Progenitor and stem cells in the circulation are largely derived from the bone marrow and contribute to repair of the vasculature and myocardium after injury [[1], [2], [3], [4]]. Circulating progenitor cells (CPCs) that express the cluster of differentiation (CD) 34 epitope have the potential to differentiate into several distinct lineages that contribute to endogenous repair capacity such as hematopoietic cells (identified by their expression of the CD34 epitope on CD45med cells), and non-hematopoietic mesenchymal progenitor cells, which lack CD45 expression [[5], [6], [7], [8]]. CD133 is a 5-transmembrance antigen that is lost during maturation and therefore identifies an early CPC-enriched subpopulation [9,10].

In the setting of injury, progenitor cells migrate from the bone marrow into the circulation, to the culprit tissue and contribute to repair and regeneration [[11], [12], [13]]. Previous studies have demonstrated that patients have a variable ability to mobilize progenitor cells [14,15]. Moreover, low CPC counts are an independent indicator of adverse cardiovascular outcomes in a variety of cardiovascular syndromes [14,[16], [17], [18], [19], [20]].

A chronic total occlusion (CTO) of the coronary artery is a 100% occlusion that is present for over 3 months and is encountered in 15–30% of patients undergoing diagnostic coronary angiography [21]. CTOs are associated with greater ischemia than non-CTO lesions [22]. Collaterals develop over time in response to myocardial ischemia and more profuse development of collaterals has been associated with lower ischemic burden [23]. A previous small study of 35 patients with ≥90% occlusion of the coronary arteries demonstrated an association between higher CD34+ CPC counts and greater collateral circulation [24], but larger studies investigating the role of CPCs in populations with a CTO are lacking. Additionally, whether CPC numbers are directly associated with the ischemic burden, estimated as circulating high sensitivity troponin-I (hsTn-I) levels [[25], [26], [27], [28]], remains unknown. In this prospective cohort of patients with stable CAD with a CTO, we aimed to investigate the association between CD34+ and CD34+/CD133+ CPCs and (a) collateral development and (b) ischemia, estimated with circulating hsTn-I levels. We hypothesized that higher CPC levels will be associated with more robust collateral development and with lower levels of hsTn-I.