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Inflammatory role and prognostic value of platelet chemokines in acute coronary syndrome

Blanchet, Xavier ; Cesarek, Katja ; Brandt, Johanna ; Herwald, Heiko LU orcid ; Teupser, Daniel ; Kuechenhoff, Helmut ; Karshovska, Ela ; Mause, Sebastian F. ; Siess, Wolfgang and Wasmuth, Hermann , et al. (2014) In Thrombosis and Haemostasis 112(6). p.1277-1287
Abstract
Activated platelets and neutrophils exacerbate atherosclerosis. Platelets release the chemokines CXCL4, CXCL4L1 and CCL5, whereas myeloperoxidase (MPO) and azurocidin are neutrophil-derived. We investigated whether plasma levels of these platelet and neutrophil mediators are affected by the acute coronary syndrome (ACS), its medical treatment, concomitant clinical or laboratory parameters, and predictive for the progression of coronary artery disease (CAD). In an observational study, the association of various factors with plasma concentrations of platelet chemokines and neutrophil mediators in 204 patients, either upon admission with ACS and 6 hours later or without ACS or CAD, was determined by multiple linear regression. Mediator... (More)
Activated platelets and neutrophils exacerbate atherosclerosis. Platelets release the chemokines CXCL4, CXCL4L1 and CCL5, whereas myeloperoxidase (MPO) and azurocidin are neutrophil-derived. We investigated whether plasma levels of these platelet and neutrophil mediators are affected by the acute coronary syndrome (ACS), its medical treatment, concomitant clinical or laboratory parameters, and predictive for the progression of coronary artery disease (CAD). In an observational study, the association of various factors with plasma concentrations of platelet chemokines and neutrophil mediators in 204 patients, either upon admission with ACS and 6 hours later or without ACS or CAD, was determined by multiple linear regression. Mediator release was further analysed after activation of blood with ACS-associated triggers such as plaque material. CXCL4, CXCL4L1, CCL5, MPO and azurocidin levels were elevated in ACS. CXCL4 and CCL5 but not CXCL4L1 or MPO were associated with platelet counts and CRP. CXCL4 (in association with heparin treatment) and MPO declined over 6 hours during ACS. Elevated CCL5 was associated with a progression of CAD. Incubating blood with plaque material, PAR1 and PAR4 activation induced a marked release of CXCL4 and CCL5, whereas CXCL4L1 and MPO were hardly or not altered. Platelet chemokines and neutrophil products are concomitantly elevated in ACS and differentially modulated by heparin treatment. CCL5 levels during ACS predict a progression of preexisting CAD. Platelet-derived products appear to dominate the inflammatory response during ACS, adding to the emerging evidence that ACS per se may promote vascular inflammation. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Acute coronary syndrome, atherosclerosis, chemokines, platelets, neutrophils
in
Thrombosis and Haemostasis
volume
112
issue
6
pages
1277 - 1287
publisher
Schattauer GmbH
external identifiers
  • wos:000346040500024
  • scopus:84914144249
  • pmid:25183015
ISSN
0340-6245
DOI
10.1160/TH14-02-0139
language
English
LU publication?
yes
id
816c1c65-0682-42d4-8dc6-77a51c04147b (old id 4957598)
date added to LUP
2016-04-01 13:49:32
date last changed
2022-02-04 17:34:02
@article{816c1c65-0682-42d4-8dc6-77a51c04147b,
  abstract     = {{Activated platelets and neutrophils exacerbate atherosclerosis. Platelets release the chemokines CXCL4, CXCL4L1 and CCL5, whereas myeloperoxidase (MPO) and azurocidin are neutrophil-derived. We investigated whether plasma levels of these platelet and neutrophil mediators are affected by the acute coronary syndrome (ACS), its medical treatment, concomitant clinical or laboratory parameters, and predictive for the progression of coronary artery disease (CAD). In an observational study, the association of various factors with plasma concentrations of platelet chemokines and neutrophil mediators in 204 patients, either upon admission with ACS and 6 hours later or without ACS or CAD, was determined by multiple linear regression. Mediator release was further analysed after activation of blood with ACS-associated triggers such as plaque material. CXCL4, CXCL4L1, CCL5, MPO and azurocidin levels were elevated in ACS. CXCL4 and CCL5 but not CXCL4L1 or MPO were associated with platelet counts and CRP. CXCL4 (in association with heparin treatment) and MPO declined over 6 hours during ACS. Elevated CCL5 was associated with a progression of CAD. Incubating blood with plaque material, PAR1 and PAR4 activation induced a marked release of CXCL4 and CCL5, whereas CXCL4L1 and MPO were hardly or not altered. Platelet chemokines and neutrophil products are concomitantly elevated in ACS and differentially modulated by heparin treatment. CCL5 levels during ACS predict a progression of preexisting CAD. Platelet-derived products appear to dominate the inflammatory response during ACS, adding to the emerging evidence that ACS per se may promote vascular inflammation.}},
  author       = {{Blanchet, Xavier and Cesarek, Katja and Brandt, Johanna and Herwald, Heiko and Teupser, Daniel and Kuechenhoff, Helmut and Karshovska, Ela and Mause, Sebastian F. and Siess, Wolfgang and Wasmuth, Hermann and Soehnlein, Oliver and Koenen, Rory R. and Weber, Christian and von Hundelshausen, Philipp}},
  issn         = {{0340-6245}},
  keywords     = {{Acute coronary syndrome; atherosclerosis; chemokines; platelets; neutrophils}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{1277--1287}},
  publisher    = {{Schattauer GmbH}},
  series       = {{Thrombosis and Haemostasis}},
  title        = {{Inflammatory role and prognostic value of platelet chemokines in acute coronary syndrome}},
  url          = {{http://dx.doi.org/10.1160/TH14-02-0139}},
  doi          = {{10.1160/TH14-02-0139}},
  volume       = {{112}},
  year         = {{2014}},
}