We compared biological repair after acute myocardial infarction (AMI) with selected porcine progenitor cell populations.

Cell types and mechanisms responsible for myocardial repair after AMI remain uncertain.

In a blinded, randomized study, we infused autologous late-outgrowth endothelial progenitor cells (EPC) (n = 10, 34 ± 22 × 10⁶CD29-31-positive, capable of tube formation), allogeneic green fluorescent peptide–labeled mesenchymal stem cells (MSC) (n = 11, 10 ± 2 × 10⁶CD29-44-90-positive, capable of adipogenic and osteogenic differentiation), or vehicle (CON) (n = 12) in the circumflex artery 1 week after AMI. Systolic function (ejection fraction), left ventricular (LV) end-diastolic and end-systolic volumes, and infarct size were assessed with magnetic resonance imaging at 1 week and 7 weeks. Cell engraftment and vascular density were evaluated on postmortem sections.

Recovery of LV ejection fraction from 1 to 7 weeks was similar between groups, but LV remodeling markedly differed with a greater increase of LV end-systolic volume in MSC and CON (+11 ± 12 ml/m²and +7 ± 8 ml/m²vs. −3 ± 11 ml/m²in EPC, respectively, p = 0.04), and a similar trend was noted for LV end-diastolic volume (p = 0.09). After EPC, infarct size decreased more in segments with >50% infarct transmurality (p = 0.02 vs. MSC and CON) and was associated with a greater vascular density (p = 0.01). Late outgrowth EPCs secrete higher levels of the pro-angiogenic placental growth factor (733 [277 to 1,214] pg/10⁶vs. 59 [34 to 88] pg/10⁶cells in MSC, p = 0.03) and incorporate in neovessels in vivo.

Infusion of late-outgrowth EPCs after AMI improves myocardial infarction remodeling via enhanced neovascularization but does not mediate cardiomyogenesis. Endothelial progenitor cell transfer might hold promise for heart failure prevention via pro-angiogenic or paracrine matrix-modulating effects.