(Circulation. 2003;107:2635.)
© 2003 American Heart Association, Inc.
Editorials |

From the Division of Cardiovascular Research, St Elizabeths Medical Center, Tufts University School of Medicine, Boston, Mass.
Correspondence to Douglas W. Losordo, MD, Chief, Cardiovascular Research, St Elizabeths Medical Center, Tufts University School of Medicine, 736 Cambridge St, Boston, MA 02135. E-mail douglas.losordo@tufts.edu
Key Words: Editorials gene therapy restenosis endothelium angioplasty
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In this world there are only two tragedies. One is not getting what one wants and the other is getting it.
Oscar Wilde
By most accounts, the field of interventional cardiology appears to have achieved one of its most elusive milestones, the virtual eradication of restenosis. In the present issue of Circulation, however, Hedman and colleagues1 report the results of a pilot study of gene therapy with vascular endothelial growth factor (VEGF) for restenosis prevention. Are these authors attempting to develop a treatment for a disease that no longer exists? Or is it possible that the mounting exuberance anticipating the release of drug-eluting stents is ignoring a major liability of these otherwise promising therapies?
See p 2677
Percutaneous transluminal coronary angioplasty (PTCA) has been used to relieve symptoms and ischemia in patients with coronary disease for more than 2 decades. Despite an initial success rate of well over 90%, coronary arterial renarrowing of initially revascularized sites, or restenosis, constitutes the principal major complication of PTCA.
The pathogenesis of restenosis has classically been regarded as involving either reactive constriction of the artery wall or neointimal thickening. The former, termed remodeling,2 has been successfully addressed to a large extent by the development of endovascular stents: Two landmark clinical trials3,4 established stents as the first mechanical intervention to have a favorable impact on restenosis.
Neointimal thickening has been inferred to result most often from vascular smooth muscle cell (VSMC) proliferation.5,6 Indeed, histological inspection of lesions retrieved by directional atherectomy from
Related Article:
Circulation 2003 107: 2677-2683.
This article has been cited by other articles:
![]() |
H. Wang, W. Zhang, R. Tang, R. P. Hebbel, M. A. Kowalska, C. Zhang, J. D. Marth, M. Fukuda, C. Zhu, and Y. Huo Core2 1-6-N-Glucosaminyltransferase-I Deficiency Protects Injured Arteries From Neointima Formation in ApoE-Deficient Mice Arterioscler Thromb Vasc Biol, July 1, 2009; 29(7): 1053 - 1059. [Abstract] [Full Text] [PDF] |
||||
![]() |
X. Wu, Q. Zhou, L. Huang, A. Sun, K. Wang, Y. Zou, and J. Ge Ageing-exaggerated proliferation of vascular smooth muscle cells is related to attenuation of Jagged1 expression in endothelial cells Cardiovasc Res, March 1, 2008; 77(4): 800 - 808. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. V. d'Uscio, L. A. Smith, A. V. Santhanam, D. Richardson, K. A. Nath, and Z. S. Katusic Essential Role of Endothelial Nitric Oxide Synthase in Vascular Effects of Erythropoietin Hypertension, May 1, 2007; 49(5): 1142 - 1148. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Adriaenssens, J. Mehilli, R. Wessely, G. Ndrepepa, M. Seyfarth, A. Wieczorek, B. Blaich, R. Iijima, J. Pache, A. Kastrati, et al. Does Addition of Estradiol Improve the Efficacy of a Rapamycin-Eluting Stent?: Results of the ISAR-PEACE Randomized Trial J. Am. Coll. Cardiol., March 27, 2007; 49(12): 1265 - 1271. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Wessely, A. Schomig, and A. Kastrati Sirolimus and Paclitaxel on Polymer-Based Drug-Eluting Stents: Similar But Different J. Am. Coll. Cardiol., February 21, 2006; 47(4): 708 - 714. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Jaschke, C. Michaelis, S. Milz, M. Vogeser, T. Mund, L. Hengst, A. Kastrati, A. Schomig, and R. Wessely Local statin therapy differentially interferes with smooth muscle and endothelial cell proliferation and reduces neointima on a drug-eluting stent platform Cardiovasc Res, December 1, 2005; 68(3): 483 - 492. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. J. Dzau, M. Gnecchi, A. S. Pachori, F. Morello, and L. G. Melo Therapeutic Potential of Endothelial Progenitor Cells in Cardiovascular Diseases Hypertension, July 1, 2005; 46(1): 7 - 18. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. W. Johnson, Y. X. Wu, C. Herdeg, A. Baumbach, A. C. Newby, K. R. Karsch, and M. Oberhoff Stent-Based Delivery of Tissue Inhibitor of Metalloproteinase-3 Adenovirus Inhibits Neointimal Formation in Porcine Coronary Arteries Arterioscler Thromb Vasc Biol, April 1, 2005; 25(4): 754 - 759. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Kappert, K. G. Peters, F. D. Bohmer, and A. Ostman Tyrosine phosphatases in vessel wall signaling Cardiovasc Res, February 15, 2005; 65(3): 587 - 598. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Langeveld, W. H. van Gilst, R. A. Tio, F. Zijlstra, and A. J.M. Roks Angiotensin-(1-7) Attenuates Neointimal Formation After Stent Implantation in the Rat Hypertension, January 1, 2005; 45(1): 138 - 141. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. G. Melo, M. Gnecchi, A. S. Pachori, D. Kong, K. Wang, X. Liu, R. E. Pratt, and V. J. Dzau Endothelium-Targeted Gene and Cell-Based Therapies for Cardiovascular Disease Arterioscler Thromb Vasc Biol, October 1, 2004; 24(10): 1761 - 1774. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. A. Liehn, A. Schober, and C. Weber Blockade of Keratinocyte-Derived Chemokine Inhibits Endothelial Recovery and Enhances Plaque Formation After Arterial Injury in ApoE-Deficient Mice Arterioscler Thromb Vasc Biol, October 1, 2004; 24(10): 1891 - 1896. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Leppanen, J. Rutanen, M. O. Hiltunen, T. T. Rissanen, M. P. Turunen, T. Sjoblom, J. Bruggen, G. Backstrom, M. Carlsson, E. Buchdunger, et al. Oral Imatinib Mesylate (STI571/Gleevec) Improves the Efficacy of Local Intravascular Vascular Endothelial Growth Factor-C Gene Transfer in Reducing Neointimal Growth in Hypercholesterolemic Rabbits Circulation, March 9, 2004; 109(9): 1140 - 1146. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2003 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |