© 1999 American Heart Association, Inc.
Original Contribution |
Balloon-Artery Interactions During Stent Placement
A Finite Element Analysis Approach to Pressure, Compliance, and Stent Design as Contributors to Vascular Injury
Presented at the 23rd Annual Meeting of the Society for Biomaterials, New Orleans, La, April 30–May 4, 1997, and the 70th Scientific Sessions of the American Heart Association, Orlando, Fla, November 9–12, 1997, and published in abstract form (Circulation. 1997;96[suppl I]:I-402).
From the Cardiac Catheterization Laboratory and Coronary Care Unit, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass, and Harvard-MIT Division of Health Science and Technology, Massachusetts Institute of Technology, Cambridge, Mass.
Correspondence to Campbell Rogers, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail cdrogers{at}bics.bwh.harvard.edu
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Abstract—Endovascular stents expand the arterial lumen more than balloon angioplasty and reduce rates of restenosis after coronary angioplasty in selected patients. Understanding the factors involved in vascular injury imposed during stent deployment may allow optimization of stent design and stent-placement protocols so as to limit vascular injury and perhaps reduce restenosis. Addressing the hypothesis that a previously undescribed mechanism of vascular injury during stent deployment is balloon-artery interaction, we have used finite element analysis to model how balloon-artery contact stress and area depend on stent-strut geometry, balloon compliance, and inflation pressure. We also examined superficial injury during deployment of stents of varied design in vivo and in a phantom model ex vivo to show that balloon-induced damage can be modulated by altering stent design. Our results show that higher inflation pressures, wider stent-strut openings, and more compliant balloon materials cause markedly larger surface-contact areas and contact stresses between stent struts. Appreciating that the contact stress and contact area are functions of placement pressure, stent geometry, and balloon compliance may help direct development of novel stent designs and stent-deployment protocols so as to minimize vascular injury during stenting and perhaps to optimize long-term outcomes.
Key Words: stent • restenosis • vascular injury • balloon • finite element analysis
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Introduction |
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Endovascular stents expand the arterial lumen more than balloon angioplasty and reduce rates of restenosis after coronary angioplasty in selected patients.1 2 However, the deep vascular trauma imposed by stent struts3 4 produces more abundant intimal hyperplasia than balloon angioplasty in experimental animals5 6 7 and in humans.1 2 8 Furthermore, understanding the practical elements that underlie in-stent restenosis is made all the more crucial in light of the failure to date to identify successful treatments for established in-stent restenosis. Understanding the factors involved in vascular injury imposed during stent deployment might allow optimization of stent design (eg, stent-strut geometry and stent material) and stent-placement protocols (eg, balloon selection and inflation pressure) so as to limit vascular injury and perhaps reduce restenosis.
In addition to mechanical factors such as focal deep injury from struts and overall arterial strain, which may play important roles in provoking in-stent restenosis, we have recently reported that stent deployment causes partial denudation of the endothelium in a pattern unique to each stent configuration, suggesting balloon-related injury.9 Assuming that endothelial denudation is a marker of the distribution of interstrut vascular injury caused during stent deployment, we now describe studies aimed at elaborating the mechanisms that underlie injury patterns during stenting. Addressing the hypothesis that the mechanism of endothelial cell denudation and therefore interstrut injury during stent deployment is balloon-artery interaction, we have examined damage to endothelial cells during deployment of stents of varied design in vivo and the balloon-stent inflation process and balloon extrusion between stent strut openings in a phantom model ex vivo. Finally, we used finite element analysis (FEA) to model how balloon-artery contact stress and area depend on stent-strut geometry, balloon compliance, and inflation pressure. Understanding more fully the mechanism of interactions among balloon, artery, and stent may help limit neointimal thickening after stenting.
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Materials and Methods |
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In Vivo Analysis of Endothelial Cell Denudation
Balloon-expandable stainless-steel stents were mounted on 3-mm angioplasty balloons (Advanced Cardiovascular Systems) and expanded at 8 atm over 20 s in the iliac arteries (2.5 to 2.75 mm)6 of New Zealand White rabbits (3.0 to 3.5 kg) treated with aspirin and heparin as described previously.10 Two distinct stent configurations,10 a slotted tube and a series of connected corrugated rings, were used. The stent struts were constructed from identical material and had the same strut thickness and surface area. Arteries (n=8 for each stent type) were harvested 1 hour after deployment, en face endothelial staining was performed using a modified Hautchen preparation, the area of intact endothelium remaining between stent struts was measured using computerized digital morphometry,9 and the percentage area of endothelial denudation was calculated.
