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(Circulation. 2001;103:429.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
Gold-Coated NIR Stents in Porcine Coronary Arteries
From the Harvard-MIT Division of Health Sciences and Technology (E.R.E., P.S., A.G., D.B., C.R.) and the Department of Mechanical Engineering (A.M.), Massachusetts Institute of Technology, Cambridge, Mass, and the Department of Medicine, Cardiovascular Division, Brigham and Women’s Hospital and Harvard Medical School (E.R.E., C.R.), Boston, Mass.
Correspondence to Dr Elazer R. Edelman, Massachusetts Institute of Technology, Division of Health Sciences and Technology, 77 Massachusetts Ave, Room 16-343, Cambridge, MA 02139. E-mail ere{at}mit.edu
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Abstract |
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Background—As endovascular stents are altered to add functionality, eg, by adding radiopaque coatings, biocompatibility may suffer.
Methods and Results—We examined the vascular response in porcine coronary arteries to stainless steel gold-coated NIR stents (7-cell, Medinol, Inc). Stents, 9 and 16 mm in length, were left bare or coated with a 7-µm layer of gold. Physical and material effects were examined in four different gold-coated stent types, two at each length that either had the coating applied to the standard strut, ie, gold coated thicker than controls, or had the coating applied to thinned struts, ie, gold coated of the same thickness as control struts. Simple gold coating exacerbated intimal hyperplastic and inflammatory reactions over 28 days, but postplating thermal processing smoothed the coating surface and negated the adverse tissue response to gold. The relative amounts of base steel and gold coating and their resistances to expansion and collapse determined the extent of stent recoil.
Conclusions—Gold coatings enhance the radiopacity of steel stents, but not without effects on vascular repair. Material effects predominate and can be abrogated by heating coated stents to alter surface finish and material purity. Clinical results may suffer unless consideration is given to material and physical effects of gold.
Key Words: restenosis • stents • thermal processing • vasculature • vascular repair
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Introduction |
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As novel designs and surface preparations have produced endovascular stents with dramatically reduced thrombosis and restenosis, the focus now is on increasing ease of use. Radiopacity in particular is poor with stainless steel and worse when struts are made thinner or spaced farther apart. Changes in design, material, or surface coatings that increase opacity cannot reduce overall functionality and biocompatibility. Stainless steel enables stents to be expanded within tortuous and eccentric lesions. Other metals and materials may not have dynamics that are as favorable. Similarly, as the biological sequelae of implantation are increasingly well defined, it becomes clear that stainless steel is relatively inert within the vasculature. Metal coatings may alter every phase of the response to vascular implantation, including thrombosis, inflammation, and proliferation.
Gold in particular has been touted as a potential coating for stents. Of all the radiopaque metals, gold is the easiest to work with by virtue of its low melting point and high malleability. On the other hand, there are disturbing reports that gold-coated stents incite an exaggerated vascular response.1 We sought to define the biological reaction to gold-coated stents implantation and to determine whether the response stemmed from a fundamental limitation of the physical and material effects of gold or the processes by which the metal was applied.
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Methods |
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Stents
Seven-cell stainless steel NIR stents (Medinol, Inc), 9 and 16 mm in length, were left intact or coated with a 7±2.5-µm gold layer. The 2-step plating process included generation of a "seed layer" to optimize adherence before plating. Because gold plating increased strut thickness by twice the coating depth, stents were electropolished to remove an equivalent 7 µm of steel from all sides of the struts before plating to maintain constant strut dimensions. In all, 5 different gold-plated stents were examined, and each coated stent was compared with uncoated devices subjected to identical processing except for gold plating. The performance of each set of gold-coated stents was compared with that of matched stainless steel controls taken from the same lot of material. Four sets of studies were performed. In the first two, 16-mm stents were used; in the latter two, 9-mm stents were used. In studies 1 and 4 (Table
),
when the coating was applied, the strut thickness was increased by the
twice the thickness of the gold coating. In studies 2 and 3, stent
struts were electropolished before coating so that the thickness after
gold coating was identical to that of the standard stainless steel
stents (the
Table).
As a frame of reference using a known standard, in concert with study
2, three animals received a single stainless steel Palmaz-Schatz stent
(Cordis/Johnson and Johnson) in two coronary arteries. In a final set
of experiments, the standard gold coating was compared with gold
coating subjected to a thermal processing step intended to smooth the
gold surface and potentially remove embedded
impurities.
