Publication

Bone marrow dysfunction in chronic heart failure patients

Westenbrink, B. D., Voors, A. A., de Boer, R. A., Schuringa, J. J., Klinkenberg, T., van der Harst, P., Vellenga, E., van Veldhuisen, D. J. & van Gilst, W. H., Jul-2010, In : European Journal of Heart Failure. 12, 7, p. 676-684 9 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Westenbrink, B. D., Voors, A. A., de Boer, R. A., Schuringa, J. J., Klinkenberg, T., van der Harst, P., Vellenga, E., van Veldhuisen, D. J., & van Gilst, W. H. (2010). Bone marrow dysfunction in chronic heart failure patients. European Journal of Heart Failure, 12(7), 676-684. https://doi.org/10.1093/eurjhf/hfq061

Author

Westenbrink, B. Daan ; Voors, Adriaan A. ; de Boer, Rudolf A. ; Schuringa, Jan J. ; Klinkenberg, Theo ; van der Harst, Pim ; Vellenga, Edo ; van Veldhuisen, Dirk J. ; van Gilst, Wiek H. / Bone marrow dysfunction in chronic heart failure patients. In: European Journal of Heart Failure. 2010 ; Vol. 12, No. 7. pp. 676-684.

Harvard

Westenbrink, BD, Voors, AA, de Boer, RA, Schuringa, JJ, Klinkenberg, T, van der Harst, P, Vellenga, E, van Veldhuisen, DJ & van Gilst, WH 2010, 'Bone marrow dysfunction in chronic heart failure patients', European Journal of Heart Failure, vol. 12, no. 7, pp. 676-684. https://doi.org/10.1093/eurjhf/hfq061

Standard

Bone marrow dysfunction in chronic heart failure patients. / Westenbrink, B. Daan; Voors, Adriaan A.; de Boer, Rudolf A.; Schuringa, Jan J.; Klinkenberg, Theo; van der Harst, Pim; Vellenga, Edo; van Veldhuisen, Dirk J.; van Gilst, Wiek H.

In: European Journal of Heart Failure, Vol. 12, No. 7, 07.2010, p. 676-684.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Westenbrink BD, Voors AA, de Boer RA, Schuringa JJ, Klinkenberg T, van der Harst P et al. Bone marrow dysfunction in chronic heart failure patients. European Journal of Heart Failure. 2010 Jul;12(7):676-684. https://doi.org/10.1093/eurjhf/hfq061


BibTeX

@article{2cefe0e3229b42dbb0b32fa8b97b4334,
title = "Bone marrow dysfunction in chronic heart failure patients",
abstract = "To investigate whether chronic heart failure (CHF) is associated with a general dysfunction of the haematopoietic compartment.Bone marrow was obtained during coronary artery bypass graft surgery from 20 patients with CHF (age 67 +/- 6 years, 75% NYHA class >= III, LVEF 32 +/- 6%), and 20 age- and gender-matched control patients with normal cardiac function. CD34(+) haematopoietic progenitor cells were isolated and cultured with increasing doses of erythropoietin (0.02-10 IU/mL, EPO), myeloid growth factors or a mix of both. After 14 days, burst forming units erythroid (BFU-E), and granulocyte or monocyte colony forming units (CFU-G, CFU-M, respectively) were counted. Apoptosis and erythropoietin-receptor (EPO-R) density were quantified by flow cytometry. Throughout the EPO dose range, the CD34(+) cells from CHF patients produced a two-fold lower number of BFU-E colonies compared with controls (P = 0.02). The resistance to EPO was associated with markedly increased apoptosis during erythroid differentiation in CHF patients compared with controls [5.3% (2.9-8.1%) vs. 1.5% (0.8-3.4%), P = 0.01]. Erythropoietin-receptor expression was, however, comparable between CHF patients and controls and the anti-apoptotic cytokine interleukin-3 did not rescue erythropoiesis. In the myeloid cultures, the number of CFU-G and CFU-M colonies was also two-fold lower in CHF patients compared with controls (both P <0.01). In the mixed-culture assay, myelopoiesis and erythropoiesis were reduced to a similar magnitude in CHF patients. The impaired clonogenic potential was independently associated with clinical and biochemical severity of CHF, but not with the presence of anaemia.Chronic heart failure is associated with profound and general bone marrow dysfunction, simultaneously affecting multiple haematopoietic lineages.",
keywords = "Haematopoiesis, Bone marrow, Heart failure, Anaemia, BLUNTED ERYTHROPOIETIN PRODUCTION, TREATMENT OPTIONS, RHEUMATOID-ARTHRITIS, CHRONIC DISEASE, ANEMIA, MORTALITY, CELLS, HEMATOPOIESIS, PATHOGENESIS, ETIOLOGY",
author = "Westenbrink, {B. Daan} and Voors, {Adriaan A.} and {de Boer}, {Rudolf A.} and Schuringa, {Jan J.} and Theo Klinkenberg and {van der Harst}, Pim and Edo Vellenga and {van Veldhuisen}, {Dirk J.} and {van Gilst}, {Wiek H.}",
year = "2010",
month = jul,
doi = "10.1093/eurjhf/hfq061",
language = "English",
volume = "12",
pages = "676--684",
journal = "European Journal of Heart Failure",
issn = "1388-9842",
publisher = "Wiley",
number = "7",

}

RIS

TY - JOUR

T1 - Bone marrow dysfunction in chronic heart failure patients

AU - Westenbrink, B. Daan

AU - Voors, Adriaan A.

