Abstract 19088: Differential Mobilization of Progenitor Cells in Smoker and Non-smoker Patients with Acute Myocardial Infarction : Insights from the Bonami Biology Sub-study
Introduction: Although autologous bone marrow cell (BMC) therapy has emerged as a promising option to treat acute myocardial infarction (AMI), randomized trials reported mixed results. This may be explained in part by great variability in the functionality of BMCs retrieved from patients with risk factors of atherosclerosis.
Hypothesis: We hypothesized that active smoking may alter bone marrow-derived progenitor cells number and functionality in patients with AMI. The aim of the current study was to investigate the characteristics of BMCs in active smokers and non-smokers with AMI and their potential impact on BMC therapy efficacy.
Methods: We compared progenitor cells in bone marrow and blood samples from 54 active smokers and 47 non-smokers with AMI enrolled in the BONAMI cell therapy trial.
Results: White bone marrow cell number per microliter and CD45dimCD34+ cell number were higher in active smokers (p=0.001, p=0.03, respectively). In marked contrast, in active smokers there was a decrease of both bone marrow and blood endothelial progenitor CD45dimCD34+KDR+ cells (EPCs) expressed as their percentage per 105 WC (p=0.005, p=0.04, respectively). Importantly, a multivariate linear regression analysis including CV risk factors that were significantly different between non- and active smokers, confirmed the association between active smoking and a lower EPC number per 105 WC in both blood (p=0.04) and bone marrow (p=0.04) Furthermore, in non-smokers not receiving BMC therapy, there were positive correlations between circulating EPC levels and the decrease in infarction defect size (p=0.02) and viability improvement (p=0.02) measured by SPECT at 3 month post-MI. This association was not observed in active smokers and in patients receiving BMC therapy.
Conclusion: These data suggest that circulating EPCs play an important role in cardiac repair post-MI in non-smokers but not in active smokers. This discrepancy may be explained by a lack of activation of the endothelial cell lineage, and of blood mobilization of EPCs in active smokers after AMI. Future studies are warranted to understand critical features of progenitor cell preparations and of patients with AMI that are predictive of a favorable response to cell transfer.
- © 2012 by American Heart Association, Inc.