(Circulation. 1997;95:2027-2031.)
© 1997 American Heart Association, Inc.
Articles |
From the Section of Vascular Medicine, University Department of Medicine, Department of Radiology, Ninewells Hospital and Medical School, Dundee, Scotland (J.J.F.B., J.W.S., G.K., M.M., R.R., C.M.); and the Department of Clinical Statistics, Scotia Pharmaceuticals Ltd, Woodbridge Meadows, Guildford, England (P.M.).
Correspondence to Dr J.J.F. Belch, Department of Medicine, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland.
Background Experimental studies have shown that endothelial dysfunction is an early event preceding restenosis. Monocytes and neutrophils have been shown to bind to damaged endothelium via the cell adhesion molecules (CAMs). The selectins are involved in capturing the leukocytes and tethering them to the endothelium. E-selectin is a CAM that is only expressed on activated endothelial cells. Its ligands are expressed on monocytes and neutrophils and it has been found to exist in a soluble form. This soluble form may represent a marker for endothelial damage and may be a precursor of smooth muscle proliferation.
Methods and Results Fifty-four patients who were undergoing peripheral arterial balloon angioplasty had blood sampled before angioplasty. E-selectin was measured in plasma with the use of an ELISA. At follow-up angiogram, 30% (n=14) of the patients had restenosed at 1 year. There was a significant difference in baseline E-selectin levels in patients who restenosed compared with those who did not (65.3 ng/mL [58.25 to 78.05] versus 52.3 [34.2 to 62.1], Mann-Whitney U, P<.007). Endothelial activation with subsequent adherence of white blood cells is an important step in restenosis.
Conclusions We have shown an increased level of shed E-selectin in patients destined for restenosis and suggest that this work further supports a role for white blood cell/endothelial interaction in restenosis after angioplasty.
Key Words: restenosis angioplasty blood cells endothelium peripheral vascular disease
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