AU - de Boer, Rudolf A.

AU - Schuringa, Jan J.

AU - Klinkenberg, Theo

AU - van der Harst, Pim

AU - Vellenga, Edo

AU - van Veldhuisen, Dirk J.

AU - van Gilst, Wiek H.

PY - 2010/7

Y1 - 2010/7

N2 - To investigate whether chronic heart failure (CHF) is associated with a general dysfunction of the haematopoietic compartment.Bone marrow was obtained during coronary artery bypass graft surgery from 20 patients with CHF (age 67 +/- 6 years, 75% NYHA class >= III, LVEF 32 +/- 6%), and 20 age- and gender-matched control patients with normal cardiac function. CD34(+) haematopoietic progenitor cells were isolated and cultured with increasing doses of erythropoietin (0.02-10 IU/mL, EPO), myeloid growth factors or a mix of both. After 14 days, burst forming units erythroid (BFU-E), and granulocyte or monocyte colony forming units (CFU-G, CFU-M, respectively) were counted. Apoptosis and erythropoietin-receptor (EPO-R) density were quantified by flow cytometry. Throughout the EPO dose range, the CD34(+) cells from CHF patients produced a two-fold lower number of BFU-E colonies compared with controls (P = 0.02). The resistance to EPO was associated with markedly increased apoptosis during erythroid differentiation in CHF patients compared with controls [5.3% (2.9-8.1%) vs. 1.5% (0.8-3.4%), P = 0.01]. Erythropoietin-receptor expression was, however, comparable between CHF patients and controls and the anti-apoptotic cytokine interleukin-3 did not rescue erythropoiesis. In the myeloid cultures, the number of CFU-G and CFU-M colonies was also two-fold lower in CHF patients compared with controls (both P <0.01). In the mixed-culture assay, myelopoiesis and erythropoiesis were reduced to a similar magnitude in CHF patients. The impaired clonogenic potential was independently associated with clinical and biochemical severity of CHF, but not with the presence of anaemia.Chronic heart failure is associated with profound and general bone marrow dysfunction, simultaneously affecting multiple haematopoietic lineages.

AB - To investigate whether chronic heart failure (CHF) is associated with a general dysfunction of the haematopoietic compartment.Bone marrow was obtained during coronary artery bypass graft surgery from 20 patients with CHF (age 67 +/- 6 years, 75% NYHA class >= III, LVEF 32 +/- 6%), and 20 age- and gender-matched control patients with normal cardiac function. CD34(+) haematopoietic progenitor cells were isolated and cultured with increasing doses of erythropoietin (0.02-10 IU/mL, EPO), myeloid growth factors or a mix of both. After 14 days, burst forming units erythroid (BFU-E), and granulocyte or monocyte colony forming units (CFU-G, CFU-M, respectively) were counted. Apoptosis and erythropoietin-receptor (EPO-R) density were quantified by flow cytometry. Throughout the EPO dose range, the CD34(+) cells from CHF patients produced a two-fold lower number of BFU-E colonies compared with controls (P = 0.02). The resistance to EPO was associated with markedly increased apoptosis during erythroid differentiation in CHF patients compared with controls [5.3% (2.9-8.1%) vs. 1.5% (0.8-3.4%), P = 0.01]. Erythropoietin-receptor expression was, however, comparable between CHF patients and controls and the anti-apoptotic cytokine interleukin-3 did not rescue erythropoiesis. In the myeloid cultures, the number of CFU-G and CFU-M colonies was also two-fold lower in CHF patients compared with controls (both P <0.01). In the mixed-culture assay, myelopoiesis and erythropoiesis were reduced to a similar magnitude in CHF patients. The impaired clonogenic potential was independently associated with clinical and biochemical severity of CHF, but not with the presence of anaemia.Chronic heart failure is associated with profound and general bone marrow dysfunction, simultaneously affecting multiple haematopoietic lineages.

KW - Haematopoiesis

KW - Bone marrow

KW - Heart failure

KW - Anaemia

KW - BLUNTED ERYTHROPOIETIN PRODUCTION

KW - TREATMENT OPTIONS

KW - RHEUMATOID-ARTHRITIS

KW - CHRONIC DISEASE

KW - ANEMIA

KW - MORTALITY

KW - CELLS

KW - HEMATOPOIESIS

KW - PATHOGENESIS

KW - ETIOLOGY

U2 - 10.1093/eurjhf/hfq061

DO - 10.1093/eurjhf/hfq061

M3 - Article

VL - 12

SP - 676

EP - 684

JO - European Journal of Heart Failure

JF - European Journal of Heart Failure

SN - 1388-9842

IS - 7

ER -

ID: 5110010