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J Am Coll Cardiol, 1995; 26:720-724
© 1995 by the American College of Cardiology Foundation
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Small stent size and intimal hyperplasia contribute to restenosis: a volumetric intravascular ultrasound analysis

GR Dussaillant, GS Mintz, AD Pichard, KM Kent, LF Satler, JJ Popma, SC Wong, and MB Leon

Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, Washington Hospital Center, Washington, D.C. 20010, USA.

OBJECTIVES. The purpose of this study was to use volumetric intravascular ultrasound analysis of Palmaz-Schatz stents to assess the in-stent restenotic process. BACKGROUND. By reducing lesion elastic recoil and chronic arterial remodeling, stents improve the long-term results of coronary angioplasty. However, stents are prone to the development of neointimal hyperplasia. Angiographic studies of stent restenosis have suggested that these hyperplastic responses are the cause of in-stent restenosis; however, it is difficult to visualize the radiolucent Palmaz-Schatz stent by angiography. Intravascular ultrasound provides detailed cross-sectional imaging of the coronary arteries, especially the intense metallic reflection of endovascular stents. METHODS. Forty-four patients with 60 Palmaz-Schatz stents underwent intravascular ultrasound imaging at follow-up ([mean +/- SD] 8.8 +/- 7.2 months after implantation). Thirty-four stents were placed in saphenous vein grafts and 26 in native coronary arteries; 30 were placed in restenotic lesions. Intravascular ultrasound with automatic transducer pullback at 0.5 mm/s allowed measurement of stent, lumen and intimal hyperplasia cross-sectional areas at 1-mm axial increments within the stents. Using Simpson's rule, stent, lumen and intimal hyperplasia volumes were calculated. Patterns of in-stent restenosis were then identified. RESULTS. Restenotic stents had smaller stent volumes (120 +/- 41 vs. 147 +/- 43 mm3, p = 0.016) and lumen volumes (62 +/- 28 vs. 118 +/- 42 mm3, p < 0.0001) but larger intimal hyperplasia volumes (58 +/- 36 vs. 29 +/- 18 mm3, p < 0.001) than nonrestenotic stents. A focal restenosis pattern was more common (20 [77%] of 26) than a diffuse restenosis pattern (6 [23%] of 26). Stents with focal restenosis and stents with diffuse restenosis had equally small stent volumes (120 +/- 44 vs. 120 +/- 31 mm3, respectively, p = NS); however, stents with diffuse restenosis had larger intimal hyperplasia volumes (84 +/- 30 vs. 50 +/- 34 mm3, p < 0.05). Focal restenosis was most commonly located at the central articulation (45%); the location of focal restenosis was related to the focal accumulation of neointimal tissue. CONCLUSIONS. Stent volume and magnitude and distribution of intimal hyperplasia are important in the development of in-stent restenosis. Stent volume was smaller and intimal hyperplasia volume greater in restenotic stents. Stent restenosis is more commonly focal in nature and located at the central articulation.


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Mechanisms of Residual Lumen Stenosis After High-Pressure Stent Implantation : A Quantitative Coronary Angiography and Intravascular Ultrasound Study
Circulation, July 14, 1998; 98(2): 112 - 118.
[Abstract] [Full Text] [PDF]


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CirculationHome page
K. Guo, V. Andres, and K. Walsh
Nitric Oxide–Induced Downregulation of Cdk2 Activity and Cyclin A Gene Transcription in Vascular Smooth Muscle Cells
Circulation, May 26, 1998; 97(20): 2066 - 2072.
[Abstract] [Full Text] [PDF]


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HeartHome page
A H Gershlick and J Baron
Dealing with in-stent restenosis
Heart, April 1, 1998; 79(4): 319 - 323.
[Full Text]


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Proc. Natl. Acad. Sci. USAHome page
M. Sata, H. Perlman, D. A. Muruve, M. Silver, M. Ikebe, T. A. Libermann, P. Oettgen, and K. Walsh
Fas ligand gene transfer to the vessel wall inhibits neointima formation and overrides the adenovirus-mediated T cell response
PNAS, February 3, 1998; 95(3): 1213 - 1217.
[Abstract] [Full Text] [PDF]


