TY - JOUR
T1 - High levels of circulating endothelial microparticles in patients with acute coronary syndromes
AU - Bernal-Mizrachi, Leon
AU - Jy, Wenche
AU - Jimenez, Joaquin J.
AU - Pastor, Juan
AU - Mauro, Lucia M.
AU - Horstman, Lawrence L.
AU - De Marchena, Eduardo
AU - Ahn, Yeon S.
N1 - Funding Information:
Supported by the Wallace H Coulter Foundation, the Roz and Cal Kovens Research Fund, the Charles and Jane Bosco Research Fund, and the Mary Beth Weiss Research Fund.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2003/6/1
Y1 - 2003/6/1
N2 - Background: Endothelial injury plays a critical role in coronary artery disease (CAD), but the assessment of this injury has been problematical. Recently, it has been shown in vitro that endothelial cells (ECs) release endothelial microparticles (EMPs) on activation or apoptosis and that an assay of EMPs can provide useful information on EC status in patients with thrombotic disorders. This study is aimed at assessing possible correlations between EMPs, which are markers of endothelial injury, and clinical subgroups of patients with CAD. Methods: A prospective, case-controlled study was conducted on 84 patients with CAD and 42 control subjects to investigate EMP profiles. Included were 64 patients with acute coronary syndromes ([ACS], 38 with myocardial infarction [MI] and 26 with unstable angina [UA]) and 20 patients with stable angina (SA). EMPs in platelet-poor plasma were measured flow cytometrically with combinations of fluorescent antibodies (anti-CD31, -51, -42), allowing distinction of EMPs from platelet microparticles (PMPs). Clinical subgroups of patients were correlated with EMP and PMP levels in blood. Results: Two species of EMPs (CD31 + and CD51 +) were evaluated. Both were significantly higher in patients with CAD than in control subjects. CD31 + EMP was higher in ACS than SA. Among patients with first MI, CD31 + EMP was higher in patients with MI than in patients with UA and was significantly higher than in patients with recurring MI. CD51 + EMP did not discriminate ACS from SA. A simultaneous assay of PMP showed correlation between EMPs and PMPs. However, PMPs did not discriminate patients with SA from control subjects. Conclusions: EMP assay appears promising for assessing EC injury in CAD.
AB - Background: Endothelial injury plays a critical role in coronary artery disease (CAD), but the assessment of this injury has been problematical. Recently, it has been shown in vitro that endothelial cells (ECs) release endothelial microparticles (EMPs) on activation or apoptosis and that an assay of EMPs can provide useful information on EC status in patients with thrombotic disorders. This study is aimed at assessing possible correlations between EMPs, which are markers of endothelial injury, and clinical subgroups of patients with CAD. Methods: A prospective, case-controlled study was conducted on 84 patients with CAD and 42 control subjects to investigate EMP profiles. Included were 64 patients with acute coronary syndromes ([ACS], 38 with myocardial infarction [MI] and 26 with unstable angina [UA]) and 20 patients with stable angina (SA). EMPs in platelet-poor plasma were measured flow cytometrically with combinations of fluorescent antibodies (anti-CD31, -51, -42), allowing distinction of EMPs from platelet microparticles (PMPs). Clinical subgroups of patients were correlated with EMP and PMP levels in blood. Results: Two species of EMPs (CD31 + and CD51 +) were evaluated. Both were significantly higher in patients with CAD than in control subjects. CD31 + EMP was higher in ACS than SA. Among patients with first MI, CD31 + EMP was higher in patients with MI than in patients with UA and was significantly higher than in patients with recurring MI. CD51 + EMP did not discriminate ACS from SA. A simultaneous assay of PMP showed correlation between EMPs and PMPs. However, PMPs did not discriminate patients with SA from control subjects. Conclusions: EMP assay appears promising for assessing EC injury in CAD.
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U2 - 10.1016/S0002-8703(03)00103-0
DO - 10.1016/S0002-8703(03)00103-0
M3 - Article
C2 - 12796750
AN - SCOPUS:0038620493
VL - 145
SP - 962
EP - 970
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 6
ER -