Far-Fetched Benefit of Inflammation

Recent observations suggest that circulating stem cells contribute to neointimal formation. For example, DNA in situ hybridization for the human Y chromosome in sex-mismatched heart transplantions has detected up to 2.6% to 16% of human coronary artery smooth muscle cells of host origin.1 This process likely contributes not only to transplant vasculopathy but also to neointimal thickening in atherosclerosis and restenosis.2 Yet, the factors that modulate this process are unknown.Article p 553 In this issue of Circulation , Inoue and coworkers3 provide tantalizing translational evidence that local arterial inflammation signals the release of bone marrow–derived stem cells. These investigators placed a coronary sinus catheter to sample blood traversing the coronary circulation before and up to 48 hours after elective percutaneous coronary intervention with bare-metal or sirolimus-eluting stents. Peripheral blood (equivalent to aorta sampling) also was sampled to determine the presence of a transcardiac gradient. Bare-metal stent deployment was accompanied by a burst of neutrophil activation across the coronary artery bed. Neutrophil activation was highest in bare-metal stent patients who subsequently developed restenosis, intermediate in bare-metal stent patients without restenosis, and lowest in patients receiving sirolimus-eluting stents. Accumulation of CD34 cells in …