Copyright © 2001 by the European Society of Cardiology.
Stent design related neointimal tissue proliferation in human coronary arteries; an intravascular ultrasound study
a Medical Clinic I, University Clinic RWTH Aachen, Aachen, Germany
b Department of Internal Medicine, Division of Cardiology, Department of Cardiology, University Munich, Munich, Germany
c Department of Cardiology, Krankenhaus Neuperlach, Munich, Germany
revised January 12, 2001; accepted January 17, 2001
Abstract
Aims Histological restenosis models in animals have indicated that stent design has a significant impact on vessel trauma during stent implantation and on the amount of subsequent neointimal tissue proliferation. The impact of different stent designs on intimal hyperplasia in human atherosclerotic coronary arteries has not been determined.
Methods and Results Angiographic and intravascular ultrasound studies were performed at the 6 month follow-up in 131 consecutive native coronary lesions of 131 patients treated with 50 Multi-LinkTM stents, 40 InFlowTM stents and 41 Palmaz–SchatzTM stents. Lumen and stent cross-sectional areas (CSA) were measured at 1mm axial increments. Mean intimal hyperplasia cross-sectional area (stent CSA–lumen CSA) and mean intimal hyperplasia thickness were calculated. Intravascular ultrasound demonstrated different levels of intimal hyperplasia proliferation for the three stents. Mean intimal hyperplasia thickness was 0·16±0·08mm for Multi-Link stents, 0·26±0·19mm for Palmaz–Schatz stents and 0·39±0·14mm for Inflow stents (P<0·001). Multivariate analysis proved that stent type was the only independent predictor of intimal hyperplasia thickness at follow-up (P<0·001).
Conclusion Coronary stent design has a significant impact on subsequent intimal hyperplasia after implantation into atherosclerotic human coronary arteries. The corrugated ring design of the Multi-Link stent proved to result in less tissue proliferation at 6-month follow-up than the tubular slotted design of Palmaz–Schatz and InFlow stents.
Key Words: Intimal hyperplasia, intravascular ultrasound, restenosis, stent
f1 Correspondence: Rainer Hoffmann, MD, FESC, Medical Clinic I, Klinikum RWTH Aachen, Pauwelsstraße, 52057 Aachen, Germany.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J Butany, K Carmichael, S W Leong, and M J Collins Coronary artery stents: identification and evaluation J. Clin. Pathol., August 1, 2005; 58(8): 795 - 804. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Chaves, A. G.M.R. Sousa, L. A. Mattos, A. Abizaid, R. Staico, F. Feres, M. Centemero, L. F. Tanajura, A. Abizaid, I. Pinto, et al. Volumetric Analysis of In-Stent Intimal Hyperplasia in Diabetic Patients Treated With or Without Abciximab: Results of the Diabetes Abciximab steNT Evaluation (DANTE) Randomized Trial Circulation, February 24, 2004; 109(7): 861 - 866. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Spanos, G. Stankovic, J. Tobis, and A. Colombo The challenge of in-stent restenosis: insights from intravascular ultrasound Eur. Heart J., January 2, 2003; 24(2): 138 - 150. [Full Text] [PDF]
|
|
|
|
|
|
M. N. Babapulle and M. J. Eisenberg Coated Stents for the Prevention of Restenosis: Part II Circulation, November 26, 2002; 106(22): 2859 - 2866. [Full Text] [PDF]
|
|
|
|
|
|
S. Windecker and B. Meier All stents are not alike or is the difference in the eye of the observer only? Eur. Heart J., November 1, 2001; 22(21): 1973 - 1977. [PDF]
|
|