Impact of red blood cell transfusion on platelet activation and aggregation in healthy volunteers: results of the TRANSFUSION study
Aims The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients are poorly understood. The aim of this paper is to determine whether RBC transfusion increases platelet activation and aggregation. Met...
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Published in | European heart journal Vol. 31; no. 22; pp. 2816 - 2821 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Oxford University Press
01.11.2010
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Subjects | |
Online Access | Get full text |
ISSN | 0195-668X 1522-9645 1522-9645 |
DOI | 10.1093/eurheartj/ehq209 |
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Abstract | Aims The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients are poorly understood. The aim of this paper is to determine whether RBC transfusion increases platelet activation and aggregation. Methods and results In vitro transfusions (n = 45) were performed by the addition of RBCs obtained from transfusion packs to fresh whole blood provided by healthy volunteers. Residual platelet aggregation (RPA) and maximal platelet aggregation (MPA) were assessed before and after in vitro transfusion using light transmission aggregometry performed with four different agonists. Flow cytometry was used for the measurement of P-selectin expression and vasodilatator-stimulated phosphoprotein (VASP) platelet reactivity index (PRI). To control for the effect of haemoconcentration, the same experiments were repeated after hematocrit adjustment using volunteer's platelet poor plasma. Transfusion increased platelet aggregation as measured by RPA with ADP 5 µM (57.7 ± 25 vs. 65.7 ± 24%; P = 0.03) or Collagen 2 µg/mL (59.4 ± 28 vs. 69.7 ± 24%; P = 0.03). There were no significant differences with Arachidonic Acid 1.25 mM or Epinephrine 20 µM and results were similar when MPA was considered. Platelet activation was also increased by transfusion as confirmed by an elevation of P-selectin expression induced by 20 µM ADP (12.2 ± 18 vs. 23.9 ± 18%; P = 0.002) or 50 µM ADP (15.4 ± 18.6 vs.26.8 ± 21.2%; P = 0.004) and an increase in VASP PRI (77.8 ± 6 vs. 81.9 ± 3%; P = 0.03). These effects were all independent of hematocrit. Conclusion Red blood cell transfusion increases platelet activation and aggregation in vitro in healthy volunteers. This effect might be mediated through the P2Y12 activation pathway. |
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AbstractList | Aims The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients are poorly understood. The aim of this paper is to determine whether RBC transfusion increases platelet activation and aggregation. Methods and results In vitro transfusions (n = 45) were performed by the addition of RBCs obtained from transfusion packs to fresh whole blood provided by healthy volunteers. Residual platelet aggregation (RPA) and maximal platelet aggregation (MPA) were assessed before and after in vitro transfusion using light transmission aggregometry performed with four different agonists. Flow cytometry was used for the measurement of P-selectin expression and vasodilatator-stimulated phosphoprotein (VASP) platelet reactivity index (PRI). To control for the effect of haemoconcentration, the same experiments were repeated after hematocrit adjustment using volunteer's platelet poor plasma. Transfusion increased platelet aggregation as measured by RPA with ADP 5 µM (57.7 ± 25 vs. 65.7 ± 24%; P = 0.03) or Collagen 2 µg/mL (59.4 ± 28 vs. 69.7 ± 24%; P = 0.03). There were no significant differences with Arachidonic Acid 1.25 mM or Epinephrine 20 µM and results were similar when MPA was considered. Platelet activation was also increased by transfusion as confirmed by an elevation of P-selectin expression induced by 20 µM ADP (12.2 ± 18 vs. 23.9 ± 18%; P = 0.002) or 50 µM ADP (15.4 ± 18.6 vs.26.8 ± 21.2%; P = 0.004) and an increase in VASP PRI (77.8 ± 6 vs. 81.9 ± 3%; P = 0.03). These effects were all independent of hematocrit. Conclusion Red blood cell transfusion increases platelet activation and