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Topographical and Elemental Analyses
The surface of the gold-coated stents was
evaluated before and after heat treatment. Surface morphology was
determined via an SEM (Leo 438VP) with a backscatter detector (Leo 400
Centaurus BSD). Elemental analysis was performed with energy dispersive
x-ray spectroscopy (IXRF Analyzer, model 500). Auger electron
spectroscopy (PHI 660) examined the outer stent surface. Surface
topography was defined with atomic force microscopic analysis
(Topometrix Explorer) of 10x10-µm areas and on two linear scans
across the face.
Surgical Procedure
Seventy-eight stents were
implanted2 in 40 domestic
swine (weight, 30 to 40 kg). Thirty-five animals survived
perioperatively; those that died were excluded from further analysis.
Animals were fed standard chow and water, and aspirin (325 mg, Sigma
Chemical Co) was administered once daily throughout the postoperative
period from the day before surgery. After anesthesia induction, animals
received nifedipine 10 mg SL, bretylium 5 mg/kg IV, and cefazolin 500
mg IV. A 7F coronary guiding catheter (AR1 or Hockey Stick, Scimed Life
Systems) was advanced to the coronary ostia via the right femoral
artery. After administration of heparin (200 U/kg IV) and nitroglycerin
(100 µg IC), angiography of the left and right coronary arteries was
performed in orthogonal planes. Sections of each coronary artery judged
to be 2.5 to 3.5 mm in diameter were chosen for stent deployment. A
single standard stainless steel or gold-coated stent was placed in two
of the three arteries.2 All
stents were mounted on 3.0- to 4.0-mm angioplasty balloons (20 mm,
SCIMED Ranger) to provide ratios of balloon/stent to artery of
1.1:1. Stents were advanced over an angioplasty guidewire
(High Torque Floppy, Guidant, Inc) to suitable segments of the coronary
artery and inflated at 8-atm pressure for 30 seconds. Nitroglycerine
100 µg IC was again administered, and angiography was repeated in
orthogonal views. On completion of the procedure, the femoral artery
was ligated, and cefazolin 500 mg IV was administered. The ratios of
balloon/stent to artery were calculated angiographically from balloon
and preplacement lumen diameters measured with digital calipers offline
on cine film.
Twenty-eight days after implantation, animals were anesthetized and euthanized with KCl 40 mEq IV. The hearts were removed, and the coronary arteries were perfused with Ringer’s lactate solution infused into the aortic root at 100 mm Hg, followed by 4% paraformaldehyde in 0.1 mol/L sodium phosphate buffer fixative. The coronaries were dissected, and stented sections were isolated and immersion fixed in 4% paraformaldehyde fixative. Stented arterial segments were oriented longitudinally and embedded with a methacrylate formulation.3 Multiple sections 5 µm thick were cut with a tungsten carbide knife (Delaware Diamond Knives) on an automated microtome (Leica, Inc) from the proximal and distal ends and the midpoint of each stented segment. Sections were stained with hematoxylin and eosin and with ver Hoeff’s elastin stain. Computer-assisted digital planimetry measured lumen, neointimal, and medial cross-sectional areas. Luminal diameter was calculated from luminal area, and stent diameter was calculated from the area bounded by the internal elastic lamina. Histological late loss of luminal diameter was calculated as the difference between stent and luminal diameters. Recoil was calculated as the difference between balloon size at implantation and histologically determined stent diameter. Inflammation was determined by quantitative determination of the number of multinucleated giant cells and by immunostaining for porcine CD45 (allotypic variant, Serotec Ltd) with a low-temperature antigen retrieval and a tyramide signal amplification system kit (Dako, Inc). The percent of immunopositive CD45 cells was semiquantitatively measured in the neointima in 5 fields.4 Injury scores were determined as described.5
Statistical Analysis
For each stented segment, results from each end and
the middle were averaged to minimize sampling error. Data are presented
as mean±SE. For each of the four studies, coated and uncoated groups
were compared with the use of unpaired Student’s
t test, with
P<0.05 considered significant.
ANOVA was used for comparisons of the three groups in the fourth
study.
