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(Circulation. 2002;106:1753.)
© 2002 American Heart Association, Inc.
Brief Rapid Communications |
From the Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories (V.M.S., S.A., N.J.W.), Cardiovascular Research Institute, Washington Hospital Center, Washington, DC; and Cardiovascular Research Foundation (G.S.M.), New York, NY.
Correspondence to Neil J. Weissman, MD, Cardiovascular Research Institute, Washington Hospital Center, 110 Irving St, NW Suite 4B-1, Washington DC 20010. E-mail neil.j.weissman{at}medstar.net
Background Late stent malapposition has been reported to be an abnormal finding after vascular brachytherapy and, possibly, implantation of drug-eluting stents. It can only be detected if intravascular ultrasound (IVUS) is performed at follow-up. However, the "background" frequency of late stent malapposition after bare-metal stent implantation is not known.
Methods and Results We studied 206 patients with native artery lesions who had tubular-slotted bare-metal stent implantation and who had IVUS performed at index and after 6±3 months of follow-up. There were 9 patients (4.4%) with late malapposition, which is separation of at least 1 stent strut from the arterial wall intima that does not overlap a side-branch, with evidence of blood flow (speckling) behind the strut, and where the immediate postimplantation IVUS revealed complete apposition of the stent to the vessel wall. The location of late malapposition was the stent edge in 8 of 9 patients. The maximum area, length, volume, and arc of late malapposition measured 3.1±2.4 mm2, 3.3±2.2 mm, 21±27 mm3, and 110±61 degrees, respectively. There was an increase in external elastic membrane (EEM) area (20.7±4.9 to 26.9±4.2 mm, P=0.0021) and plaque area (10.1±3.7 to 14.8±3.6 mm, P=0.0022); however, the increase in EEM was greater than the increase in plaque. The area of late malapposition correlated directly with the increase in EEM area (r=0.75, P=0.0205).
Conclusion Late malapposition occurs in 4% to 5% of slotted-tube bare-metal stents, usually at stent edges. The main cause is positive remodeling out of proportion to the increase in peri-stent intimal hyperplasia.
Key Words: stents remodeling restenosis
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