Ex Vivo Visualization and Analysis of Balloon-Artery
Interactions
To visualize how stent and artery interact during the
stent-balloon inflation process and perhaps explain the observed
patterns of in vivo endothelial injury, we used a
glass-tube arterial phantom model. A glass tube (Pyrex, ID
2.75 mm, 10 cm long) was filled with water colored with black
India ink and placed under a stereomicroscope (model M5A; Wild).
Stents of corrugated-ring or slotted-tube design were mounted on 3-mm
angioplasty balloons (Advanced Cardiovascular
Systems/Guidant), and each was inserted into the center portion
of a glass tube. After positioning the stent-mounted balloon, colored
water was injected into the glass tube, and air bubbles were removed.
The balloon was then inflated to 8 atm over 20 s. Magnified video
images were recorded before inflation and at 8 atm pressure.
Finite Element Analysis
To study how individual components of the balloon-artery
interaction may affect associated contact stress and thereby vascular
injury, we developed an FEA model, using Automatic Dynamic
Incremental Nonlinear Analysis software (ADINA 7.0, ADINA R&D,
Inc) on a dedicated workstation (Silicon Graphics). Our model included
input of the following: individual stent-strut width and thickness and
interstrut distances of the corrugated-ring and slotted-tube stents
described above, Young's modulus and Poisson's ratio for the balloon
material, arterial-wall thickness, Young's modulus
(circumferential) and Poisson's ratio for the artery, and pressure
loaded into the balloon.
The relationship of balloon-artery contact stress and contact area with the distance between 2 adjacent stent struts, balloon materials, and inflation pressure was analyzed by a 2-dimensional FEA model. The FEA model used in this analysis included both displacement and pressure loading to represent arterial displacement and balloon extrusion between struts, respectively. The model assumed the following: (1) a balloon membrane with no thickness; (2) frictionless contact between balloon surface and artery; (3) no slip between stent struts and luminal surface; and (4) no other substrates, such as blood, present between the balloon surface and the arterial wall. The distance between balloon and luminal surfaces before inflation was set as the same as stent-strut thickness (100 µm). Eight-node 2-dimensional solid plane-strain elements and 2-node isobeam plane-strain elements were used for arterial and balloon surface, respectively. Constant step-time functions were used to control artery displacement and balloon extrusion between struts during analysis. The correlations of maximum contact stress and contact area with balloon pressure and the distance between adjacent stent struts at different Young's moduli of balloon materials were analyzed.
Dimensions of the slotted-tube stent design were measured. Young's modulus (circumferential) and Poisson's ratio for the arterial wall, based on previously published studies, were 100 kPa and 0.27, respectively.11 12 Arterial-wall thickness was input as 500 µm. The Young's moduli of balloon materials were measured on a strain-stress measurement instrument (Instron) with a 50-kg load. The Young's modulus was 2.58x104 kPa for a compliant balloon (LEAP, Boston Scientific Co/Scimed) and 7.03x105 kPa for a semicompliant balloon (TRIAD, Boston Scientific Co). Because of difficulty measuring the Young's moduli of noncompliant balloon materials, this value was estimated on the basis of material properties. For FEA, 3 values for Young's modulus of a balloon within the range of the measured values were chosen (1.38x106 kPa, 6.9x105 kPa, and 3.45x105 kPa) to give a ratio of 2:1:0.5 for low-compliant, semicompliant, and compliant balloons, respectively. Poisson's ratio for the balloons was chosen as 0.30.13 The arterial displacement was based on the assumption that a 3.0-mm-ID vessel was expanded to 3.1 mm ID.
Statistical Analysis
All data are presented as mean±SE. Comparison of
endothelial denudation of slotted-tube and
corrugated-ring stents used an unpaired Student t test.
Probability values <0.05 were considered significant.
