Severity of endothelial dysfunction is associated with the occurrence of hemorrhagic complications in COPD patients trea
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LETTER
Severity of endothelial dysfunction is associated with the occurrence of hemorrhagic complications in COPD patients treated by extracorporeal CO2 removal Jean‑Luc Diehl1,2* , Jean Loup Augy1, Nadia Rivet2,3, Coralie Guerin2,4, Richard Chocron5,6 and David M. Smadja2,3 © 2020 Springer-Verlag GmbH Germany, part of Springer Nature
Dear Editor, In chronic obstructive pulmonary disease (COPD) patients extracorporeal CO2 removal (ECCO2R) has been associated with both hemorrhagic and thrombotic complications [1], which could be related to an endothelial dysfunction promoted in part by extracorporeal life support [2]. Moreover, endothelial dysfunction is a hallmark of severe COPD: an imbalance between repair capacity and endothelial damage has been reported in stable patients [3], with a changing profile during acute exacerbations [4]. We planned to rigorously study these points using a formalized E CCO2R register (NCT02965079) combined with a study project (Hector: Hemostasis and ECCO2R). We counted circulating endothelial cells (CEC) by CD146-coated beads and CD34+CD45dim circulating hematopoietic progenitor cells (HPC) by flow cytometry according to the ISHAGE (International Society of Hematotherapy and Graft Engineering) protocol (see also ESM). We also quantified in plasma VEGF-A, a mobilizing factor of endothelial progenitor cells, and its main soluble receptor sVEGFR-2. Sixteen severe COPD patients were admitted and studied prior to ECCO2R initiation (Hemolung device, ALung, Pittsburgh, USA, and iLA Activve device, Xenios/Novalung, Heilbronn, Germany), *Correspondence: jean‑[email protected] 1 Service de Médecine Intensive ‑ Réanimation, Hôpital Européen Georges Pompidou, Assistance Publique – Hôpitaux de Paris, 20 rue Leblanc, 75015 Paris, France Full author information is available at the end of the article
then daily during the E CCO2R course and after E CCO2R. We recorded severe hemorrhagic events (types 3–5 of the Bleeding Academic Research Consortium standardized classification) and thrombotic events [5]. Cell counts were compared to control values obtained from healthy subjects. Quantitative variables were summarized using mean with standard deviation. Quantitative variables determined to follow non-normal distributions are summarized using median presented with IQR and evaluated for associations using a nonparametric equality-of-medians test. Demographics and cellular counts are presented in Table 1. We observed a high level of both CEC and CD34+CD45dim prior to ECCO2R initiation as compared to controls, confirming previous results [4]. Daily CEC count during ECCO2R was not different in the whole group from CEC count prior to ECCO2R initiation. Daily CD34+CD45dim count in the whole group was higher than CD34+CD45dim count prior to ECCO2R initiation (p = 0.031). A severe hemorrhagic event was observed in five patients. As compared to the mean daily count during the full E CCO2R therapy in the other patients, these patients exhibited higher mean CEC count, lower mean CD34+CD45
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