Circulating microparticle signature in coronary and peripheral blood of ST elevation myocardial infarction patients in relation to pain-to-PCI elapsed time. (1st January 2016)

• Record Type: Journal Article
• Authors: Suades, R.; Padró, T.; Crespo, J.; Ramaiola, I.; Martin-Yuste, V.; Sabaté, M.; Sans-Roselló, J.; Sionis, A.; Badimon, L.
• Is Part Of: International journal of cardiology. Volume 202(2016)
• Page Start: 378
• Page End: 387
• Publication Date: 2016-01-01
• Subjects: ACS acute coronary syndrome -- AUC area under the curve -- AV annexin V -- CAD coronary artery disease -- cMP circulating microparticle -- CV cardiovascular -- ECs endothelial cells -- eMPs endothelial-derived microparticles -- ErMPs erythrocyte-derived microparticles -- FH familial hypercholesterolemia -- gMPs granulocyte-derived microparticles -- IQR interquartile range -- IT ischemic time -- LMPs leukocyte-derived microparticles -- ℓMPs lymphocyte-derived microparticles -- mAbs monoclonal antibodies -- MI myocardial infarction -- mMPs monocyte-derived microparticles -- PCI percutaneous coronary intervention -- PFP platelet-free plasma -- pMPs platelet-derived microparticles -- ROC receiver operating characteristic curve -- STEMI ST elevation myocardial infarction -- TF tissue factor; Biomarkers -- Circulating cell-derived microparticles -- Myocardial revascularization -- Myocardial infarction -- Thrombosis; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2015.09.011
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: 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-to-PCI 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. Highlights: STEMI patients show changes in circulating microparticle (cMP) signature. Prothrombotic and proinflammatory cMPs vary both at systemic and coronary levels. The cMP intracoronary profile associates to duration of pain-to-PCI ischemic time. Peripheral cMPs associate to the number of diseased vessels. cMPs may be considered as sensitive prognostic multi-biomarkers in STEMI.