(Circulation. 2000;101:841.)
© 2000 American Heart Association, Inc.
Brief Rapid Communications |
Elevated Levels of Shed Membrane Microparticles With Procoagulant Potential in the Peripheral Circulating Blood of Patients With Acute Coronary Syndromes
From the Institut National de la Santé et la Recherche Médicale, INSERM U141, IFR Circulation, Hôpital Lariboisière, Paris (Z.M., A.T.); Service de Cardiologie (H.B., P.G.S.) and Service de Biochimie (J.B.), Hôpital Bichat, Paris; Institut d’Hématologie et d’Immunologie, Faculté de Médecine, Université Louis Pasteur, Strasbourg; and INSERM U143, Le Kremlin-Bicêtre (B.H., J.-M.F.), France.
Correspondence to Alain Tedgui, PhD, INSERM U 141, 41 boulevard de la Chapelle, 75475 Paris Cedex 10, France. E-mail tedgui{at}infobiogen.fr
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—High 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.
Key Words: atherosclerosis • complications • thrombosis • microparticles • endothelium.
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H J Ankersmit, T Weber, J Auer, G Roth, M Brunner, E Kvas, B Moser, S Spreitzer, E Lassnig, E Maurer, et al. Increased serum concentrations of soluble CD95/Fas and caspase 1/ICE in patients with acute angina Heart, February 1, 2004; 90(2): 151 - 154. [Abstract] [Full Text] [PDF]
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F. D. Kolodgie, A. Petrov, R. Virmani, N. Narula, J. W. Verjans, D. K. Weber, D. Hartung, N. Steinmetz, J. L. Vanderheyden, M. A. Vannan, et al. Targeting of Apoptotic Macrophages and Experimental Atheroma With Radiolabeled Annexin V: A Technique With Potential for Noninvasive Imaging of Vulnerable Plaque Circulation, December 23, 2003; 108(25): 3134 - 3139. [Abstract] [Full Text] [PDF]
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A. Sambola, J. Osende, J. Hathcock, M. Degen, Y. Nemerson, V. Fuster, J. Crandall, and J. J. Badimon Role of Risk Factors in the Modulation of Tissue Factor Activity and Blood Thrombogenicity Circulation, February 25, 2003; 107(7): 973 - 977. [Abstract] [Full Text] [PDF]
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P. K. Shah Mechanisms of plaque vulnerability and rupture J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 15S - 22S. [Abstract] [Full Text] [PDF]
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R. A. Preston, W. Jy, J. J. Jimenez, L. M. Mauro, L. L. Horstman, M. Valle, G. Aime, and Y. S. Ahn Effects of Severe Hypertension on Endothelial and Platelet Microparticles Hypertension, February 1, 2003; 41(2): 211 - 217. [Abstract] [Full Text] [PDF]
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D. Proudfoot, J.D. Davies, J.N. Skepper, P.L. Weissberg, and C.M. Shanahan Acetylated Low-Density Lipoprotein Stimulates Human Vascular Smooth Muscle Cell Calcification by Promoting Osteoblastic Differentiation and Inhibiting Phagocytosis Circulation, December 10, 2002; 106(24): 3044 - 3050. [Abstract] [Full Text] [PDF]
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V. Schachinger and A. M. Zeiher Atherogenesis--recent insights into basic mechanisms and their clinical impact Nephrol. Dial. Transplant., December 1, 2002; 17(12): 2055 - 2064. [Full Text] [PDF]
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M. Diamant, R. Nieuwland, R. F. Pablo, A. Sturk, J. W.A. Smit, and J. K. Radder Elevated Numbers of Tissue-Factor Exposing Microparticles Correlate With Components of the Metabolic Syndrome in Uncomplicated Type 2 Diabetes Mellitus Circulation, November 5, 2002; 106(19): 2442 - 2447. [Abstract] [Full Text] [PDF]
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V. Balasubramanian, E. Grabowski, A. Bini, and Y. Nemerson Platelets, circulating tissue factor, and fibrin colocalize in ex vivo thrombi: real-time fluorescence images of thrombus formation and propagation under defined flow conditions Blood, September 26, 2002; 100(8): 2787 - 2792. [Abstract] [Full Text] [PDF]
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F. Sabatier, P. Darmon, B. Hugel, V. Combes, M. Sanmarco, J.-G. Velut, D. Arnoux, P. Charpiot, J.-M. Freyssinet, C. Oliver, et al. Type 1 And Type 2 Diabetic Patients Display Different Patterns of Cellular Microparticles Diabetes, September 1, 2002; 51(9): 2840 - 2845. [Abstract] [Full Text] [PDF]
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R. Gonzalez-Conejero, J. Corral, V. Roldan, C. Martinez, F. Marin, J. Rivera, J. A. Iniesta, M. L. Lozano, P. Marco, and V. Vicente A common polymorphism in the annexin V Kozak sequence (-1C>T) increases translation efficiency and plasma levels of annexin V, and decreases the risk of myocardial infarction in young patients Blood, August 28, 2002; 100(6): 2081 - 2086. [Abstract] [Full Text] [PDF]
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E. I. Lev, J. D. Marmur, M. Zdravkovic, J. I. Osende, J. Robbins, J. A. Delfin, M. Richard, E. Erhardtsen, M. S. Thomsen, A. M. Lincoff, et al. Antithrombotic Effect of Tissue Factor Inhibition by Inactivated Factor VIIa: An Ex Vivo Human Study Arterioscler Thromb Vasc Biol, June 1, 2002; 22(6): 1036 - 1041. [Abstract] [Full Text] [PDF]
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D. Bonderman, A. Teml, J. Jakowitsch, C. Adlbrecht, M. Gyongyosi, W. Sperker, H. Lass, W. Mosgoeller, D. H. Glogar, P. Probst, et al. Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque Blood, April 15, 2002; 99(8): 2794 - 2800. [Abstract] [Full Text] [PDF]
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J. Huber, A. Vales, G. Mitulovic, M. Blumer, R. Schmid, J. L. Witztum, B. R. Binder, and N. Leitinger Oxidized Membrane Vesicles and Blebs From Apoptotic Cells Contain Biologically Active Oxidized Phospholipids That Induce Monocyte-Endothelial Interactions Arterioscler Thromb Vasc Biol, January 1, 2002; 22(1): 101 - 107. [Abstract] [Full Text] [PDF]
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C. M. Boulanger, A. Scoazec, T. Ebrahimian, P. Henry, E. Mathieu, A. Tedgui, and Z. Mallat Circulating Microparticles From Patients With Myocardial Infarction Cause Endothelial Dysfunction Circulation, November 27, 2001; 104(22): 2649 - 2652. [Abstract] [Full Text] [PDF]
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Z. Mallat and A. Tedgui Current Perspective on the Role of Apoptosis in Atherothrombotic Disease Circ. Res., May 25, 2001; 88(10): 998 - 1003. [Abstract] [Full Text] [PDF]
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A. Tedgui and Z. Mallat Smooth Muscle Cells : Another Source of Tissue Factor-Containing Microparticles in Atherothrombosis? Circ. Res., July 21, 2000; 87(2): 81 - 82. [Full Text] [PDF]
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J.-R. Nofer, B. Levkau, I. Wolinska, R. Junker, M. Fobker, A. von Eckardstein, U. Seedorf, and G. Assmann Suppression of Endothelial Cell Apoptosis by High Density Lipoproteins (HDL) and HDL-associated Lysosphingolipids J. Biol. Chem., September 7, 2001; 276(37): 34480 - 34485. [Abstract] [Full Text] [PDF]
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