Circulating humoral factors and endothelial progenitor cells in patients with differing coronary collateral support.
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.


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 > or =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.
Lambiase
Pier D
PD
Department of Cardiology, GKT School of Medicine, The Rayne Institute, St Thomas' Hospital, London, UK.
Edwards
Richard J
RJ
Anthopoulos
Prodromos
P
Rahman
Salman
S
Meng
Y Gloria
YG
Bucknall
Clifford A
CA
Redwood
Simon R
SR
Pearson
Jeremy D
JD
Marber
Michael S
MS
D000368:Aged; D000943:Antigens, Differentiation / Q000032:analysis; D006328:Cardiac Catheterization; D002404:Catheterization; D002465:Cell Movement; D002478:Cells, Cultured / Q000378:metabolism; D003326:Coronary Circulation; D003327:Coronary Disease / Q000097:blood* / Q000473:pathology; D004730:Endothelium, Vascular / Q000473:pathology*; D005080:Exercise Test; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000097:blood*; D014644:Genetic Variation; D006801:Humans; D008297:Male; D059630:Mesenchymal Stem Cells / Q000737:chemistry / Q000166:cytology*; D008875:Middle Aged; D018919:Neovascularization, Physiologic; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000097:blood*; D011312:Pressure; D011446:Prospective Studies; D012307:Risk Factors; D016037:Single-Blind Method; D042461:Vascular Endothelial Growth Factor A / Q000097:blood*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000032:analysis
D000943:Antigens, Differentiation; C000608036:PGF protein, human; D011257:Pregnancy Proteins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D016222:Fibroblast Growth Factor 2; D000072483:Placenta Growth Factor; D040301:Vascular Endothelial Growth Factor Receptor-2