(Circulation. 1995;91:2995-3001.)
© 1995 American Heart Association, Inc.
Articles |
Endovascular Stent Design Dictates Experimental Restenosis and Thrombosis
From the Department of Medicine (Cardiovascular Division, Brigham and Women's Hospital) (C.R., E.R.E.), Harvard Medical School, Boston, Mass; and the Harvard-MIT Division of Health Sciences and Technology (E.R.E.), Massachusetts Institute of Technology, Cambridge, Mass.
Correspondence to Campbell Rogers, MD, Department of Medicine, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115.
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Abstract |
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Background Vascular interventions that maximize initial lumen diameter provoke extensive neointimal hyperplasia but minimize its effects, causing long-term lumen size to be greater. Nevertheless, interventions such as endovascular stents, which increase lumen size above that achieved with balloon angioplasty, are subject to frequent thrombosis and restenosis. It has been unclear whether the response to stent-induced injury is determined solely by the degree of stent-induced arterial expansion or whether the geometric configuration of the stent or the material left in contact with the vessel wall also contribute.
Methods and Results We examined the vascular response to steel stents deployed in denuded rabbit iliac arteries for 14 days. In one set of experiments, the effects of stent configuration were examined, holding diameter, mass, surface area, and stent surface material constant. In another set, stent surface material was changed, with mass, configuration, and diameter unaltered. Changing stent configuration to reduce strut-strut intersections by 29% without affecting mass or surface area reduced vascular injury by 42%, thrombosis by 69%, and neointimal hyperplasia by 38%. Monocyte adhesion to stented arteries correlated linearly with vascular trauma and neointimal hyperplasia (r=.96, P<.01 for each). When the stainless steel surface was coated with an inert polymer material, vascular injury and neointimal hyperplasia were unchanged, but thrombosis was eliminated.
Conclusions Surface material and geometric configuration of stents may be more important than postplacement diameter in determining neointimal hyperplasia and thrombosis. Alterations in configuration affect vascular injury and neointimal hyperplasia, while surface material plays a greater role in thrombosis. Monocytes may be important modulators of stent-induced intimal thickening. Clinical confirmation of these findings may alter coronary stent deployment techniques and future stent designs.
Key Words: restenosis • thrombosis • stents
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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The promise of endovascular coronary artery stents is their ability to increase luminal diameter beyond that achieved with balloon angioplasty and potentially to reduce late complications such as restenosis.1 2 3 Currently available metal endovascular stents are extremely thrombogenic, and prevention of subacute thrombosis necessitates potent anticoagulation regimens.4 5 6 7 8 9 10 Only by accepting a 7% to 13% risk of peripheral hemorrhagic complications have subacute stent thrombosis rates been kept below 5%.1 2 Similarly, substantial expansion and overexpansion of the arterial lumen by the stent comes at the expense of a potent stimulus for smooth muscle cell proliferation and neointimal hyperplasia. Cell proliferation is prolonged in stented arteries compared with balloon angioplasty,11 12 13 so much so that 20% to 40% of patients who receive endovascular coronary stents develop significant restenosis.1 2 4 5 10 14 15 The extent and duration of smooth muscle cell proliferation observed after stenting also make it less likely that stent-induced vascular injury can be controlled by experimentally effective drugs, which have thus far failed to reduce restenosis after other less injurious coronary interventions.16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 It has been hoped that better understanding of the mechanisms that drive these complications will enable more rational design of endovascular devices and reduce the need for adjunctive pharmacological treatments.
Clinical and animal studies have suggested that deformation and expansion of the vessel wall are principal determinants of the response to arterial injury.33 34 35 36 Under such a paradigm, redesign of endovascular devices should have little impact on vascular repair unless arterial lumen size is also altered. We tested this hypothesis and examined the effects of stent configuration and material on vascular injury, thrombosis, and neointimal hyperplasia. Stainless steel stents of two distinct designs but of identical mass and surface area were expanded to a fixed diameter. Bare stents of each configuration were compared with others whose surfaces were coated with an inert polymer material. Exploration of mechanisms of stent-induced vascular injury may lead to more optimal stent deployment protocols as well as to novel stent designs, reducing the need for concomitant antithrombotic and antiproliferative drug treatment.
