Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes

被引:788
作者
Mallat, Z
Benamer, H
Hugel, B
Benessiano, J
Steg, PG
Freyssinet, JM
Tedgui, A
机构
[1] Hop Lariboisiere, INSERM, U141, IFR Circulat, F-75475 Paris, France
[2] Hop Bichat Claude Bernard, Serv Cardiol, F-75877 Paris, France
[3] Hop Bichat Claude Bernard, Serv Biochim, F-75877 Paris, France
[4] Univ Strasbourg, Fac Med, Inst Hematol & Immunol, Strasbourg, France
[5] INSERM, U143, F-94275 Le Kremlin Bicetre, France
关键词
atherosclerosis; complications; thrombosis; microparticles; endothelium;
D O I
10.1161/01.CIR.101.8.841
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background-Apoptotic microparticles are responsible for almost all tissue factor activity of the plaque lipid core. We hypothesized that elevated levels of procoagulant microparticles could also circulate in the peripheral blood of patients with recent clinical signs of plaque disruption and thrombosis; Methods and Results-We studied 39 patients with coronary heart disease, including 12 patients with stable angina and 27 patients with acute coronary syndromes (ACS), and 12 patients with noncoronary heart disease. We isolated the circulating microparticles by capture with annexin V and determined their procoagulant potential with a prothrombinase assay. The cell origins of microparticles were determined in an additional 22 patients by antigenic capture with specific antibodies. The level of procoagulant microparticles did not differ between stable angina patients and noncoronary patients (10.1 +/- 1.6 nmol/L phosphatidylserine [PS] equivalent versus 9.9 +/- 1.6 nmol/L PS equivalent, respectively). However, procoagulant microparticles were significantly elevated in patients with ACS (22.2 +/- 2.7 nmol/L PS equivalent) compared with other coronary (P<0.01) or noncoronary (P<0.01) patients. Microparticles of endothelial origin were significantly elevated in patients with ACS (P<0.01), which suggests an important role for endothelial injury in inducing the procoagulant potential. Conclusions-Hihh levels of procoagulant endothelial microparticles are present in the circulating blood of patients with ACS and may contribute to the generation and perpetuation of intracoronary thrombi.
引用
收藏
页码:841 / 843
页数:3
相关论文
共 17 条
  • [1] Tissue-factor antigen and activity in human coronary atherosclerotic plaques
    Ardissino, D
    Merlini, PA
    Ariens, R
    Coppola, R
    Bramucci, E
    Mannucci, PM
    [J]. LANCET, 1997, 349 (9054) : 769 - 771
  • [2] The significance of shed membrane particles during programmed cell death in vitro, and in vivo, in HIV-1 infection
    Aupeix, K
    Hugel, B
    Martin, T
    Bischoff, P
    Lill, H
    Pasquali, JL
    Freyssinet, JM
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (07) : 1546 - 1554
  • [3] Transcellular activation of platelets and endothelial cells by bioactive lipids in platelet microparticles
    Barry, OP
    Pratico, D
    Lawson, JA
    FitzGerald, GA
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (09) : 2118 - 2127
  • [4] Surface blebs on apoptotic cells are sites of enhanced procoagulant activity: Implications for coagulation events and antigenic spread in systemic lupus erythematosus
    CasciolaRosen, L
    Rosen, A
    Petri, M
    Schlissel, M
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (04) : 1624 - 1629
  • [5] In vitro generation of endothelial microparticles and possible prothrombotic activity in patients with lupus anticoagulant
    Combes, V
    Simon, AC
    Grau, GE
    Arnoux, D
    Camoin, L
    Sabatier, F
    Mutin, M
    Sanmarco, M
    Sampol, J
    Dignat-George, F
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (01) : 93 - 102
  • [6] SECRETORY PHOSPHOLIPASE A(2) GENERATES THE NOVEL LIPID MEDIATOR LYSOPHOSPHATIDIC ACID IN MEMBRANE MICROVESICLES SHED FROM ACTIVATED CELLS
    FOURCADE, O
    SIMON, MF
    VIODE, C
    RUGANI, N
    LEBALLE, F
    RAGAB, A
    FOURNIE, B
    SARDA, L
    CHAP, H
    [J]. CELL, 1995, 80 (06) : 919 - 927
  • [7] Freyssinet JM, 1999, THROMB HAEMOSTASIS, V82, P727
  • [8] MECHANISMS OF DISEASE - THE PATHOGENESIS OF CORONARY-ARTERY DISEASE AND THE ACUTE CORONARY SYNDROMES .1.
    FUSTER, V
    BADIMON, L
    BADIMON, JJ
    CHESEBRO, JH
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1992, 326 (04) : 242 - 250
  • [9] Treatment with a GPIIb/IIIa antagonist inhibits thrombin generation in platelet rich plasma from patients
    Keularts, IMLW
    Béguin, S
    de Zwaan, C
    Hemker, HC
    [J]. THROMBOSIS AND HAEMOSTASIS, 1998, 80 (03) : 370 - 371
  • [10] The unstable atheroma
    Lee, RT
    Libby, P
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (10) : 1859 - 1867