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Results |
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Topographic and Elemental Analysis
The surface of the gold-plated stents is evident in the microscopic images (Figure 1
). The roughness of the standard gold plating was
equivalent to that of standard stainless steel, and heat treatment
smoothed the surface of the gold plating without erosion. Heated gold
layers were smooth but thin enough to reveal the underlying granular
interface of the stainless steel
(Figure 1c and 1d). The differences between the surfaces were
confirmed by atomic force microscopy. The average roughness of
the unheated gold-coated stents was more than twice the value for
heated stents, with a 3.3-fold–greater mean peak-to-valley height in
profile
(Figure 2). Although surface roughness was reduced with
heating, there was no discernible difference in surface elemental
density by energy dispersive x-ray spectroscopy or Auger analysis
between the nonheated and heated surfaces. More iron was detected to
have diffused into the gold coating of the heated stent, but in none of
the stents did iron reach the stent surface. Initial Auger surveys of
the gold-coated and heated gold-coated stents showed only oxygen and
carbon at the outermost surface. After several cycles of sputtering,
the carbon layer was greatly reduced, and only gold was detected. No
trace contaminants were detected on the surface of the
stents.
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Biological Response
The biological responses to stainless steel and
gold-coated stents 28 days after implantation were compared. Ratios of
balloon to artery for all devices ranged from 1.03 to 1.2 (the
Table
)
and did not correlate with ultimate neointimal size. Two different
stent lengths (9 and 16 mm) were examined, and the coating either was
applied to struts whose thickness was equivalent to that of the control
stents or reduced by twice the thickness coating depth. No
stents were thrombosed at harvest. Differences were observed in the
reaction of stainless steel stents of different dimensions
(Table);
comparisons were made only within specific experiments, not across
experiments.
In every experiment, gold-coated stents produced a greater
neointima than their stainless steel counterparts, the difference being
more profound with shorter stents. Neointimal thickness was increased
by 24% and 26% in the long stents and by 33% and 57% in the short
stents of standard and thinned strut thicknesses, respectively (the
Table
and
Figure 3). In marked contrast, heat processing rendered the
responses to gold-coated stents indistinguishable from uncoated
stainless steel stents
(Figure 3). Although the injury scores in all sections were
low (<0.2), in all but study 1, they were higher in the gold-coated
stents. Because the ratios of balloon to artery were similar between
stent types, the observed differences in injury score likely reflect
late effects rather than acute implantation-related injury alone.
Palmaz-Schatz stents provoked greater intimal thickness (0.34±0.04 mm)
at a higher injury score (0.6±0.3) with lower lumen areas (2.21±0.4
mm2) than any of the gold-coated
devices.
|
The reduction in neointima with thermal processing of
gold-coated stents correlated with a reduction in inflammation to
levels equivalent to uncoated stents. The number of porcine
CD45-positive cells per five high-power neointimal fields in nonheated
gold-coated stents (134.0±18.5) was 2.6-fold greater than the reaction
in uncoated stainless steel stents (45.6±9.1) or heated gold devices
(41.3±7.6, P<0.0001;
Figure 3). Similarly, CD45-positive cells in the neointima
represented 14.8±0.4%, 5.6±0.8%, and 5.7±1.5% of the total cells
for steel, gold-coated, and heated gold stents, respectively, and the
number of multinucleated giant cells increased in gold-plated but not
heated gold-coated stents: 8.4±0.6, 13.2±2.2
(P<0.02), and 8.6±0.9 giant
cells per section for steel, gold-coated, and heated, gold-coated
stents, respectively.
Strut Thickness
The application of a coating by necessity changes
the thickness of the stent strut. We examined struts of two
thicknesses, one that increased the strut thickness by virtue of the
gold coating and one with the same strut thickness achieved by
electropolishing of the steel stent before coating. When the coated
stent struts were polished to equalize coated and uncoated stent
thickness, there was less stainless steel and more soft gold in coated
struts, and these stents exhibited a greater propensity for recoil
(Table).
Correspondingly, when the amount of steel was kept constant and the
gold-coated struts were therefore thicker, recoil dropped. The impact
of recoil on luminal diameter is synergistic with intimal hyperplasia.
For example, recoil was so much less in the coated 16-mm stents when
the 7-µm coating was added to a standard thickness strut that the
ultimate lumen size was greater for the gold-coated stents despite
greater tissue growth.
