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. 2007 Jul 31;119(3):344-8.
doi: 10.1016/j.ijcard.2006.07.191. Epub 2006 Oct 27.

Circulating endothelial progenitor cells in congestive heart failure

Mutsuko Nonaka-Sarukawa  1 , Keiji Yamamoto, Hirotaka Aoki, Yoshioki Nishimura, Hidenori Tomizawa, Masaru Ichida, Takayuki Eizawa, Kazuo Muroi, Uichi Ikeda, Kazuyuki Shimada
Affiliations

Circulating endothelial progenitor cells in congestive heart failure

Mutsuko Nonaka-Sarukawa et al. Int J Cardiol. .

Abstract

Background: Endothelial progenitor cells (EPCs) circulate in the adult peripheral blood and contribute to neovascularization. EPCs are considered to be included in CD34 positive mononuclear cells (CD34+ MNCs). Kinetics of circulating EPCs in congestive heart failure (CHF) has not been fully investigated.

Methods: We determined the numbers of white blood cells (WBCs), plasma brain natriuretic peptide (BNP), serum erythropoietin, vascular endothelial growth factor (VEGF) and thrombomodulin levels in 16 mild CHF patients (NYHA I, II), 10 severe CHF patients with acute exacerbation (NYHA III, IV), and 22 control subjects. The number of CD34+ MNCs in peripheral blood was quantified by flow cytometry.

Results: The ratio of CD34+ MNCs:10(3) WBCs in mild CHF patients was higher than that in control subjects (P<0.05). Interestingly, the ratio of CD34+ MNCs:10(3) WBCs in severe CHF patients at admission was significantly lower than that in control subjects (P<0.005) or in mild CHF patients (P<0.05). Levels of BNP and erythropoietin in severe CHF patients were significantly higher than those in mild CHF patients. However, VEGF and thrombomodulin levels were not different between mild and severe CHF patients. In addition, the ratio of CD34+ MNCs:10(3) WBCs in severe CHF patients increased in proportion to the amelioration of CHF during hospitalization, and this increase correlated with the decrease in BNP level.

Conclusions: The ratio of CD34+ MNCs:10(3) WBCs was decreased in severe CHF. These findings suggest that impaired EPC recruitment might be involved in the pathophysiology of severe CHF.

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