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Results |
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In Vivo Analysis of Endothelial Cell Denudation
Denudation of endothelial cells during stent expansion, as a marker of balloon-induced damage, was determined by en face staining 1 hour after stent placement in rabbit iliac arteries. Stents of slotted-tube and corrugated-ring designs were compared. Although endothelial denudation occurred at the center of each interstrut opening (Figure 1
),
less endothelium was denuded after deployment of
corrugated-ring design stents (42.6±4.6%, n=8) than after
slotted-tube design stents (63.0±4.3%, n=8, P<0.01,
Figure 2).
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Ex Vivo Visualization and Analysis of Balloon-Artery
Interactions
To examine possible mechanisms of balloon-artery interactions
during stent deployment, the stent-balloon inflation process was
visualized inside a glass-tube arterial model. The
inflation process included 2 stages. The first stage was gradual
inflation of the balloon and stent until the stent just made contact
with the luminal surface of the glass tubing. The second stage, as
balloon pressure continued to increase, included portions of the
balloon being extruded between stent struts to make contact with the
luminal surface of the glass tube, after the stent had contacted the
glass tubing. Digital images of balloon extruded between stent-strut
openings were recorded for slotted-tube and corrugated-ring design
stents (Figure 3). The pattern of the
balloon-tubing contact identified in this model was identical to the
pattern of endothelial-cell denudation identified from
en face staining after in vivo stent deployment (Figure 1
).
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Finite Element Analysis
FEA was used to investigate in a continuous fashion independent
effects of distance between stent struts, balloon-material properties,
and balloon inflation pressures on balloon-artery surface stress and
contact area. In the 2-dimensional FEA contact model with 0.05 mm
displacement and 8 atm deployment pressure, the balloon-artery
displacement (including arterial displacement and balloon
extrusion) and balloon-artery interactions were modeled (Figure 4).
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The correlations between balloon-artery surface stress or contact area
and the distance between 2 adjacent stent struts, the placement
pressure, and different balloon materials, were analyzed. With
constant interstrut distance and balloon compliance, the effective
surface stress increased with deployment pressure (Figure 5a) and reached a maximum at the center
of the intrastrut opening primarily caused by contact between artery
and balloon. Maximum contact stress rose exponentially with deployment
pressure in the range of 12 to 18 atm pressure (Figure 5b).
Examining how balloon compliance affects surface stress in the elastic
region of balloon materials, we found that normalized contact area
between balloon and artery (Figure 6a)
and maximum contact stress (Figure 6b) also increased with
interstrut distance and balloon compliance.
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Discussion |
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How an artery is injured experimentally or clinically may be a critical determinant of the biological events that ensue. We now report a new approach to quantifying the unique forces applied to vessel walls during a particular form of vascular injury, endovascular stent placement. To date, stent-induced arterial injury has been considered to be limited to the sites of stent struts, where depending on stent design and size, deep wall laceration translates into greater vascular responses.3 4 10 14 At the same time, with current clinical stent-deployment techniques including balloon predilation, stent expansion at moderate balloon pressures, and postdilation at significantly higher balloon pressures to ensure that all stent struts are fully expanded and abutting the arterial wall,15 elements of stent implantation such as balloon inflation pressure, balloon material, and arterial stretching, independent of stent design, have taken on tremendous importance in clinical practice. Our report now provides data for the first time that suggest how these various elements may contribute to vascular injury. In particular, in vivo and bench-top stent expansion demonstrate contact of the expansion balloon with the vessel wall between stent struts, and FEA demonstrates that small alterations in inflation pressure, balloon material, or stent design can each have large effects on the area of balloon-artery contact and the stress applied by the balloon to the arterial wall.
Sites of Injury
In addition to the deep injury associated with stent expansion,
more superficial vascular injury occurs during stent expansion in areas
removed from stent struts themselves.9 First, asking
whether the shape of the areas bounded by stent struts influenced the
degree of damage, we altered stent design so as to alter this shape.
Using stents of which the total surface area and strut thickness were
the same but the geometric configuration different, and using
endothelial loss as a marker for superficial injury, we
demonstrated that the stent design in which the struts created a more
complex and closed area (corrugated-ring design) permitted 33% less
injury in the spaces bounded by each strut than did the stent design in
which the interstrut areas were more simple and open in shape
(slotted-tube design). In contrast, in the absence of a stent,
balloon-artery contact during an angioplasty covers 100% of the
luminal surface, and one would anticipate that denudation would
encompass 100% of the arterial surface.
