4.7 Article

Intracoronary microparticles and microvascular obstruction in patients with ST elevation myocardial infarction undergoing primary percutaneous intervention

Journal

EUROPEAN HEART JOURNAL
Volume 33, Issue 23, Pages 2928-2938

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehs065

Keywords

Microparticles; Intracoronary; Myocardial blush grade; Quantitative blush grade; Thrombus score

Funding

  1. Fondazione Cassa di Risparmio di Roma

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Aims Microparticles (MP) are cell-derived fragments known to be increased in the blood of patients with acute coronary syndromes. We aimed to assess, in ST elevation myocardial infarction (STEMI), the systemic and local (in the culprit coronary artery) levels of platelet-derived MP (PMP, CD42CD31) and endothelial-derived MP (EMP, CD42CD31) and their relation to indexes of microvascular obstruction (MVO). Methods and results In 78 STEMI patients undergoing successful primary percutaneous coronary intervention, blood samples were sequentially drawn from the aorta and the culprit coronary artery for cytofluorimetric MP detection. Thrombolysis in myocardial infarction (TIMI) flow, thrombus score (TS), corrected TIMI frame count (cTFC), myocardial blush grade (MBG), quantitative blush evaluator (QuBE) score, and 90 min ST resolution (SigmaSTR) were calculated. Both PMP and EMP levels were significantly higher in the intracoronary than in the aortic blood samples. Intracoronary PMP and EMP levels were positively related to TS and cTFC and inversely related to MBG and QuBE. Aortic PMP (but not EMP) levels were related to TS and cTFC and, inversely, to QuBE. Intracoronary PMP were independently related to angiographic and electrocardiographic MVO in a multivariate model. Conclusion The correlations of intracoronary EMP and of both systemic and intracoronary PMP levels with TS support the role of MP as markers of ongoing thrombosis. Moreover, the correlation of intracoronary MP with indexes of microvascular dysfunction suggests, for the first time, a possible direct role of MP in the pathogenesis of MVO.

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