Intracoronary Infusion of CD133+ Endothelial Progenitor Cells Improves Heart Function and Quality of Life in Patients with Chronic Post-infarct Heart Insufficiency

Aim: To assess the safety and efficacy of the intracoronary infusion of CD133+ hematopoietic stem cells to improve ventricular function and quality of life in candidates for heart transplantation due to post-infarct chronic heart failure.

Methods: We selected seven candidates for heart transplantation (six males/one female, age range 44-65 years) in whom all treatment alternatives were exhausted (angioplasty/stent and bypass surgery). These subjects had a symptomatic New York Heart Association (NYHA) scale of at least II and ejection fractions (EFs) below 35%. After obtaining informed consent, CD133+ cells were obtained by stimulation with granulocyte-colony stimulating factor, apheresis, and separation with magnetic beads. Stem cells were implanted in the infarcted zone via intracoronary percutaneous angiography. Evaluations (NYHA scale classification, plasma concentration of pro-B-natriuretic-peptide and the risk of sudden death, echocardiography, cardiac magnetic resonance, and gated-SPECT with MIBI) were performed at baseline and at 3, 6, 12, and 24 months after cell infusion.

Results: Stem cell isolation was efficient and safe (around 10(7) cells/patient and >92% CD133+ viable cells). Two patients died during observation due to noncardiac conditions. In the five remaining subjects, the NYHA scale improved and no accounts of hospital admissions for heart failure were documented. Plasma concentrations of pro-B-natriuretic peptide and the risk of sudden death clearly decreased, while the EF increased significantly to 35% and 40% by echocardiography and cardiac MRI, respectively (P=.013 and .009, respectively) 24 months after treatment. No other major adverse events were noticed.

Conclusions: The intracoronary inoculation of CD133+ stem cells was safe and effective to improve ventricular contraction and symptomatic class function in patients with refractory post-infarct heart failure.