BACKGROUND: Recent evidence indicates that circulating endothelial progenitor cells (EPCs), a population of bone marrow-derived cells, have an important role in the process of vascular repair. Impairment of EPCs is related to endothelial dysfunction, coronary artery disease, and to the pathophysiology of congestive heart failure (CHF). Early EPCs have been shown to express the mineralocorticoid receptor (MR) and MR blockers have been shown to improve EPC function in patients with hyper-aldosteronism. We therefore hypothesized, that MR blockers may enhance EPC levels and function in patients with CHF as well,
possibly as part of their beneficial effect in this patient population.
METHODS: Patients with compensated CHF not under MR blocker therapy were recruited. Either Eplerenone (25 mg/d) or Spironolactone (12.5-25 mg/d) therapy was initiated under CHF specialist discretion. EPCs recruitment and function was evaluated before therapy initiation and 8 weeks following initiation using the following methods: Circulating EPC level was quantified by measurement of surface markers—VEGFR-2, CD34, and CD133 by flow cytometry. Functional aspects of EPCs were evaluated by measurement of colony forming units (CFU), migration and the MTT assays of the cultured cells after 7 days of culture.
PERLIMINARY RESULTS: Ten patients have completed the study protocol thus far (mean age 70, 20% women, 50% diabetes, mean NYHAFC 2.6, mean EF 27% ). Median CD34+/VEGFR2+ count increased from 2.1% (IQR 0.9-5.3) to 5.1% (IQR 1.1-12.3) of peripheral mononuclear cells (PMN), (p=0.3). Median CD133+/VEGFR2+ count increased from 1.1% (IQR 0.4-3.3) to 4.45% (IQR 2.6-5.6) of PMN cells (P= 0.05).
CONCLUSIONS: Preliminary results suggest that MR blocker therapy appears to enhance EPC recruitment in patients with compensated CHF.
