the individuals who would benefit most from 
      these interventions.
FAU - Zakynthinos, Epaminondas
AU  - Zakynthinos E
AD  - Critical Care Department, School of Medicine, University Hospital of Thessaly, 
      Larissa, Greece. ezakynth@yahoo.com
FAU - Pappa, Nikolitsa
AU  - Pappa N
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20090129
PL  - Netherlands
TA  - J Cardiol
JT  - Journal of cardiology
JID - 8804703
RN  - 0 (Biomarkers)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Serum Amyloid A Protein)
RN  - 147205-72-9 (CD40 Ligand)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - EC 1.11.1.7 (Peroxidase)
SB  - IM
CIN - J Cardiol. 2009 Oct;54(2):344-5; author reply 345-6. PMID: 19782279
MH  - Biomarkers/blood
MH  - C-Reactive Protein/*analysis
MH  - CD40 Ligand/blood
MH  - Cell Adhesion Molecules/blood
MH  - Coronary Artery Disease/*diagnosis/etiology/prevention & control
MH  - Cytokines/blood
MH  - Humans
MH  - Inflammation/complications/*diagnosis
MH  - Inflammation Mediators/blood
MH  - Peroxidase/blood
MH  - Predictive Value of Tests
MH  - Primary Prevention
MH  - Risk
MH  - Serum Amyloid A Protein/analysis
EDAT- 2009/05/30 09:00
MHDA- 2011/02/17 06:00
CRDT- 2009/05/30 09:00
PHST- 2008/10/10 00:00 [received]
PHST- 2008/12/24 00:00 [revised]
PHST- 2008/12/26 00:00 [accepted]
PHST- 2009/05/30 09:00 [entrez]
PHST- 2009/05/30 09:00 [pubmed]
PHST- 2011/02/17 06:00 [medline]
AID - S0914-5087(09)00011-2 [pii]
AID - 10.1016/j.jjcc.2008.12.007 [doi]
PST - ppublish
SO  - J Cardiol. 2009 Jun;53(3):317-33. doi: 10.1016/j.jjcc.2008.12.007. Epub 2009 Jan 
      29.