Inflammatory role and prognostic value of platelet chemokines in acute coronary syndrome
Inflammatory role and prognostic value of platelet chemokines in acute coronary syndrome
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DOI：
10.1160/th14-02-0139
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发表时间：
2014-12-01
影响因子：
6.7
通讯作者：
von Hundelshausen, Philipp
中科院分区：
文献类型：
--
作者：
Blanchet, Xavier;Cesarek, Katja;von Hundelshausen, Philipp
活化的血小板和中性粒细胞加剧动脉粥样硬化。血小板释放趋化因子CXCL4、CXCL4L1和CCL5，而髓过氧化物酶（MPO）和天青霉素是嗜中性粒细胞衍生的。我们研究了这些血小板和中性粒细胞介质的血浆水平是否受急性冠状动脉综合征（ACS），其药物治疗，伴随的临床或实验室参数的影响，并预测冠状动脉疾病（CAD）的进展。在一项观察性研究中，通过多元线性回归确定了204例ACS患者入院后6小时或无ACS或CAD患者的各种因素与血小板趋化因子和中性粒细胞介质血浆浓度的相关性。在用ACS相关触发物（如斑块材料）活化血液后，进一步分析介质释放。ACS患者血清CXCL4、CXCL4L1、CCL5、MPO和azurocidin水平升高。CXCL 4和CCL 5与血小板计数和CRP相关，但CXCL 4L1或MPO与血小板计数和CRP无关。CXCL4（与肝素治疗相关）和MPO在ACS期间下降超过6小时。升高的CCL5与CAD的进展相关。将血液与斑块材料一起孵育，PAR 1和PAR 4活化诱导CXCL 4和CCL 5的显著释放，而CXCL 4L1和MPO几乎没有或没有改变。血小板趋化因子和中性粒细胞产物在ACS中伴随升高，并受到肝素治疗的差异调节。ACS期间的CCL5水平可预测既存CAD的进展。血小板衍生的产物似乎在ACS期间的炎症反应中占主导地位，增加了ACS本身可能促进血管炎症的新证据。
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.