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Methods |
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Surgical Procedure
New Zealand White rabbits (Millbrook Farm Breeding Labs) weighing 3 to 4 kg, housed individually in steel mesh cages and fed rabbit chow and water ad libitum, were anesthetized with 35 mg/kg IM ketamine (Aveco Co) and 4 mg/kg IV sodium Nembutal (Abbott Laboratories). Each femoral artery was exposed and ligated, and iliac arterial endothelium was removed by a 3F balloon embolectomy catheter (Baxter Healthcare Corp, Edwards Division) passed via arteriotomy retrograde into the abdominal aorta and withdrawn inflated three times. A stainless steel stent of one of four designs described below (Fig 1
) was mounted coaxially on a 3-mm angioplasty balloon
(Advanced Cardiovascular Systems), passed retrograde via arteriotomy
into each iliac artery, and expanded with a 15-second inflation at 8-
to 10-atm pressure. Four iliac arteries subjected only to balloon
withdrawal injury without stent placement and four normal iliac
arteries were also harvested and processed for histological
analysis.
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Rabbits were begun on aspirin (Sigma Chemical Co) 0.07 mg/mL in drinking water 1 day before surgery to achieve an approximate dose of 5 mg/kg per day for the duration of the experiment and received a single bolus of standard anticoagulant heparin (100 U/kg, Elkin-Sinn Inc) intravenously at the time of surgery. All animal care conformed to institutional guidelines of Harvard Medical School.
Stents were 7 mm
long, and stent struts were 50 µm thick. One
configuration was a slotted tube13 (Fig 1
,
n=16), and the
other was a series of corrugated rings connected by short longitudinal
bridges (MULTI-LINK, Advanced Cardiovascular Systems; Fig 1,
n=17). An
inert, nonpolar, hydrophobic, and nonbioerodable polymer material
(Thrombo-Shield, Advanced Cardiovascular Systems) was applied as a
3-µm-thick coating to additional stents of either configuration:
slotted tube (n=12) or corrugated ring (n=8).
Tissue Processing
Iliac arteries were harvested either 1 hour
(n=4 each for
slotted tube design or corrugated ring designs) or 14 days after
surgery. Under deep anesthesia with intravenous sodium Nembutal,
inferior vena caval exsanguination was followed by perfusion with
lactated Ringer's solution via left ventricular puncture. Both iliac
arteries were excised and fixed by immersion in Carnoy's solution
(60% methanol, 30% chloroform, 10% glacial acetic acid). Stented
arterial segments were oriented for distal and proximal ends, embedded
in DDK-plast (Delaware Diamond Knives, Inc), and sectioned with a
tungsten carbide knife. Multiple 5-µm cross sections were taken from
each end and from the middle of each stent. Nonstented arteries were
embedded in paraffin and cut on a standard microtome.
The extent of deep arterial injury in each cross section caused by stent struts was quantified histologically in Verhoeff elastin–stained sections using the method of Schwartz et al.36 Each stent strut seen in each arterial cross section was graded as to the extent to which it disrupted the vessel wall: 0 for no disruption of the internal elastic lamina; 1 for disruption of the internal elastic lamina; 2 for laceration of the tunica media; and 3 for disruption of the external elastic lamina. An overall injury score for each cross section was calculated by averaging the scores for individual struts within that section.
As described previously,13 cross-sectional neointimal area was determined using computer-assisted digital planimetry. Arterial circumferences were measured and diameters calculated in four normal arteries from animals of the same weight as those included in balloon-injured or stent-injured groups. In stented arteries, stent diameter was derived from the measured circumference of the internal elastic lamina. Thrombosis was measured by determining both the frequency of complete occlusive stent thrombosis and the portion of the circumference of patent stent-bearing arteries covered with laminar thrombus (measured on histological sections). Nuclear morphology was well preserved in these arteries, allowing differentiation of leukocyte classes. Cells adherent to stented arterial lumina and identified in cross sections stained with hematoxylin and eosin as having monocytoid morphology were counted. Thrombosis, arterial injury, arterial diameter, intimal area, and monocyte number were determined at proximal, middle, and distal sites from each stent, and the results were averaged to minimize sampling error.
Ex Vivo Analysis
One stent of each configuration with or
without polymer material
coating was balloon-expanded ex vivo. Analysis of digitized magnified
video images provided precise measurements of stent diameter after
expansion and metal as well as total surface areas subtended by stent
struts. Four stents of each design were also weighed.
Statistics
All data are presented as mean±SEM.
Comparisons between
stent groups used two-way ANOVA for a factorial design. Comparison of
the balloon-injured group with the stent-injured group used a
two-tailed t test. Probability values less than .05 were
considered significant.
