TY - JOUR
TI - Circulating Erythrocyte Microparticles and the Biochemical Extent of
Myocardial Injury in ST Elevation Myocardial Infarction
AU - Giannopoulos, Georgios
AU - Vrachatis, Dimitrios A.
AU - Oudatzis,
AU - Georgios
AU - Paterakis, Georgios
AU - Angelidis, Christos
AU - Koutivas,
AU - Athanasios
AU - Sianos, Georgios
AU - Cleman, Michael W.
AU - Filippatos,
AU - Gerasimos
AU - Lekakis, John
AU - Deftereos, Spyridon
JO - Cardiology (Switzerland)
PY - 2017
VL - 136
TODO - 1
SP - 15-20
PB - Karger
SN - null
TODO - 10.1159/000447625
TODO - Red blood cell; Flow cytometry; Myocardial infarction; Creatine kinase;
Troponin; Acute myocardial infarction
TODO - 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 rho = 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 x
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 beta = 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. (C) 2016 S. Karger AG, Basel
ER -