Abstract 2495: Long-term Safety and Efficacy of Autologous Bone Marrow-derived Stem Cell Transfer after Acute Myocardial Infarction
Background. Progenitor cell transfer may enhance myocardial functional recovery after AMI but whether these effects are sustained remains unknown. We investigated long-term safety and efficacy of intracoronary autologous bone marrow-derived stem cell (BMSC) transfer 1 year after AMI in a randomized, double-blind, and placebo-controlled study.
Methods. We enrolled 69 patients, who presented more than 2 h after AMI and randomly assigned them 24 h after successful recanalisation to intracoronary injection of BMSC or placebo (CON). We measured changes in LV global and regional function and remodeling at 1-y follow-up using MRI (n=30 per group). Coronary flow velocity reserve (CFVR) was calculated from Doppler flow velocities at baseline and during adenosine-induced hyperemia in a subset of patients.
Results. LV volumes and global function did not differ with time between the CON and BMSC groups (table⇓). In contrast, regional contraction in segments with >75% transmural extent of hyperenhance-ment improved significantly more following BMSC (improved contraction in 31 of 83 segments versus in 14 of 87 segments in CON, P=0.013). Wall motion of the infarct border zone increased more over time in BMSC (from 4.3Â ±1.9 to 5.9Â ±2.0 mm versus from 3.0Â ±2.1 to 3.7Â ±1.9 mm in CON, P=0.039). The reduction in infarct size following BMSC (28% treatment effect at 4 months, P=0.03) was less prominent at 1-y (23% treatment effect, P=0.12) but hypertrophic remodeling was significantly reduced in BMSC (reduction in ED-wall thickness of adjacent and remote myocardium −0.6Â ±1.1 and -0.2Â ±1.0 mm in CON versus -1.1Â ±1.3 and -0.7Â ±1.0 mm in BMSC, P=0.001 and 0.0001, respectively). CFVR in infarct-related arteries was normal (2.9Â ±0.4 in CON versus 2.8Â ±0.7 in BMSC).
Conclusions. Intracoronary BMSC transfer after AMI is safe, has a sustained beneficial effect on regional systolic function recovery and reduces hypertrophic remodeling in adjacent and remote myocardium.