Circulation. 2004;110:1209-1212
Published online before print July 12, 2004, doi: 10.1161/01.CIR.0000136813.89036.21
Published online before print July 12, 2004, doi: 10.1161/01.CIR.0000136813.89036.21
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(Circulation. 2004;110:1209-1212.)
© 2004 American Heart Association, Inc.
Original Articles |
CD34+ and Endothelial Progenitor Cells in Patients With Various Degrees of Congestive Heart Failure
From the Chair of Cardiology (M.V., A.F., O.S., P.M., G.F., R.F.), University of Ferrara and Cardiovascular Research Center, Salvatore Maugeri Foundation, IRCCS, Gussago, Italy, and Section of Haematology (G.M.R., M.D.P., A.M.B., L.Z.B., E.M., G.C.), University of Ferrara, Ferrara, Italy.
Correspondence to Marco Valgimigli, Chair of Cardiology, University of Ferrara, Cardiovascular Institute, Arcispedale S. Anna, Corso Giovecca 203, 44100 Ferrara, Italy. E-mail vlgmrc{at}unife.it
Received February 6, 2004; de novo received April 12, 2004; revision received May 26, 2004; accepted May 28, 2004.
Background— Peripheral blood CD34+ cells and circulating endothelial progenitor cells (EPCs) increase in myocardial infarction and vascular injuries as a reflection of endothelial damage. Despite the occurrence of endothelial dysfunction in heart failure (HF), no data are available on EPC mobilization in this setting. We investigated the pattern of CD34+ cells and EPC mobilization during HF and their correlation with the severity and origin of the disease.
Methods and Results— Peripheral blood CD34+ cells (n=91) and EPCs (n=41), assessed both as CD34+ cells coexpressing AC133 and vascular endothelial growth factor (VEGF) receptor-2 and as endothelial colony-forming units, were studied in HF patients (mean age 67±11 years) and 45 gender- and age-matched controls. Tumor necrosis factor-
(TNF-) and its receptors (sTNFR-1 and sTNFR-2), VEGF, stromal derived factor-1 (SDF-1), granulocyte-colony stimulating factor (G-CSF), and B-type natriuretic peptide were also measured. CD34+ cells, EPCs, TNF- and receptors, VEGF, SDF-1, and B-type natriuretic peptide were increased in HF. CD34+ cells and EPCs were inversely related to functional class and to TNF-, being decreased in New York Heart Association class IV compared with class I and II and controls. No role was found for the origin of the disease.
Conclusions— CD34+ cells and EPC mobilization occurs in HF and shows a biphasic response, with elevation and depression in the early and advanced phases, respectively. This could be related to the myelosuppressive role of TNF-.
Key Words: cells • heart failure • interleukins • angiogenesis • endothelium
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