Suades R, Padró T, Crespo J, Ramaiola I, Martin-Yuste V, Sabaté M, Sans-Roselló J, Sionis A, Badimon L
Cardiovascular Research Center, CSIC-ICCC, IIB-Sant Pau, Barcelona, Spain.
Department of Interventional Cardiology, Hospital Clinic, Barcelona, Spain.
Int J Cardiol. 2016 Jan 1;202:378-87. doi: 10.1016/j.ijcard.2015.09.011. Epub 2015 Sep 12.
Circulating microparticle (cMP) levels are increased in the acute phase of ST-elevation myocardial infarction (STEMI) and associate with microvascular obstruction; however, the precise cMP-parental cell signature and activation level are not elucidated. Here, we aimed to study the cMP signature in STEMI-patients and whether cMP phenotype changes in relation to onset of pain-to-PCI [ischemic time (IT)]-elapsed time.
Blood was taken at PCI from the culprit coronary and the peripheral circulation in STEMI-patients (N=40). Two control groups were included: peripheral blood of age-matched patients recovering from STEMI [after 72 h] and of control individuals (N=20/group). cMP-parental origin and activation level were characterized by triple-labeling flow cytometry.
Procoagulant annexin V-positive cMPs bearing parental cell markers as well as markers of activated cells displayed a significantly different profile in STEMI-patients, in control individuals and in patients recovering from STEMI. cMPs derived from monocytes, endothelium, and activated vascular cells were higher in the culprit coronary artery than in peripheral blood in STEMI-patients, especially in patients intervened at short IT. Indeed, cMP levels in coronary blood were inversely related to IT duration (more abundant in thrombi with pain-to-PCI time<180 min).
A characteristic [CD66b+/CD62E+/CD142+] cMP signature in the systemic circulation reflects the formation of coronary thrombotic occlusions in STEMI-patients. Changes in the cMP signature in the culprit coronary artery blood reveal the sensitivity of MPs to detect the ischemia-elapsed time. Interestingly, cMPs in peripheral blood may be sensitive markers of the thrombo-occlusive vascular process developing in the coronary arteries of STEMI-patients.
循环微粒(cMP)水平在ST段抬高型心肌梗死(STEMI)急性期升高,并与微血管阻塞相关;然而,cMP的精确亲代细胞特征和激活水平尚未阐明。在此,我们旨在研究STEMI患者的cMP特征,以及cMP表型是否随疼痛至经皮冠状动脉介入治疗(PCI)[缺血时间(IT)]的经过时间而变化。
在STEMI患者(N = 40)接受PCI时,从罪犯冠状动脉和外周循环采集血液。纳入两个对照组:年龄匹配的STEMI恢复患者[72小时后]的外周血和对照组个体(每组N = 20)。通过三重标记流式细胞术对cMP的亲代来源和激活水平进行表征。
携带亲代细胞标记物以及激活细胞标记物的促凝血膜联蛋白V阳性cMPs在STEMI患者、对照组个体和STEMI恢复患者中显示出显著不同的特征。STEMI患者罪犯冠状动脉中源自单核细胞、内皮细胞和激活血管细胞的cMPs高于外周血,尤其是在短IT时接受干预的患者中。实际上,冠状动脉血液中的cMP水平与IT持续时间呈负相关(在疼痛至PCI时间<180分钟的血栓中更丰富)。
全身循环中特征性的[cMP特征(CD66b + / CD62E + / CD142 +)]反映了STEMI患者冠状动脉血栓性闭塞的形成。罪犯冠状动脉血液中cMP特征的变化揭示了微粒检测缺血经过时间的敏感性。有趣的是,外周血中的cMPs可能是STEMI患者冠状动脉中正在发展的血栓闭塞性血管过程的敏感标志物。