These endothelial progenitor cells (EPC) are produced in the bone marrow, and one of their roles is to repair damage to the lining of blood vessels. Duke cardiologists believe that one cause of coronary artery disease is an increasing inability over time of these EPCs to keep up with the damage caused to the arterial lining, or endothelium.
"In our study we found that patients with multi-vessel disease had many fewer EPCs, which supports our hypothesis that these cells play an important role in protecting blood vessels," said cardiologist Geoffrey Kunz, M.D., of the Duke Clinical Research Institute. "If you don't have enough of the cells, the ongoing damage to the endothelium from traditional risk factors occurs faster than the body's ability for repair."
Kunz presented the results of the Duke analysis March 9, 2004, at the annual scientific sessions of the American College of Cardiology.
In an article published last year in Circulation (July 29, 2003), Duke researchers reported discovering in mouse studies that a major outcome of aging is an unexpected failure of the bone marrow to produce EPCs needed to repair and rejuvenate arteries exposed to a genetically induced risk of high lipid levels. The researchers demonstrated that an age-related loss of these particular cells is critical to determining the onset and progression of atherosclerosis, which causes arteries to clog and become less elastic.
For the current study, the researchers measured the levels of EPCs in 122 patients undergoing diagnostic cardiac catheterization procedures at Duke and
Contact: Richard Merritt
Duke University Medical Center