Introduction: Although autologous bone marrow cell (BMC) therapy has emerged as a promising treatment for\r\nacute myocardial infarction (AMI), trials reported mixed results. In the BONAMI trial, active smoking reduced cardiac\r\nfunction recovery after reperfused AMI. Therefore, we hypothesized that variability in the functionality of BMCs retrieved\r\nfrom patients with cardiovascular risk factors may partly explain these mixed results. We investigated the characteristics of\r\nprogenitor cells in active smokers and non-smokers with AMI and their potential impact on BMC therapy efficacy.\r\nMethods: Bone marrow and blood samples from 54 smoking and 47 non-smoking patients enrolled in the BONAMI\r\ncell therapy trial were analyzed.\r\nResults: The white BMC and CD45dimCD34+ cell numbers were higher in active smokers (P = 0.001, P = 0.03,\r\nrespectively). In marked contrast, either bone marrow or blood endothelial progenitor CD45dimCD34 + KDR + cells\r\n(EPCs) were decreased in active smokers (P = 0.005, P = 0.04, respectively). Importantly, a multivariate analysis including\r\ncardiovascular risk factors confirmed the association between active smoking and lower EPC number in bone marrow\r\n(P = 0.04) and blood (P = 0.04). Furthermore, baseline circulating EPC count predicted infarct size decrease at three\r\nmonths post-AMI in non-smokers (P = 0.01) but not in active smokers. Interestingly, baseline circulating EPCs were no\r\nlonger predictive of cardiac function improvement in the BMC therapy group.\r\nConclusions: These data suggest that circulating EPCs play an important role in cardiac repair post-AMI only in\r\nnon-smokers and that active smoking-associated EPC alterations may participate in the impairment of cardiac\r\nfunction recovery observed in smokers after AMI, an effect that was overridden by BMC therapy.
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