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J Thorac Cardiovasc Surg 2002;124:950-956
© 2002 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology (CSP) |
From the Bristol Heart Institute, Bristol Royal Infirmary, Bristol, United Kingdom.
Supported by the British Heart Foundation.
Received for publication Feb 7, 2002. Revisions requested April 4, 2002; revisions received, May 28, 2002. Accepted for publication June 5, 2002. Address for reprints: Andrew Newby, PhD, Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW, United Kingdom (E-mail: A.Newby{at}bris.ac.uk).
Background: Reducing neointima formation and atherosclerosis are key goals in preventing late vein graft failure. Although pharmacologic and mechanical solutions have been proposed, the demonstration that these influence both aspects of vein graft pathology have been lacking. Supporting grafts externally with an oversized, highly porous polyester stent dramatically reduces neointima formation in normocholesterolemic pigs. However, its effects in the presence of hypercholesterolemia are unknown.
Methods: We compared wall thickening, cholesterol concentration, foam-cell formation, and the expression of the leukocyte adhesion molecule vascular cell adhesion molecule 1 after 3 months in stented and unstented saphenous vein interposition grafts into the carotid arteries of pigs fed cholesterol to cause modest hypercholesterolemia (11.2 ± 1.2 mmol/L).
Results: Stenting reduced neointima formation from 5.6 ± 0.4 to 1.2 ± 0.2 mm2 (n = 7; P < .00002, paired t test) and graft cholesterol concentration from 4.7 ± 1.2 to 2.1 ± 1.3 mg/g wet weight (P < .02). Foam cells were observed in unstented grafts (mean, 1.5% ± 0.5% of all cells) but never in stented grafts. Vascular cell adhesion molecule 1 was strongly expressed in 53% ± 8% of intimal and medial cells in unstented grafts but was weakly expressed in only 19% ± 3% (n = 4, P < .05) of stented grafts.
Conclusions: We conclude that external stenting with polyester favorably influences both neointima formation and early atherosclerosis, both of which are key aspects of vein graft disease, and that decreased expression of vascular cell adhesion molecule 1 is part of the underlying mechanism.
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