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Discussion |
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As endovascular stents are altered to add functionality, biocompatibility may suffer. Indeed, gold coatings of a stent type other than that used here elicited greater restenosis than similar uncoated stainless steel devices.1 We now report that although gold coating of stainless steel improves radiopacity, the mode of coating processing determines the hyperplastic and inflammatory reactions. The reduced compatibility of gold-coated stents was completely negated by postplating heating. Moreover, the relative amounts of base and coating metals, and their respective resistances to expansion and collapse, determine stent recoil.
Biomedical Applications of
Gold
Because of its malleability and relatively low melting
point, gold is one of the easiest metals to manipulate, and for >5000
years, gold has adorned jewelry, weapons, goblets and silverware,
homes, and statuary.6 Gold
dental fillings and prostheses were used >3000 years
ago.7 8 9
Early rehabilitation in facial nerve paralysis involved placement of
gold weights or springs in the lower
eyelid,10 and gold materials
were a major part of
cranioplasty.11 Gold has
been used in electromechanical devices by virtue of high electrical
conductivity and corrosion resistance and in a broad spectrum of
applications in biology, pharmacology, and medicine. The cellular
compatibility of this material is high, as evidenced by its use as a
tracer compound following cell motility and defining cell structure
with electron microscopy. Ease of use, coupled with atomic weight and
density, might make gold a natural material for enhancing endovascular
implant radiovisibility. Gold is, however, subject to corrosion in
chlorine-rich environments and is perhaps 100 times less resistant than
316L stainless steel.12
Thus, a central question is whether stents with surface gold would
elicit untoward tissue responses and, if so, whether such a response
was an obligate material reaction or controllable through manipulation
of metal or surface properties.
Our knowledge of gold biocompatibility stems in part from studies of the effects of dental prostheses and other gold-plated implants. The most biocompatible of six single-phase dental metal alloys was the one with the greatest gold content.13 Gold has been used to mark catheters, the ends of balloons, portions of guidewires, and stents. Gold markings have extended from isolated dots to coatings over terminal rings or the entire stent surface. The juxtaposition of two dissimilar materials and differences in surface and mechanical properties can generate profound effects. Surface applications that remove the oxide layer that covers stainless steel may make this inert material less compatible. Surface modifications can create substrate-film mismatches, film defects, volume changes, alterations in film microstructure, impurities, anisotropic growth, or electrostatic effects. Thus, the possibility of surface breaks and cracks from tensile stress or of buckling or curling with compression arises. Metallic coating alterations in charge, hydrophobicity, and texture, as well as surface composition, can influence thrombogenic potential, endothelial regeneration, and intimal hyperplasia. Rougher surfaces increase thrombosis, mural injury, intimal hyperplasia,14 and altered endothelial cell migration,15 and platelets adhere with greater affinity to materials with high surface potential materials and hydrophobicity.16
The earliest clinical use of gold-plated stents was in the genitourinary tract.17 18 Gold-plated stainless-steel prostatic stents produced fewer acute irritative symptoms, no greater infections, and minimally greater encrustations than nitinol stents.17 Gold-coated endovascular stents have also fared well, especially compared with other metals such as copper. Copper, but not gold,19 increased the thrombogenic potential of stents, and gold-plated stents produced fewer macroscopic and histopathologic changes in dog aortae than silver- or copper-plated or Teflon- or silicone-coated devices. Copper-plated stents in particular eroded the vessel wall, with marked thrombus formation and aortic rupture.20 Hehrlein et al14 coated the surface of stainless steel Palmaz-Schatz stents with platinum, gold, or copper by electrochemical deposition or argon ion bombardment. Four weeks after implantation, 6 of 14 galvanized stents, but none of the uncoated or ion-bombarded stents, were occluded by a thrombus. Similarly, neointimal hyperplasia was increased in galvanized coated stents compared with stents coated by ion implantation. In both study groups, the most electropositive coating (platinum or gold) induced markedly less neointimal formation than the least electropositive (copper). Thrombogenic properties of bare and gold-coated stents in flow loops did not differ.21
Nonetheless, recent articles1 have indicated that gold coatings on stents may not be as compatible as their stainless steel counterparts. Seven hundred thirty patients at a single center were randomized to receive a standard stainless steel or 5-µm gold-coated slotted tube stents. Stent occlusion at 30 days was 4-fold higher and the probability of death, myocardial infarction or target lesion revascularization after 1 year was almost twice as great in the gold-plated group. The stents used in that study (InFlow Gold) were different in design and material than those we examined, and the reaction to the gold coating reported in that study1 was far greater than anything we observed. Gold-coated stents in our study failed to elicit a reaction greater than that observed in clinically used devices; the neointima formed in all of the gold-coated stents was less than that observed with Palmaz-Schatz stents placed in identical animals under similar conditions. Thus, it is increasingly clear that even subtle changes in the processing of metal plating can have profound effects on the biocompatibility of a coated device. Some gold-plating techniques clearly endow stents with an excessive inflammatory or proliferative reaction. However, others may not, and those that do can be made more compatible with additional processing.