aggregation in vitro in healthy volunteers. This effect might be mediated through the P2Y12 activation pathway. The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients are poorly understood. The aim of this paper is to determine whether RBC transfusion increases platelet activation and aggregation.AIMSThe underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients are poorly understood. The aim of this paper is to determine whether RBC transfusion increases platelet activation and aggregation.In vitro transfusions (n = 45) were performed by the addition of RBCs obtained from transfusion packs to fresh whole blood provided by healthy volunteers. Residual platelet aggregation (RPA) and maximal platelet aggregation (MPA) were assessed before and after in vitro transfusion using light transmission aggregometry performed with four different agonists. Flow cytometry was used for the measurement of P-selectin expression and vasodilatator-stimulated phosphoprotein (VASP) platelet reactivity index (PRI). To control for the effect of haemoconcentration, the same experiments were repeated after hematocrit adjustment using volunteer's platelet poor plasma. Transfusion increased platelet aggregation as measured by RPA with ADP 5 µM (57.7 ± 25 vs. 65.7 ± 24%; P = 0.03) or Collagen 2 µg/mL (59.4 ± 28 vs. 69.7 ± 24%; P = 0.03). There were no significant differences with Arachidonic Acid 1.25 mM or Epinephrine 20 µM and results were similar when MPA was considered. Platelet activation was also increased by transfusion as confirmed by an elevation of P-selectin expression induced by 20 µM ADP (12.2 ± 18 vs. 23.9 ± 18%; P = 0.002) or 50 µM ADP (15.4 ± 18.6 vs.26.8 ± 21.2%; P = 0.004) and an increase in VASP PRI (77.8 ± 6 vs. 81.9 ± 3%; P = 0.03). These effects were all independent of hematocrit.METHODS AND RESULTSIn vitro transfusions (n = 45) were performed by the addition of RBCs obtained from transfusion packs to fresh whole blood provided by healthy volunteers. Residual platelet aggregation (RPA) and maximal platelet aggregation (MPA) were assessed before and after in vitro transfusion using light transmission aggregometry performed with four different agonists. Flow cytometry was used for the measurement of P-selectin expression and vasodilatator-stimulated phosphoprotein (VASP) platelet reactivity index (PRI). To control for the effect of haemoconcentration, the same experiments were repeated after hematocrit adjustment using volunteer's platelet poor plasma. Transfusion increased platelet aggregation as measured by RPA with ADP 5 µM (57.7 ± 25 vs. 65.7 ± 24%; P = 0.03) or Collagen 2 µg/mL (59.4 ± 28 vs. 69.7 ± 24%; P = 0.03). There were no significant differences with Arachidonic Acid 1.25 mM or Epinephrine 20 µM and results were similar when MPA was considered. Platelet activation was also increased by transfusion as confirmed by an elevation of P-selectin expression induced by 20 µM ADP (12.2 ± 18 vs. 23.9 ± 18%; P = 0.002) or 50 µM ADP (15.4 ± 18.6 vs.26.8 ± 21.2%; P = 0.004) and an increase in VASP PRI (77.8 ± 6 vs. 81.9 ± 3%; P = 0.03). These effects were all independent of hematocrit.Red blood cell transfusion increases platelet activation and aggregation in vitro in healthy volunteers. This effect might be mediated through the P2Y(12) activation pathway.CONCLUSIONRed blood cell transfusion increases platelet activation and aggregation in vitro in healthy volunteers. This effect might be mediated through the P2Y(12) activation pathway. The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients are poorly understood. The aim of this paper is to determine whether RBC transfusion increases platelet activation and aggregation. In vitro transfusions (n = 45) were performed by the addition of RBCs obtained from transfusion packs to fresh whole blood provided by healthy volunteers. Residual platelet aggregation (RPA) and maximal platelet aggregation (MPA) were assessed before and after in vitro transfusion using light transmission aggregometry performed with four different agonists. Flow cytometry was used for the measurement of P-selectin expression and vasodilatator-stimulated phosphoprotein (VASP) platelet reactivity index (PRI). To control for the effect of haemoconcentration, the same experiments were repeated after hematocrit adjustment using volunteer's platelet poor plasma. Transfusion increased platelet aggregation as measured by RPA with ADP 5 µM (57.7 ± 25 vs. 65.7 ± 24%; P = 0.03) or Collagen 2 µg/mL (59.4 ± 28 vs. 69.7 ± 24%; P = 0.03). There were no significant differences with Arachidonic Acid 1.25 mM or Epinephrine 20 µM and results were similar when MPA was considered. Platelet activation was also increased by transfusion as confirmed by an elevation of P-selectin expression induced by 20 µM ADP (12.2 ± 18 vs. 23.9 ± 18%; P = 0.002) or 50 µM ADP (15.4 ± 18.6 vs.26.8 ± 21.2%; P = 0.004) and an increase in VASP PRI (77.8 ± 6 vs. 81.9 ± 3%; P = 0.03). These effects were all independent of hematocrit. Red blood cell transfusion increases platelet activation and aggregation in vitro in healthy volunteers. This effect might be mediated through the P2Y(12) activation pathway. |
Author | Pena, Ana Vignalou, Jean-Baptiste Brieger, David Barthelemy, Olivier Bellemain-Appaix, Anne Cayla, Guillaume Chastre, Thomas Beygui, Farzin Montalescot, Gilles Collet, Jean-Philippe Silvain, Johanne |
Author_xml | – sequence: 1 givenname: Johanne surname: Silvain fullname: Silvain, Johanne organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 2 givenname: Ana surname: Pena fullname: Pena, Ana organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 3 givenname: Guillaume surname: Cayla fullname: Cayla, Guillaume organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 4 givenname: David surname: Brieger fullname: Brieger, David organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 5 givenname: Anne surname: Bellemain-Appaix fullname: Bellemain-Appaix, Anne organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 6 givenname: Thomas surname: Chastre fullname: Chastre, Thomas organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 7 givenname: Jean-Baptiste surname: Vignalou fullname: Vignalou, Jean-Baptiste organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 8 givenname: Farzin surname: Beygui fullname: Beygui, Farzin organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 9 givenname: Olivier surname: Barthelemy fullname: Barthelemy, Olivier organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 10 givenname: Jean-Philippe surname: Collet fullname: Collet, Jean-Philippe organization: Institut de Cardiologie, Bureau 2-236, INSERM CMR937, Pitié-Salpêtrière Hospital (AP-HP), Université Paris 6, 47-83 bld de l'Hôpital, 75013 Paris, France – sequence: 11 givenname: Gilles surname: Montalescot fullname: Montalescot, Gilles email: gilles.montalescot@psl.aphp.fr organization: E-mail: gilles.montalescot@psl.aphp.fr |
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Keywords | Human Transfusion Healthy subject Red blood cell Activation Antiplatelet agent Result Response ACS Platelet Platelet response Clopidogrel Circulatory system Cardiology |
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Snippet | Aims The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome... The underlying mechanisms leading to recurrent ischaemic events or mortality after red blood cell (RBC) transfusion in anaemic acute coronary syndrome patients... |
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SubjectTerms | ACS Adult Biological and medical sciences Cardiology. Vascular system Cell Adhesion Molecules - metabolism Clopidogrel Erythrocyte Transfusion Female Flow Cytometry Hematocrit - methods Hemoglobins - metabolism Humans Male Medical sciences Microfilament Proteins - metabolism P-Selectin - metabolism Phosphoproteins - metabolism Phosphorylation - physiology Platelet Activation - drug effects Platelet Activation - physiology Platelet Aggregation - drug effects Platelet Aggregation - physiology Platelet Aggregation Inhibitors - pharmacology Platelet response Transfusion |
Title | Impact of red blood cell transfusion on platelet activation and aggregation in healthy volunteers: results of the TRANSFUSION study |
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