Hoop dreams. Stents without restenosis.

Spanning ribs enable canoes and massive sailing ships to float and withstand the battering of the seas. Bronze-age huts were supported by massive wooden hoops embedded in the walls, and the great cathedrals of Europe rose only by virtue of innovative buttress supports. Endovascular stents were designed with the expectation that they would similarly buttress the collapsible artery against deforming stress with the hope that they might break the vicious cycle of arterial stenosis, intervention, and restenosis. As these devices stretch vessels to their greatest extent, they represent the extreme of the notion that “bigger is better.” This prevailing paradigm in interventional cardiology holds that relative restenosis is minimized by maximization of the initial lumen diameter; the larger the diameter is immediately after any form of angioplasty, the greater is the degree but the less is the impact of luminal encroachment from elastic recoil, thrombosis, intimal hyperplasia, and matrix remodeling.1 The attraction of this paradigm arises in part from frustration with attempted control of the vascular response to injury. To date, even the most promising pharmacological agents have failed to stem the tide of restenosis, and the most sophisticated of mechanical interventions have, if anything, exacerbated the problem. Only the simplest approach beyond balloon angioplasty, endovascular stenting, now appears to offer some relief,2 3 4 5 yet even these devices are limited by the vascular counterreaction they elicit. If the “bigger is better” paradigm holds true, the only recourse is to use larger stents expanded to their maximal extent. Furthermore, if size alone dictates restenosis, no single stent design should be superior to any other. Extensive experimental data, however, suggest that the pathobiological response to implantation of an endovascular device involves a complex interplay among design, material, and deployment technique. Reconciling clinical dogma with experimental observations will require …

[1]  Karnovsky Mj,et al.  Endothelial regeneration in the rat carotid artery and the significance of endothelial denudation in the pathogenesis of myointimal thickening. , 1975 .

[2]  E. Edelman,et al.  Monocyte recruitment and neointimal hyperplasia in rabbits. Coupled inhibitory effects of heparin. , 1996, Arteriosclerosis, thrombosis, and vascular biology.

[3]  E. Edelman,et al.  Inhibition of experimental neointimal hyperplasia and thrombosis depends on the type of vascular injury and the site of drug administration. , 1993, Circulation.

[4]  E J Topol,et al.  The restenosis paradigm revisited: an alternative proposal for cellular mechanisms. , 1992, Journal of the American College of Cardiology.

[5]  E. Edelman,et al.  Endovascular stent design dictates experimental restenosis and thrombosis. , 1995, Circulation.

[6]  K. Robinson,et al.  Coronary intimal proliferation after balloon injury and stenting in swine: an animal model of restenosis. , 1992, Journal of the American College of Cardiology.

[7]  F Joffre,et al.  Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. , 1987, The New England journal of medicine.

[8]  S Glagov,et al.  Cyclic stretching stimulates synthesis of matrix components by arterial smooth muscle cells in vitro. , 2003, Science.

[9]  M. Leon,et al.  Patterns and mechanisms of in-stent restenosis. A serial intravascular ultrasound study. , 1996, Circulation.

[10]  D. McPherson,et al.  Accurate three-dimensional reconstruction of intravascular ultrasound data. Spatially correct three-dimensional reconstructions. , 1996, Circulation.

[11]  R. Virmani,et al.  Morphologic characteristics of lesion formation and time course of smooth muscle cell proliferation in a porcine proliferative restenosis model. , 1994, Journal of the American College of Cardiology.

[12]  W. Edwards,et al.  Polymeric stenting in the porcine coronary artery model: differential outcome of exogenous fibrin sleeves versus polyurethane-coated stents. , 1994, Journal of the American College of Cardiology.

[13]  Julio C. Palmaz,et al.  Clinical Experience With the Palmaz‐Schatz Coronary Stent: Initial Results of a Multicenter Study , 1991, Circulation.

[14]  E. Edelman,et al.  Endogenous cell seeding. Remnant endothelium after stenting enhances vascular repair. , 1996, Circulation.

[15]  W Rutsch,et al.  A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. Benestent Study Group. , 1994, The New England journal of medicine.

[16]  W. Baxley,et al.  Vascular pathology of balloon-expandable flexible coil stents in humans. , 1992, Journal of the American College of Cardiology.

[17]  P Hall,et al.  Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. , 1995, Circulation.

[18]  P. Serruys,et al.  Histology after stenting of human saphenous vein bypass grafts: observations from surgically excised grafts 3 to 320 days after stent implantation. , 1993, Journal of the American College of Cardiology.

[19]  M. Savage,et al.  Restenosis after coronary angioplasty: A multilvariate statistical model to relate lesion and procedure variables to restenosis☆ , 1991 .

[20]  R E Vlietstra,et al.  Restenosis and the proportional neointimal response to coronary artery injury: results in a porcine model. , 1992, Journal of the American College of Cardiology.

[21]  M. Reidy,et al.  Kinetics of cellular proliferation after arterial injury. I. Smooth muscle growth in the absence of endothelium. , 1983, Laboratory investigation; a journal of technical methods and pathology.

[22]  J. Fallon,et al.  Morphology after transluminal angioplasty in human beings. , 1981, The New England journal of medicine.

[23]  C M Gibson,et al.  Generalized model of restenosis after conventional balloon angioplasty, stenting and directional atherectomy. , 1993, Journal of the American College of Cardiology.

[24]  H Yokoi,et al.  Three-year follow-up after implantation of metallic coronary-artery stents. , 1996, The New England journal of medicine.

[25]  P. Teirstein,et al.  A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. Stent Restenosis Study Investigators. , 1994, The New England journal of medicine.

[26]  J. Isner,et al.  Three‐Dimensional Reconstruction of Human Coronary and Peripheral Arteries From Images Recorded During Two‐Dimensional Intravascular Ultrasound Examination , 1991, Circulation.

[27]  N. Ratliff,et al.  Intimal proliferation of smooth muscle cells as an explanation for recurrent coronary artery stenosis after percutaneous transluminal coronary angioplasty. , 1985, Journal of the American College of Cardiology.

[28]  R E Vlietstra,et al.  Percutaneous Polymeric Stents in Porcine Coronary Arteries: Initial Experience With Polyethylene Terephthalate Stents , 1992, Circulation.