Endothelial Progenitor Cells

Vascular stenosis as a result of neointimal hyperplasia is a major clinical problem that has an impact on multiple and diverse disciplines, including cardiology (coronary restenosis), cardiothoracic and vascular surgery (saphenous vein and polytetrafluoroethylene [PTFE] graft failure), neurology (carotid stenosis), nephrology (dialysis access dysfunction), and transplant medicine (chronic allograft rejection in hearts and kidneys). [1] In marked contrast to the deleterious effects of smooth muscle progenitor cells on neointimal hyperplasia, circulating endothelial progenitor cells (EPCs) are believed to play an important role in vascular repair and in the inhibition of neointimal hyperplasia. [2] Endothelial progenitor cells (EPCs) circulate in adult peripheral blood and contribute to neovascularization. Satoshi et al. have demonstrated that lineage-committed EPCs and CD34-positive mononuclear cells, their putative precursors, are mobilized during an acute ischemic event in humans. [3] Reduced levels of circulating EPCs independently predict atherosclerotic disease progression, thus supporting an important role for endogenous vascular repair to modulate the clinical course of coronary artery disease. [4] These observations prompt the hypothesis that circulating EPCs may provide an endogenous repair mechanism to counteract surgery-induced endothelial cell injury and to replace dysfunctional endothelium perioperatively. Therefore, the investigators examined whether levels of circulating EPCs correlate with time course and outcomes of coronary artery bypass surgery to establish a clinical role of endogenous endothelial repair mediated by circulating EPCs.