To visualize balloon-"vessel" interactions at the sites of superficial endothelial injury, we constructed a phantom model using a glass tube in lieu of an artery. During inflation, after the stent struts had contacted the vessel wall, further increases in balloon pressure led to the balloon material being extruded through the openings bounded by stent struts. Balloon extrusion was sufficient to cause direct contact between balloon and glass tube, and the shape of this contact area matched the area of vascular injury previously identified in vivo. For any given stent design, as balloon pressure rises, the area of balloon-artery contact would also rise but would reach a limit of <100% of the arterial surface, always leaving a cuff of surface directly adjacent to the struts free from contact.
Sources of Injury
We next sought to examine what force and stress would be
transmitted to the arterial wall via balloon-artery
contact. Using FEA, we constructed a model to determine the force
applied by a balloon to the arterial surface with boundary
conditions chosen to mimic a balloon extruding between 2 stent struts.
From this surface force, we modeled the amount of stress developed
within the arterial wall. The input variables we
studied were interstrut distance (reflecting stent design) and balloon
expansion pressure and compliance. FEA showed that as interstrut
distance grew, so too did the maximum surface-contact stress and
normalized contact area (Figure 6). This again confirmed that
increasing the geometric complexity of stent design, or increasing the
number of struts for a given arterial surface area, would
reduce the surface-contact stress and contact area imparted by the
balloon to the artery during stent deployment.
Holding interstrut distance and balloon compliance constant, FEA
demonstrated that maximum surface-contact force grew in a nonlinear
fashion as balloon pressure climbed (Figure 5). There was a
rapid rise in predicted maximum arterial-surface force
between 12 and 18 atm followed by a plateau at higher pressures. This
finding is of particular importance, as the pressures chosen to dilate
stents in clinical practice range between 12 and 18 atm.15
Of note, some data suggest that high stent postdilation pressures may
be correlated with greater restenosis.16 Potential
adverse ramifications of high pressure dilation after stent deployment,
particularly with stents imbued with enhanced
thromboresistance,17 will need to be addressed.
Finally, FEA demonstrated that maximum surface-contact stress and
normalized contact area grew as balloon compliance increased,
reflecting greater degrees of balloon extrusion between struts (Figure 6). There was a 15-fold difference in maximum surface-contact
stress between a compliant balloon and a semicompliant balloon at 8
atm. This finding pertains to both stent-deployment balloons and
postdilation balloons, indicating that lower balloon compliance will
lead to lower arterial-wall stress and perhaps less
vascular injury.
Surface-Contact Force and Vascular Injury
Balloon-Artery Interactions
Injury to endothelial cells and the underlying
smooth muscle cells produces experimental neointimal
hyperplasia.18 19 20 21 While denudation of
endothelial cells alone produces mild
neointimal thickening,22 more substantial
neointimal hyperplasia requires direct injury to medial
smooth muscle cells.23 24 In stented arteries, a
correlation exists between the depth of arterial injury and
the extent of intimal thickening.3 4 10 In humans, higher
inflation pressures and larger balloon sizes may also cause greater
neointimal hyperplasia.16 25 26 27 Possible
mechanisms whereby balloon-induced stress may be a determinant of
restenosis include effects of either transient or cyclical
stress on vascular smooth muscle cells.24 28 29 30 31 Also,
acute luminal stretching at the time of angioplasty has been shown to
be an accurate predictor of later luminal loss.32 33 34 35
Superficial injury during stent deployment is the result of balloon and artery vessel wall interactions. During stent placement, the balloon and arterial vessel interactions include 2 opposite elements, balloon extrusion and arterial displacement, as both balloon surface and arterial wall are not totally rigid. If we assumed total rigidity of artery, the balloon would extrude. On the other hand, if we assumed total rigidity (low compliance) of the balloon, the artery would prolapse into the stent-strut interstices during and after balloon expansion. Because neither vessel nor balloon is totally rigid, we included both arterial displacement and balloon deformation in FEA modeling. To represent arterial displacement and balloon extrusion, displacement and pressure loadings were used. The model assumed this highly nonlinear contact as a planar-contact problem. The solution procedures to address contact problems can be found in previous studies.36 37
Our data suggest 3 ways to alter contact stress. First, the contact-stress distribution at the balloon-artery interface is a function of stent-placement pressure. In the elastic region of the balloon material, the maximum surface-contact force increased with increasing deployment pressure. Increasing deployment pressure from 4 to 16 atm, the effective surface stress increased in a nonlinear fashion and reached a maximum in the center of the intrastrut opening. Second, contact area and stress created at the balloon-artery interface are functions of stent geometry. The greater the distance between 2 adjacent stent struts, the more the balloon extrusion, and the greater arterial displacement during and after expansion. The normalized contact area and maximum contact force increased with increasing interstrut distance. Third, balloon-material properties affect the contact area and surface-contact stress. Balloon material with higher compliance would allow more balloon extrusion and more arterial displacement between struts at any given pressure. As the compliance of balloon material chosen for FEA modeling fell, the normalized contact area and maximum contact stress both decreased.
