Johanne Silvain1, Jérémie Abtan1, Mathieu Kerneis1, Réjane Martin1, Jonathan Finzi1, Jean-Baptiste Vignalou1, Olivier Barthélémy1, Stephen A O'Connor1, Charles-Edouard Luyt2, Nicolas Brechot2, Anne Mercadier3, Delphine Brugier1, Sophie Galier1, Jean-Philippe Collet1, Jean Chastre2, Gilles Montalescot4. 1. Institut de Cardiologie, Institut National de la Santé et de la Recherche Médicale CMR937, Allies in Cardiovascular Trials Initiatives and Organized Networks Group, Pitié-Salpêtrière Hospital (Assistance Publique - Hôpitaux de Paris), Université Pierre et Marie Curie, Paris, France. 2. Service de Réanimation Médicale, Pitié-Salpêtrière Hospital (Assistance Publique - Hôpitaux de Paris), Université Pierre et Marie Curie, Paris, France. 3. Etablissement Français du Sang Ile-de-France, CR4, Pitié-Salpêtrière Hospital (Assistance Publique - Hôpitaux de Paris), Paris, France. 4. Institut de Cardiologie, Institut National de la Santé et de la Recherche Médicale CMR937, Allies in Cardiovascular Trials Initiatives and Organized Networks Group, Pitié-Salpêtrière Hospital (Assistance Publique - Hôpitaux de Paris), Université Pierre et Marie Curie, Paris, France. Electronic address: gilles.montalescot@psl.aphp.fr.
Abstract
OBJECTIVES: This study sought to determine whether red blood cell (RBC) transfusion increases in vivo platelet aggregation and inflammation in coronary and noncoronary patients. BACKGROUND:RBC transfusion increases in vitro platelet activation and aggregation in healthy volunteers, providing a possible explanation for the increase in recurrent ischemic events and mortality reported after RBC transfusion in patients with acute coronary syndromes (ACS). METHODS:Platelet reactivity was measured before and after RBC transfusion in 61 patients (33 with ACS patients and 28 without ACS). Relative changes between baseline and post-transfusion measurements of maximal and residual platelet aggregation were considered with different agonists as well as changes in vasodilator-stimulated phosphoprotein platelet reactivity index and P-selectin expression. Inflammatory and thrombotic biomarkers were also measured before and after transfusion. RESULTS: After RBC transfusion, platelet reactivity was increased when measured using adenosine diphosphate-induced light transmission aggregometry (11.6% relative increase in maximal platelet aggregation, p = 0.004; 10.8% increase in residual platelet aggregation, p = 0.005) and vasodilator-stimulated phosphoprotein platelet reactivity index (20.7% relative increase, p = 0.002), and there was a nonsignificant trend toward an increase in P-selectin expression. Similar results were found with the nonspecific agonist thrombin receptor-activated peptide (relative increases of 11.7% for maximal platelet aggregation, p = 0.04, and 12.7% for residual platelet aggregation, p = 0.02) but not with collagen or arachidonic acid agonists. There were no significant differences in inflammatory and thrombotic biomarkers before and after transfusion. CONCLUSIONS: After RBC transfusion, there is an increase in platelet reactivity, especially with tests measuring the adenosine diphosphate-P2Y12 receptor pathway, without significant variations in inflammatory or thrombotic biomarkers. This in vivo effect may account for the excess of ischemic events observed in the context of patients with ACS treated using percutaneous coronary intervention and P2Y12 inhibitors.
RCT Entities:
OBJECTIVES: This study sought to determine whether red blood cell (RBC) transfusion increases in vivo platelet aggregation and inflammation in coronary and noncoronary patients. BACKGROUND: RBC transfusion increases in vitro platelet activation and aggregation in healthy volunteers, providing a possible explanation for the increase in recurrent ischemic events and mortality reported after RBC transfusion in patients with acute coronary syndromes (ACS). METHODS: Platelet reactivity was measured before and after RBC transfusion in 61 patients (33 with ACS patients and 28 without ACS). Relative changes between baseline and post-transfusion measurements of maximal and residual platelet aggregation were considered with different agonists as well as changes in vasodilator-stimulated phosphoprotein platelet reactivity index and P-selectin expression. Inflammatory and thrombotic biomarkers were also measured before and after transfusion. RESULTS: After RBC transfusion, platelet reactivity was increased when measured using adenosine diphosphate-induced light transmission aggregometry (11.6% relative increase in maximal platelet aggregation, p = 0.004; 10.8% increase in residual platelet aggregation, p = 0.005) and vasodilator-stimulated phosphoprotein platelet reactivity index (20.7% relative increase, p = 0.002), and there was a nonsignificant trend toward an increase in P-selectin expression. Similar results were found with the nonspecific agonist thrombin receptor-activated peptide (relative increases of 11.7% for maximal platelet aggregation, p = 0.04, and 12.7% for residual platelet aggregation, p = 0.02) but not with collagen or arachidonic acid agonists. There were no significant differences in inflammatory and thrombotic biomarkers before and after transfusion. CONCLUSIONS: After RBC transfusion, there is an increase in platelet reactivity, especially with tests measuring the adenosine diphosphate-P2Y12 receptor pathway, without significant variations in inflammatory or thrombotic biomarkers. This in vivo effect may account for the excess of ischemic events observed in the context of patients with ACS treated using percutaneous coronary intervention and P2Y12 inhibitors.
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