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CirculationHome page
C. von Birgelen, E. A. de Vrey, G. S. Mintz, A. Nicosia, N. Bruining, W. Li, C. J. Slager, J. R. T. C. Roelandt, P. W. Serruys, and P. J. de Feyter
ECG-Gated Three-dimensional Intravascular Ultrasound : Feasibility and Reproducibility of the Automated Analysis of Coronary Lumen and Atherosclerotic Plaque Dimensions in Humans
Circulation, November 4, 1997; 96(9): 2944 - 2952.
[Abstract] [Full Text]


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CirculationHome page
R. Mehran, G. S. Mintz, L. F. Satler, A. D. Pichard, K. M. Kent, T. A. Bucher, J. J. Popma, and M. B. Leon
Treatment of In-Stent Restenosis With Excimer Laser Coronary Angioplasty : Mechanisms and Results Compared With PTCA Alone
Circulation, October 7, 1997; 96(7): 2183 - 2189.
[Abstract] [Full Text]


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Cardiovasc ResHome page
L. Maillard, E. Van Belle, R. C Smith, A. Le Roux, P. Denefle, G. Steg, J. J Barry, D. Branellec, J. M Isner, and K. Walsh
Percutaneous delivery of the gax gene inhibits vessel stenosis in a rabbit model of balloon angioplasty
Cardiovasc Res, September 1, 1997; 35(3): 536 - 546.
[Abstract] [Full Text] [PDF]


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NEJMHome page
P. S. Teirstein, V. Massullo, S. Jani, J. J. Popma, G. S. Mintz, R. J. Russo, R. A. Schatz, E. M. Guarneri, S. Steuterman, N. B. Morris, et al.
Catheter-Based Radiotherapy to Inhibit Restenosis after Coronary Stenting
N. Engl. J. Med., June 12, 1997; 336(24): 1697 - 1703.
[Abstract] [Full Text] [PDF]


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CirculationHome page
M. Kearney, A. Pieczek, L. Haley, D. W. Losordo, V. Andres, R. Schainfeld, K. Rosenfield, and J. M. Isner
Histopathology of In-Stent Restenosis in Patients With Peripheral Artery Disease
Circulation, April 15, 1997; 95(8): 1998 - 2002.
[Abstract] [Full Text]


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CirculationHome page
H. Mudra, E. Regar, V. Klauss, F. Werner, K.-H. Henneke, E. Sbarouni, and K. Theisen
Serial Follow-up After Optimized Ultrasound-Guided Deployment of Palmaz-Schatz Stents: In-Stent Neointimal Proliferation Without Significant Reference Segment Response
Circulation, January 21, 1997; 95(2): 363 - 370.
[Abstract] [Full Text]


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CirculationHome page
M. K. Hong, K. M. Kent, R. Mehran, G. S. Mintz, F. O. Tio, M. Foegh, S. C. Wong, S. S. Cathapermal, and M. B. Leon
Continuous Subcutaneous Angiopeptin Treatment Significantly Reduces Neointimal Hyperplasia in a Porcine Coronary In-Stent Restenosis Model
Circulation, January 21, 1997; 95(2): 449 - 454.
[Abstract] [Full Text]


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CirculationHome page
A. J. Carter, J. R. Laird, L. R. Bailey, T. G. Hoopes, A. Farb, D. R. Fischell, R. E. Fischell, T. A. Fischell, and R. Virmani
Effects of Endovascular Radiation From a ß-Particle–Emitting Stent in a Porcine Coronary Restenosis Model: A Dose-Response Study
Circulation, November 15, 1996; 94(10): 2364 - 2368.
[Abstract] [Full Text]


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NEJMHome page
J. A. Bittl
Advances in Coronary Angioplasty
N. Engl. J. Med., October 24, 1996; 335(17): 1290 - 1302.
[Full Text] [PDF]


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CirculationHome page
R. Hoffmann, G. S. Mintz, G. R. Dussaillant, J. J. Popma, A. D. Pichard, L. F. Satler, K. M. Kent, J. Griffin, and M. B. Leon
Patterns and Mechanisms of In-Stent Restenosis: A Serial Intravascular Ultrasound Study
Circulation, September 15, 1996; 94(6): 1247 - 1254.
[Abstract] [Full Text]


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CirculationHome page
G. S. Mintz, J. A. Kovach, S. P. Javier, A. D. Pichard, K. M. Kent, J. J. Popma, L. F. Salter, and M. B. Leon
Mechanisms of Lumen Enlargement After Excimer Laser Coronary Angioplasty : An Intravascular Ultrasound Study
Circulation, December 15, 1995; 92(12): 3408 - 3414.
[Abstract] [Full Text]



 
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