Permanent mechanical stress imposed by stent struts and strain imposed by stent deformation even after balloon withdrawal could also contribute to superficial and deep arterial injury. However, the stress and strain caused by stent deformation after balloon removal are actually lower at the center of interstrut openings than that at the stent struts themselves (data not shown). The mechanical tearing or scraping imposed by stent struts as they traverse the arterial surface during expansion might also contribute to superficial injury.38 Another contributing factor might be fluid-shear stress caused by blood confined to the closed space between balloon surface, stent strut, and arterial luminal wall, a mechanism that distributes surface stress equally over the entire interstrut area. However, none of these mechanisms are consistent with the pattern of endothelial denudation observed.
Study Limitations
This study constructs a theoretical basis for measuring
balloon-artery interactions during stent deployment. Input
parameters for physical arterial-wall
characteristics were taken from published data, and values for diseased
arteries may differ. Specifically, more rigid diseased arteries
undergoing more substantial degrees of dilation would demonstrate much
greater surface-contact stresses. Nevertheless, the relative effects of
varying chosen variables such as balloon material, stent design, or
inflation pressure are not likely to change. We have not examined late
in vivo ramifications of varying balloon-related vascular injury
through altering stent design, balloon material, or inflation pressure.
Stent expansion also imposes injury in the direct vicinity of stent
struts not included in our FEA model. Developing techniques for
3-dimensional FEA analysis and for studying stress
analysis in vivo39 will allow extension of this
model from comparing effects of different parameters in a
relative fashion to identifying optimal design
parameters.
Implications
Balloon-artery interactions during stent placement were observed
and verified by in vivo and in vitro visualization and modeled by FEA.
These interactions may contribute to vascular injury during stent
placement. The acute contact of balloon with artery wall may have
direct impact on vascular injury above and beyond that caused by
balloon angioplasty alone and explain in part the greater degree of
neointimal thickening seen after stent implantation in
experimental animals5 6 7 and humans.1 2 8
Appreciating that the contact stress and contact area are functions of
placement pressure, stent geometry, and balloon compliance may help
direct development of novel stent designs and stent-deployment
protocols so as to minimize vascular injury and optimizing long-term
outcomes.
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Acknowledgments |
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This work was supported by American Heart Association National Center Grant 95004400 (to C.R.), National Institutes of Health Grants HL03104 (to C.R.) and GM/HL 49039 (to E.R.E.), and grants from the Burroughs Wellcome Fund for Experimental Therapeutics and the Whitaker Foundation (both to E.R.E.). We are grateful to Philip Seifert for technical assistance.
Received August 7, 1998; accepted December 4, 1998.
