Circulating Erythrocyte Microparticles and the Biochemical Extent of Myocardial Injury in ST Elevation Myocardial Infarction

Abstract

Objectives: Red blood cell microparticles (RBCm) have potential adverse vascular effects and they have been shown to be elevated in ST elevation myocardial infarction (STEMI). The purpose of this study is to investigate their relationship with biochemical infarct size. Methods: RBCm were quantified with flow cytometry in blood drawn from 60 STEMI patients after a primary angioplasty. The creatine kinase-myocardial brain fraction (CK-MB) was measured at predefined time points and the area under the curve (AUC) was calculated. Results: RBCm count was correlated with CK-MB AUC (Spearman's ρ = 0.83, p < 0.001). The CK-MB AUC values per RBCm quartile (lower to upper) were: 3,351 (2,452-3,608), 5,005 (4,450-5,424), 5,903 (4,862-10,594), and 8,406 (6,848-12,782) ng × h/ml, respectively. From lower to upper quartiles, the maximal troponin I values were: 42.2 (23.3-49.3), 49.6 (28.8-54.1), 59.2 (41.4-77.3), and 69.1 (48.0-77.5) ng/ml (p = 0.005). In multivariable analysis, RBCm remained a significant predictor of CK-MB AUC (standardized β = 0.63, adjusted p = 0.001). Conclusions: Erythrocyte microparticles appear to be related to the total myocardial damage biomarker output. The exact pathophysiologic routes, if any, for this interaction remain to be identified. However, these results suggest that erythrocytes may be a - thus far virtually ignored - player in the pathogenesis of ischemic injury.

The number of red blood cell-derived microparticles in predicting periprocedural adverse effects in acute STsegment elevation myocardial infarction patients

“…In ST elevation myocardial infarction (STEMI) patients treated with primary circulating level of PCI RBC-MPs have exhibited significant approximately double elevation compared to volunteers. Moreover, the concentration of PCI RBC-MPs appears to be strongly positively associated with adverse clinical events in short-term follow-up [53].…”

“…There is evidence regarding close relationship between circulating number of RBC-MPs and biochemical infarct size, circulating troponins, associate with microvascular obstruction and reverse of ischemia-induced myocardial dysfunction [53], although the exact pathophysiologic routes for these interactions remain to be uncertain. Probably, the pro-coagulant activity of RBC-MPs seems to provide beneficial intrinsic and extrinsic clotting in patients after primary PCI.…”

Red blood cell-derived extracellular vesicles mediate intercellular communication in ischemic heart failure

“…Recent therapeutic strategies that target inflammation to reduce heart failure (Ridker et al, 2017) suggest that interaction between hematopoietic cells and cardiac cells may be important in cardiac remodeling. Notably, recent evidence demonstrates the prognostic significance of RBC-EVs in post-MI patients (Cheow et al, 2016, Giannopoulos et al, 2014, Giannopoulos et al, 2017, and plasma miRNAs derived from circulating hematopoietic cells (HCs), have been implicated in cardiac remodeling in several studies (Collino et al, 2010, Wen et al, 2012. However, the functional contribution of RBC-EVs as mediators of intercellular signaling (Thery et al, 2009) that contribute to post-MI LV remodeling remains unexplored, largely due to the limitations in tools for in-vivo tracking of EVs (Gangadaran et al, 2017).…”

Biosensing of periprocedural events in acute ST-segment elevation myocardial infarction patients with the erythrocyte-derived microparticles

“…RBC-MPs have potential adverse vascular effects and they have been shown to be elevated in ST elevation myocardial infarction (STEMI) [28]. There is evidence regarding close relationship between circulating number of RBC-MPs and biochemical infarct size, circulating troponins and reverse of ischemia-induced myocardial dysfunction [28], although the exact pathophysiologic routes for these interactions remain to be uncertain.…”

“…RBC-MPs have potential adverse vascular effects and they have been shown to be elevated in ST elevation myocardial infarction (STEMI) [28]. There is evidence regarding close relationship between circulating number of RBC-MPs and biochemical infarct size, circulating troponins and reverse of ischemia-induced myocardial dysfunction [28], although the exact pathophysiologic routes for these interactions remain to be uncertain. Probably, pro-coagulant thrombotic activity of RBC-MPs and their ability inducing platelet activation and aggregation might explain the role of them in the pathogenesis of periprocedural microvascular obstruction and left ventricular remodeling [29,30].…”