Abstract 14775: Intracoronary and Systemic Microparticle Expression is Associated with Activated Platelet Monocyte Aggregate Formation, Platelet Activation, Myocardial Necrosis and Inflammation in St Elevation Myocardial Infarction
Background: In acute coronary syndrome (ACS) activated platelets bind to monocytes forming platelet monocyte aggregates (PMA), a sensitive marker of platelet activation. Microparticles (MP) are submicron membrane vesicles derived from many cell types in response to cell activation. Recent data suggests that MP are implicated in the pathogenesis of ACS. Aim: To investigate the relationship between intracoronary and systemic MP expression, PMA, markers of myocardial necrosis, platelet activation and inflammation in ST elevation myocardial infarction (STEMI).
Methods: Patients undergoing primary angioplasty for STEMI were recruited. Blood samples from the infarct related artery [intracoronary (IC)] and arterial sheath [systemic arterial (SA)] were collected. PMA and MP levels were estimated using fluorescent monoclonal antibodies (MonAb) and flow cytometry. PMA were identified as CD14+CD61+CD62P+ events. All MP were AnV+ events. We used CD62P MonAb for platelet derived MP (PMP); CD105 and CD31 MonAb for endothelial derived MP (EMP); CD14/CD142 MonAb for monocyte derived MP (TF+ MMP). MP was expressed as x106 per ml of plasma. ELISA was used for p-selectin, vWF and TNF-α measurement.
Results: Total MP (mean ± SD) in IC were 3.8 ± 2.6 vs 1.3 ± 1.6 in SA (p=0.02). Cell-specific MP expression was IC: PMP 1.7 ± 1.5; EMP 1.2±1.4; MMP 0.09 ± 0.08 and SA: PMP 1.1 ± 1.6; EMP 0.76 ± 0.9; MMP 0.23 ± 0.2. IC PMP and EMP were higher than SA (p=0.02 for PMP and p=0.1 for EMP) but SA MMP was higher than IC (p=0.07). IC PMA correlated with EMP (r=0.7; p=0.03). IC soluble p-selectin also correlated with total MP, PMP and CD105+ EMP (r=0.7; p=0.04, r=0.9; p=0.0002, r=0.8; p=0.008). IC MMP correlated well with IC soluble vWF (r=0.7; p=0.02). SA total MP and CD31+ EMP correlated strongly with peak Troponin-T (r=0.9; p=0.01) and total CK (r=0.9; p=0.01 and r=0.8; p=0.005). SA TNF-α correlated strongly with MMP (r=0.9; p=0.01).
Conclusions: This study demonstrates local and systemic differential MP expression in STEMI. Our data suggests distinct functional roles for different cell-specific MP phenotypes including pro-thrombosis, platelet activation, inflammation and myocardial necrosis. This may suggest a novel role for MPs as effectors of cellular injury in ACS.
- © 2012 by American Heart Association, Inc.