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 B. Balakrishnan, A. R. Tzafriri, P. Seifert, A. Groothuis, C. Rogers, and E. R. Edelman Strut Position, Blood Flow, and Drug Deposition: Implications for Single and Overlapping Drug-Eluting Stents Circulation, June 7, 2005; 111(22): 2958 - 2965. [Abstract] [Full Text] [PDF]
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 F. Vogt, A. Stein, G. Rettemeier, N. Krott, R. Hoffmann, J. v. Dahl, A.-K. Bosserhoff, W. Michaeli, P. Hanrath, C. Weber, et al. Long-term assessment of a novel biodegradable paclitaxel-eluting coronary polylactide stent Eur. Heart J., August 1, 2004; 25(15): 1330 - 1340. [Abstract] [Full Text] [PDF]
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 J. F. LaDisa Jr., L. E. Olson, I. Guler, D. A. Hettrick, S. H. Audi, J. R. Kersten, D. C. Warltier, and P. S. Pagel Stent design properties and deployment ratio influence indexes of wall shear stress: a three-dimensional computational fluid dynamics investigation within a normal artery J Appl Physiol, July 1, 2004; 97(1): 424 - 430. [Abstract] [Full Text] [PDF]
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 J Gunn, N Arnold, K H Chan, L Shepherd, D C Cumberland, and D C Crossman Coronary artery stretch versus deep injury in the development of in-stent neointima Heart, October 1, 2002; 88(4): 401 - 405. [Abstract] [Full Text] [PDF]
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 C. Briguori, C. Sarais, P. Pagnotta, F. Liistro, M. Montorfano, A. Chieffo, F. Sgura, N. Corvaja, R. Albiero, G. Stankovic, et al. In-stent restenosis in small coronary arteries: Impact of strut thickness J. Am. Coll. Cardiol., August 7, 2002; 40(3): 403 - 409. [Abstract] [Full Text] [PDF]
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M. Haude and R. Erbel How big is small? Eur. Heart J., February 1, 2002; 23(3): 198 - 199. [Full Text] [PDF]
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C. Briguori, J. Tobis, T. Nishida, M. Vaghetti, R. Albiero, C. Di Mario, and A. Colombo Discrepancy between angiography and intravascular ultrasound when analysing small coronary arteries Eur. Heart J., February 1, 2002; 23(3): 247 - 254. [Abstract] [Full Text] [PDF]
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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]
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R. Hoffmann, C. Jansen, A. Konig, P.K. Haager, G. Kerckhoff, J. Vom Dahl, V. Klauss, P. Hanrath, and H. Mudra Stent design related neointimal tissue proliferation in human coronary arteries; an intravascular ultrasound study Eur. Heart J., November 1, 2001; 22(21): 2007 - 2014. [Abstract] [PDF]
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S. Windecker, I. Mayer, G. De Pasquale, W. Maier, O. Dirsch, P. De Groot, Y.-P. Wu, G. Noll, B. Leskosek, B. Meier, et al. Stent Coating With Titanium-Nitride-Oxide for Reduction of Neointimal Hyperplasia Circulation, August 21, 2001; 104(8): 928 - 933. [Abstract] [Full Text] [PDF]
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 H. Vernhet, R. Demaria, J. M. Juan, M. C. Oliva-Lauraire, J. P. Senac, and M. Dauzat Changes in Wall Mechanics After Endovascular Stenting in the Rabbit Aorta: Comparison of Three Stent Designs Am. J. Roentgenol., March 1, 2001; 176(3): 803 - 807. [Abstract] [Full Text] [PDF]
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D. E. Drachman, E. R. Edelman, P. Seifert, A. R. Groothuis, D. A. Bornstein, K. R. Kamath, M. Palasis, D. Yang, S. H. Nott, and C. Rogers Neointimal thickening after stent delivery of paclitaxel: change in composition and arrest of growth over six months J. Am. Coll. Cardiol., December 1, 2000; 36(7): 2325 - 2332. [Abstract] [Full Text] [PDF]
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R. Hoffmann and G.S. Mintz Coronary in-stent restenosis--predictors, treatment and prevention Eur. Heart J., November 1, 2000; 21(21): 1739 - 1749. [PDF]
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J. M. Ahmed, G. S. Mintz, N. J. Weissman, A. J. Lansky, A. D. Pichard, L. F. Satler, and K. M. Kent Mechanism of Lumen Enlargement During Intracoronary Stent Implantation : An Intravascular Ultrasound Study Circulation, July 4, 2000; 102(1): 7 - 10. [Abstract] [Full Text] [PDF]
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J. M. Garasic, E. R. Edelman, J. C. Squire, P. Seifert, M. S. Williams, and C. Rogers Stent and Artery Geometry Determine Intimal Thickening Independent of Arterial Injury Circulation, February 22, 2000; 101(7): 812 - 818. [Abstract] [Full Text] [PDF]
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 M. Overhaus, J. Heckenkamp, S. Kossodo, D. Leszczynski, and G. M. LaMuraglia Photodynamic Therapy Generates a Matrix Barrier to Invasive Vascular Cell Migration Circ. Res., February 18, 2000; 86(3): 334 - 340. [Abstract] [Full Text] [PDF]
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