The dysfunctional nature of CD34+ cells from patients with heart failure (HF) may make them unsuitable for autologous stem-cell therapy. In view of evidence that the vasoprotective axis of the renin–angiotensin system (RAS) improves CD34+ cell functions, we hypothesized that CD34+ cells from patients with HF will be dysfunctional and that angiotensin-(1–7) [Ang-(1–7)] would improve their function. Peripheral blood was collected from New York Heart Association class II-IV patients with HF (n = 31) and reference subjects (n = 16). CD34+ cell numbers from patients with HF were reduced by 47% (P < 0.05) and also displayed 76% reduction in migratory capacity and 56% (P < 0.05) lower production of nitric oxide. These alterations were associated with increases in RAS genes angiotensin-converting enzyme and AT2R (595%, P < 0.05) mRNA levels and 80% and 85% decreases in angiotensin-converting enzyme 2 and Mas mRNA levels, respectively. Treatment with Ang-(1–7) enhanced CD34+ cell function through increased migratory potential and nitric oxide production, and reduced reactive oxygen species generation. These data show that HF CD34+ cells are dysfunctional, and Ang-(1–7) improves their functions. This suggests that activation of the vasoprotective axis of the RAS may hold therapeutic potential for autologous stem-cell therapy in patients with HF.