Benefits of Postplating
Processing
A number of possible interrelated effects might
explain why heating gold-coated stents removed adverse material-tissue
interactions, including smoothing of the stent surface, removal of
impurities, and strengthening of the gold stent interface. The relative
bioinertness of stainless steel arises primarily from the overlying
oxide layer. Application of a metal coat requires removal of this
layer. The intergranular spaces of the stainless steel must then be
covered by the coating or establish nidi for corrosion and potential
reservoirs for contaminants. Coatings that are incomplete, are highly
porous, flake with wear, or crack with stent expansion expose the
underlying metal. Organic contaminants, such as long-chain acids used
as surfactants or cyanate salts used in plating process, can become
trapped in these intergranular spaces. Heating can disintegrate these
contaminants and smooth the surface of the gold coating. Average
roughness values for the heated stents were half of the nonheated and
comparable to plain stainless steel devices. Intergranular spaces or
pores in a porous material within the coating might be sealed or
covered over.
Noble metals are minimally chemically reactive, and within the transition elements, gold is the noblest. Mineral gold is not a pure metal but rather an alloy. Harvested ores may contain more silver than gold. Even gold processed to 99.99% purity retains 100 ppm silver, 20 ppm copper, and 30 ppm other base metals.22 Although it is not clear whether these levels of impurities can alter tissue responses, minor amounts of nickel, molybdenum, and chromium eluted from metal stents can increase thrombogenicity and leukocyte activation in bench-top assays.23 The diffusivity of a compound is temperature dependent, and at some temperatures, the diffusivity is so low that no movement can be detected. The distance one metal will traverse into another during heating is the square root of the product of the diffusivity of the one metal into the other at the specific heating temperature and the time that the material is exposed to that temperature. The diffusivity of gold into stainless steel is so low that it will not move substantially from the coating even at elevated temperatures. Iron, in contrast, which is 74% of 316L stainless steel, will not flow through gold at room temperature but can diffuse completely through a 7-µm gold layer with 100-second exposure to a temperature that will raise its diffusivity to 10-8 cm2/s. We did observe enhanced iron diffusion into the heated gold coating (although it was not sufficient to reach the surface), virtually no impurities in the coating, and no difference in the surface gold elemental content of baked and unheated gold-plated stents.
Nonetheless, even limited metal diffusion can have significant mechanical advantages. Elemental diffusion creates a tighter bond between the gold coat and underlying stainless steel that minimizes the mechanical trauma from buckling or cracking with differential expansion. These theoretical effects, coupled with our data, suggest that if gold coatings are to be applied to stents, they should undergo some type of thermal processing.
Recoil, Intimal Hyperplasia, and
Luminal Stenosis
Coatings by necessity changes strut thickness and
expansion dynamics. The latter may become especially problematic when
stent and coating metals are of different material strengths. Standard
coating techniques increase strut thicknesses by twice the coating
depth and strengthen devices against expansion and recoil. If the
thickness is kept constant but some of the original metal is replaced
with a softer substitute, there will be less resistance to expansion
and recoil. When the thrombotic, inflammatory, and proliferative
responses to the metal coating combine with recoil, there is a
complementary effect on luminal integrity. A metal that elicits a
greater vascular response but resists recoil to a greater extent than
control stents may in fact produce a greater luminal diameter. This was
the case for the 16-mm stents used in the second set of studies whose
coating was laid down on unmodified struts. In contrast, when there is
enhanced recoil and a significant vascular response, luminal diameter
may be decreased even more than anticipated. That we did not observe
the expected lower recoil of gold-coated stents in study 4 likely
reflects the difficulty in making these measurements in an animal model
system at the terminus of the experiments. Further work in metallurgy
and material science will enable independent optimization of stent
coatings and strength.
