Trial Information

Endothelial Progenitor Cells and Risk Factors for Coronary Artery Disease

Evidence suggests that risk factors for atherosclerosis contribute to atherogenesis by
causing endothelial injury. However, little is known about determinants of endothelial cell
repair and regeneration. We propose that mobilization of endothelial progenitor cells
(EPCs) constitutes one mechanism for ongoing endothelial repair. EPCs are a bone marrow
derived cell population that can be isolated from peripheral blood. Among human peripheral
mononuclear cells, EPCs are relatively abundant with an estimated frequency of 1 in 500 to 1
in 1000 cells. Evidence suggests that EPCs can participate in angiogenesis under
pathophysiological circumstances. Under normal conditions, however, adult organisms
undergo little if any active angiogenesis. One explanation for this set of observations is
that high circulating levels of EPCs may exist to allow these cells to participate in
functions beyond angiogenesis. We hypothesize that one such function is in the repair of
ongoing endothelial injury. To test this hypothesis, we will measure peripheral blood EPC
activity by ascertaining the number of EPC colony forming units from peripheral blood
sampling. We intend to correlate this biological determinant with the degree of endothelial
dysfunction assessed by flow-mediated brachial artery reactivity, and an atherosclerotic
risk stratification method developed by the Framingham study. We hypothesize that a
correlation will exist between the atherosclerotic risk profile, endothelial function and
EPC activity and that the EPC activity will therefore become a novel surrogate biological
marker for cumulative cardiovascular risk.