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Results |
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Efficacy of Stent Expansion
Metal stents of either configuration were 7 mm long. Slotted tube stents weighed 4.7±0.4 mg, and corrugated ring stents weighed 5.4±0.2 mg (P=NS). In each case, after expansion, metal accounted for 30±1% of the total surface area. Ex vivo analysis in the absence of vascular constraint to expansion demonstrated full expansion of each configuration to the nominal diameter of 3.0 mm. As in other experimental models and clinical trials,15 elastic recoil in vivo accounted for loss of 10% of the initial diameter: 1 hour after in vivo expansion, stent diameters of 2.66±0.19 mm and 2.69±0.10 mm were observed for slotted tube and corrugated ring designs, respectively (P=NS). Normal iliac arterial diameter in animals of the same size was 2.5±0.1 mm, yielding an initial stent/balloon to artery ratio of 1.2:1.
Vascular Injury
Disruption of normal arterial wall
architecture by the struts of
purposefully overexpanded stents correlates with subsequent
neointimal hyperplasia in a porcine model.36
We measured stent-induced mural disruption in rabbit iliac arteries
undergoing expansion to a balloon/stent to artery ratio of 1.2:1, using
the same scoring system. Corrugated ring stents achieved the same
initial lumen diameters but imposed an arterial injury score of
0.31±0.04, 42% lower than slotted tube stents (injury score,
0.58±0.09,13 P<.0001; see
Table and Fig 2). The application of an
inert polymer coating to stent struts had no effect on vascular injury
imposed by either stent configuration (injury scores of 0.28±0.05 for
coated corrugated ring stents and 0.56±0.05 for coated slotted tube
stents; see Table and Fig 2). The internal
elastic lamina was intact in
all arteries subjected to balloon withdrawal injury alone and as a
result, an injury score of 0 was reported (Fig 2).
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Although the number of strut-strut intersections was 29% lower in the corrugated ring stents than in the slotted tube stents, the surface area of metal in each design was the same, and therefore the number of sites of strut-vessel interaction was not different between the two stent configurations: 10.5±0.3 or 11.4±0.4 struts per cross section for slotted tube or corrugated ring designs, respectively (P=NS).
Neointimal Hyperplasia
Corrugated ring stents caused 38% less
neointimal
hyperplasia than slotted tube stents after 14 days. Intimal area was
0.69±0.05 mm2 for corrugated ring stents and
1.11±0.09
mm2 for slotted tube stents13
(P<.0001; see Table and Figs 3 and
4). As with vascular injury, neointimal
hyperplasia was not significantly affected by the polymer material
coating (intimal areas of 0.69±0.04 mm2
for coated corrugated ring stents and 1.14±0.08 mm2 for
coated slotted tube stents; see Table and Figs 3
and 4).
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It is now established that neointimal hyperplasia provoked by stents is greater than that after balloon injury.11 12 13 In the current experiments, balloon injury alone resulted in an intimal area of 0.22±0.06 mm2 after 14 days, one fifth of that seen after slotted tube stent placement (P<.001) and one third of that after corrugated ring stent placement (P<.01). Comparison of injury scores36 and neointimal areas showed a linear relation across groups receiving stents of either configuration after balloon injury and the group undergoing balloon injury alone (r=.99, P<.0009). Corrugated ring stents caused injury scores and elicited intimal growth midway between those of balloon injury and of slotted tube stents.
Monocyte Adhesion
We and others have reported that
mononuclear cell adhesion and
infiltration into stented arteries may contribute to prolonged
neointimal hyperplasia after this form of arterial
injury.37 38 In the current study, the number of
monocytes
adherent to the luminal surface of stented arteries after 14 days was
markedly reduced in arterial segments containing corrugated ring stents
(22.5±1.8 cells) compared with those containing slotted tube stents
(31.1±2.8 cells, P<.001; see Table). Coating
the stents
did not significantly affect monocyte adhesion (19.0±2.7 cells for
coated corrugated ring stents and 28.2±2.7 for coated slotted tube
stents, P=NS; see Table), and monocytes were
not seen
adherent to the surface of arteries 14 days after balloon injury alone.
A close linear relation was found between monocyte adhesion and
neointimal hyperplasia (r=.96,
P<.008) or vascular injury (r=.96,
P<.01) when stents of both configurations and surface
materials were pooled. These findings support a possible contributory
role for monocytes in the pathogenesis of stent-induced
neointimal hyperplasia.
