Journal
INTERNATIONAL JOURNAL OF CARDIOLOGY
Volume 202, Issue -, Pages 378-387Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.ijcard.2015.09.011
Keywords
Biomarkers; Circulating cell-derived microparticles; Myocardial revascularization; Myocardial infarction; Thrombosis
Categories
Funding
- Spanish Ministry of Science Plan Estatal I+D+I - Fondo Europeo de Desarrollo Regional (FEDER-Una manera de hacer Europa) [SAF2013-42962-R]
- AGAUR (Agencia de Gestio d'Ajuts Universitaris i de Recerca) [2009SGR826]
- TerCel (Red de Terapia Celular) [RD/12/0019/0026]
- Red de Investigacion Cardiovascular (RIC) [RD12/0042/0027]
- Spanish Ministry of Health from Instituto de Salud Carlos III (ISCIII) [FIS-PI13/02850]
- Fundacion de Investigacion Cardiovascular (FIC)-Fundacion Jesus Serra
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Background: 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. Methods: 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. Results: 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-toPCI time <180 min). Conclusions: 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. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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