Conclusions
Coated, plated, and surface-modified stents are the
devices of the future. Analysis of their reactivity is complex and
multifactorial, including interdependence of surface and bulk
properties of the materials and composite devices. There is a tradeoff
between radiopacity and the dynamics of stent expansion, recoil, and
intimal hyperplasia. In a 21st century version of the alchemist’s
dream, postplating processing can turn "plain gold" into "better
gold," reducing inflammatory and intimal hyperplastic
reactions.
Quo ferrea primum desinet ac toto surget gens aurea mundo [The age of iron comes to an end. In every region of the world the golden race appears anew.] P. Vergili Maronis. Ecloga Quarta, 8–10.
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Acknowledgments |
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We acknowledge grant support from the National Institutes of Health (GM/HL-49039, HL-60407 to Dr Edelman; HL-03104 to Dr Rogers) and a gift from Medinol, Ltd. Dr Edelman is an Established Investigator of the American Heart Association. We are further grateful for intellectual input from Dr Jacob Richter and Professors Larry Kaufman and Robert Rose and for the expert technical assistance of Stefan Hesselberg. Surface analysis made use of MRSEC Shared Facilities supported by the National Science Foundation (DMR-9400334).
Received July 14, 2000; revision received August 30, 2000; accepted September 1, 2000.
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References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Kastrati
A, Schomig A, Dirschinger J, et al. Increased risk of restenosis after
placement of gold-coated stents: results of a randomized trial
comparing gold-coated with uncoated steel stents in patients with
coronary artery disease.
Circulation. 2000;101:2478–2483.
[Abstract/Free Full Text]
-
Kjelsberg MA,
Seifert P, Edelman ER, et al. Design dependent variations in coronary
stent stenosis are measured as precisely by angiography as by
histology. Journal of Invasive
Cardiology. 1998;10:142–150.
-
Rogers C, Welt FG,
Karnovsky MJ, et al. Monocyte adhesion and neointimal hyperplasia in
rabbits: coupled inhibitory effects of heparin.
Arterioscler Thromb Vasc Biol. 1996;16:1312–1318.
[Abstract/Free Full Text]
-
Garasic J, Edelman
ER, Squire JC, et al. Stent and artery geometry determine intimal
thickening independent of deep arterial injury.
Circulation. 2000;101:812-818.
[Abstract/Free Full Text]
-
Schwartz RS, Huber
KC, Murphy JG, et al. Restenosis and proportional neointimal response
to coronary artery injury: results in a porcine model.
J Am Coll Cardiol. 1992;19:267–274.[Abstract]
-
Niemi L. Structure,
corrosion and biocompatibility of dental Ag-Pd-Cu-(Au)-(Zn) alloys.
Proc Finn Dent Soc.
1986;82(suppl 1-2):1–30.
-
Hagman HC. 3,000
years of dental gold. Dent Lab
Rev. 1979;54:28–30.
-
Harris JE, Iskander
Z, Farid S. Restorative dentistry in ancient Egypt: an archaeologic
fact! J Mich Dent Assoc. 1975;57:401–404.[Medline]
[Order article via Infotrieve]
-
Loevy HT, Kowitz
AA. The dawn of dentistry: dentistry among the Etruscans.
Int Dent J. 1997;47:279–284.[Medline]
[Order article via Infotrieve]
-
Linder TE, Pike
VE, Linstrom CJ. Early eyelid rehabilitation in facial nerve paralysis.
Laryngoscope. 1996;106:1115–1118.[Medline]
[Order article via Infotrieve]
-
Sanan A, Haines
SJ. Repairing holes in the head: a history of cranioplasty [see
comments]. Neurosurgery. 1997;40:588–603.[Medline]
[Order article via Infotrieve]
-
Steinemann SG.
Metal implants and surface reactions.
Injury. 1996;27(suppl
3):SC16–SC22.
-
Grill V,
Sandrucci MA, Basa M, et al. The influence of dental metal alloys on
cell proliferation and fibronectin arrangement in human fibroblast
cultures. Arch Oral Biol. 1997;42:641–647.[Medline]
[Order article via Infotrieve]
-
Hehrlein C,
Zimmermann M, Metz J, et al. Influence of surface texture and charge on
the biocompatibility of endovascular stents.
Coron Artery Dis. 1995;6:581–586.[Medline]
[Order article via Infotrieve]
-
Palmaz J,
Benson A, Sprague E. Influence of surface topography on
endothelialization of intravascular metallic material.
