Published online before print June 7, 2004, doi: 10.1161/01.CIR.0000130639.97284.EC
(Circulation. 2004;109:2986-2992.)
© 2004 American Heart Association, Inc.
Clinical Investigation and Reports |
Circulating Humoral Factors and Endothelial Progenitor Cells in Patients With Differing Coronary Collateral Support
From the Department of Cardiology, GKT School of Medicine, The Rayne Institute, St Thomas’ Hospital, London; Department of Cardiovascular Biology (J.D.P.), Guy’s, King’s and St Thomas’ School of Biomedical Sciences, Guy’s Hospital, London; and Genetech Inc (Y.G.M.), San Francisco, Calif.
Correspondence to Professor M.S. Marber, PhD, FRCP, FACC, Department of Cardiology, Rayne Institute, St Thomas’ Hospital, Lambeth Palace Rd, London SE1 7EH, UK. E-mail mike.marber{at}kcl.ac.uk
Received January 6, 2004; revision received February 27, 2004; accepted March 4, 2004.
Background— The mechanisms underlying the variation in collateral formation between patients, even with similar patterns of coronary artery disease, remain unclear. This study investigates whether circulating humoral or cellular factors can provide an insight into this variation.
Methods and Results— Thirty patients with isolated left anterior descending coronary artery disease underwent percutaneous coronary intervention with collateral flow index (CFI) determined using a pressure wire. Patients with inadequate (CFI <0.25) compared with those with adequate (CFI 
0.25) collateral support had, or tended to have, lower concentrations of coronary sinus growth factors and plasma exerting a weaker effect on endothelial cell migration and angiogenesis in vitro. However, there was an inverse correlation between serum mitogenicity and CFI (r=–0.61, P<0.01). No significant differences were detected between the 2 groups in plasma levels of total vascular endothelial growth factor, vascular endothelial growth factor165, or placental growth factor. There was a strong positive correlation between numbers of CD34/CD133-positive circulating hemopoietic precursor cells and CFI (r=0.75, P<0.001). In patients with inadequate, compared with those with adequate, CFI, the numbers of differentiated endothelial progenitor cells (EPCs) appearing in the circulation and in culture were significantly reduced by 75% (P<0.05) and 70% (P<0.05), respectively.
Conclusions— In this study, inadequate coronary collateral development is associated with reduced numbers of circulating EPCs and impaired chemotactic and proangiogenic but not mitogenic activity. These findings are consistent with current efforts to enhance collateral formation by augmentation of circulating EPCs.
Key Words: collateral circulation • angiogenesis • coronary disease
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