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(Circulation. 2007;115:548-549.)
© 2007 American Heart Association, Inc.

Editorial

Far-Fetched Benefit of Inflammation

Daniel I. Simon, MD; Vincent J. Pompili, MD

From the Division of Cardiovascular Medicine, University Hospitals–Case Medical Center, Case Cardiovascular Center, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Correspondence to Daniel I. Simon, MD, Chief, Division of Cardiovascular Medicine, 11100 Euclid Ave, Cleveland, OH 44022. E-mail daniel.simon@uhhospitals.org

Key Words: Editorials • bone marrow • endothelium • inflammation • restenosis • stem cells • stents

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 the peripheral blood peaked at 7 days and correlated with the extent of transcardiac inflammation at 48 hours and, importantly, with late lumen loss within the stent at follow-up angiography. CD34 cell number was lowest in patients with sirolimus-eluting stents. Most interestingly, endothelial precursor cells in peripheral blood were increased after deployment of bare-metal stents but markedly reduced . . . [Full Text of this Article]