JVIR. 1999;10:439–444.[Medline]
[Order article via Infotrieve]
-
Seeger J, Ingegno
MP, Bigatan E, et al. Hydrophilic surface modification of metallic
endoluminal stents. J Vasc
Surg. 1995;22:327–336.[Medline]
[Order article via Infotrieve]
-
Yachia D,
Aridogan IA. Comparison between first-generation (fixed-caliber), and
second- generation (self-expanding, large caliber) temporary prostatic
stents. Urol Int. 1996;57:165–169.[Medline]
[Order article via Infotrieve]
-
Holmes SA, Miller
PD, Crocker PR, et al. Encrustation of intraprostatic stents: a
comparative study. Br J
Urol. 1992;69:383–387.[Medline]
[Order article via Infotrieve]
-
Nikolaychik
V, Sahota H, Keelan MH Jr, et al. Influence of different stent
materials on endothelialization in vitro.
J Invasive Cardiol. 1999;11:410–415.[Medline]
[Order article via Infotrieve]
-
Tanigawa N,
Sawada S, Kobayashi M. Reaction of the aortic wall to six metallic
stent materials. Acad Radiol. 1995;2:379–384.[Medline]
[Order article via Infotrieve]
-
Herrmann R,
Schmidmaier G, Markl B, et al. Antithrombogenic coating of stents using
a biodegradable drug delivery technology.
Thromb Haemost. 1999;82:51–57.[Medline]
[Order article via Infotrieve]
-
Dähne W. Gold
refining and gold recycling. In: Schmidbaur H, ed.
Gold: Progress in Chemistry, Biochemistry,
and Technology. New York, NY: John Wiley & Sons Inc;
1999:119–142.
-
Tarnok A, Mahnke
A, Muller M, et al. Rapid in vitro biocompatibility assay of
endovascular stents by flow cytometry using platelet activation and
platelet-leukocyte aggregation.
Cytometry. 1999;38:30–39. [Medline]
[Order article via Infotrieve]
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S. Windecker, R. Simon, M. Lins, V. Klauss, F. R. Eberli, M. Roffi, G. Pedrazzini, T. Moccetti, P. Wenaweser, M. Togni, et al. Randomized Comparison of a Titanium-Nitride-Oxide-Coated Stent With a Stainless Steel Stent for Coronary Revascularization: The TiNOX Trial Circulation, May 24, 2005; 111(20): 2617 - 2622. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ohyama, T. Nishide, H. Iwata, and W. Taki Development of Gold Stents for the Treatment of Intracranial Aneurysms: An Experimental Study in a Canine Model AJNR Am. J. Neuroradiol., January 1, 2004; 25(1): 53 - 59. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Schurmann, J. Lahann, P. Niggemann, B. Klosterhalfen, J. Meyer, A. Kulisch, D. Klee, R. W. Gunther, and D. Vorwerk Biologic Response to Polymer-coated Stents: In Vitro Analysis and Results in an Iliac Artery Sheep Model Radiology, January 1, 2004; 230(1): 151 - 162. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. F. Maitz, M.-T. Pham, E. Wieser, and I. Tsyganov Blood Compatibility of Titanium Oxides with Various Crystal Structure and Element Doping J Biomater Appl, April 1, 2003; 17(4): 303 - 319. [Abstract] [PDF]
|
|
|
|
|
|
R. S. Schwartz, E. R. Edelman, A. Carter, N. Chronos, C. Rogers, K. A. Robinson, R. Waksman, J. Weinberger, R. L. Wilensky, D. N. Jensen, et al. Drug-Eluting Stents in Preclinical Studies: Recommended Evaluation From a Consensus Group Circulation, October 1, 2002; 106(14): 1867 - 1873. [Full Text] [PDF]
|
|
|
|
 |
|
 M. R. Ward, A. Agrotis, P. Kanellakis, J. Hall, G. Jennings, and A. Bobik Tranilast Prevents Activation of Transforming Growth Factor-{beta} System, Leukocyte Accumulation, and Neointimal Growth in Porcine Coronary Arteries After Stenting Arterioscler. Thromb. Vasc. Biol., June 1, 2002; 22(6): 940 - 948. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E Regar, G Sianos, and P W Serruys Stent development and local drug delivery Br. Med. Bull., October 1, 2001; 59(1): 227 - 248. [Abstract] [Full Text] [PDF]
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