Thrombosis
Complete thrombosis of endovascular stents in
clinical trials
occurs within a few days of placement and has mandated potent
antithrombotic regimens that include heparin, aspirin, dipyridamole,
dextran, and warfarin. There is increasing pressure to limit the use of
these agents because they raise the rate of peripheral vascular
complications to as high as 7% to 13% of
patients.1 2 3 7 8 9 39
We measured complete and partial
thrombosis 14 days after experimental stent placement. Similar to early
clinical trials, 42% of uncoated slotted tube stents were occluded
with thrombus.13 Polymer material coating reduced this
incidence in slotted tube stents to 8% (P<.01; see
Table
and Fig 5). Partial thrombosis (the fraction of lumen
circumference covered with laminar thrombus) was also reduced 63%,
from 0.29±0.0613 in uncoated to 0.10±0.03 in coated
slotted tube stents (P<.03). Changing stent configuration
alone, without altering surface area, mass, or the material in contact
with the blood vessel wall and lumen, also reduced complete thrombosis
(15% for uncoated corrugated ring stents and 0% for coated corrugated
ring stents, P<.04 and P<.01, respectively,
compared with uncoated slotted tube stents; see Table and Fig
5).
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No difference was seen between the elastic recoil of stents of different configurations after in vitro or in vivo expansion, implying that different incidences of thrombosis were not related to different degrees of acute vessel dilation. No relation was found between the number of adherent monocytes and the presence or amount of partial thrombosis. Thus, thrombosis in this model, like neointimal hyperplasia, was not dependent on the extent of acute arterial dilation. In contrast to intimal growth, however, thrombosis could be altered by changes in the stent material in contact with the blood vessel wall.
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Discussion |
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Endovascular stents increase arterial lumen size at the expense of early thrombosis and prolonged neointimal hyperplasia. Drugs directed at limiting these responses prolong hospitalizations because of the need for intravenous infusions, increased risks of bleeding, and arterial complications at the site of vascular access or stent expansion.1 2 3 7 8 9 39 We wondered whether stent-induced vascular injury and its sequelae were the results of (1) the ultimate deformation of the arterial wall, ie, the strain exerted on the wall, (2) the means by which this deformation was achieved, ie, the geometric allocation of forces necessary to generate this strain, or (3) the stent material that remained in contact with the blood vessel wall after deformation.
Our data show that a reduction in the number of immobile interfaces with the wall was an important determinant of neointimal hyperplasia. Although the stent mass and surface area and the ultimate diameter achieved by stent expansion were all held constant, different degrees of vascular injury, thrombosis, and neointimal hyperplasia were observed with different stent configurations. In contrast, when we altered the stent surface material, we found that the material contacting the vessel wall did not affect vascular injury or neointimal thickening but was an important determinant of thrombosis. The implications of these results are first, that vascular repair after endovascular stent placement is multifactorial, and second, that each factor is dictated by a series of parameters and not simply by lumen size.
Stent Configuration
The two endovascular stent configurations
differed in the way in
which they applied force to the expanded artery. The amount of metal in
each was the same, but the corrugated ring design reduced the frequency
of radial force application by including 29% fewer strut-strut
intersections than the slotted tube configuration. Both stent
configurations were expanded to the same initial diameter with the same
balloon/stent to artery ratio and suffered the same degree of early
recoil (10% loss of diameter). Thus, the acute gains and early losses
for each stent design were similar, with late losses comprising
primarily neointimal hyperplasia.
Disruption of the arterial wall by endovascular stents is greater than that caused by balloon inflation alone,11 12 13 and in models using overexpanded coil stents in swine coronary arteries36 or balloon dilation alone,40 variations in vascular injury matched the variations in neointimal hyperplasia. Our data demonstrate that such injury is not determined by arterial wall stretching and increased lumen size regardless of the means of vessel enlargement. On the contrary, keeping the amount of metal the same but reducing the number of strut-strut intersections by one third reduced disruption of the internal elastic lamina and tunica media by nearly one half. Coincident and commensurate with this reduction were a twofold reduction in neointimal hyperplasia and near elimination of thrombosis. Applying a polymer material coating to stents did not alter arterial injury, attesting to the primary importance of the forces applied by the stent rather than the surface material of the stent in causing vascular disruption.
Our data also suggest a possible biological mechanism for the correlation between vascular injury and neointimal hyperplasia: Monocytes adherent to stented arterial walls were present in increased numbers when increased vascular injury was observed. Cells of the monocyte/macrophage lineage have been reported previously by us and by others to be prominent constituents of stent-induced neointimal hyperplasia.13 37 Mechanisms whereby mural disruption would enhance mononuclear cell recruitment might include medial cell death, release of cellular or extracellular chemoattractants, or delayed endothelial regrowth over the injured vessel wall. Covering stent struts with a thin polymer material reduced monocyte recruitment only slightly, whereas altering vascular injury reduced their number markedly. Hence, this component of the vascular response to stents may be provoked more by mechanical vascular disruption than by an inflammatory response to stent material.
Stent configuration also may alter endothelial regrowth over the denuded artery. In our model, stent placement is preceded by complete balloon denudation of the endothelial lining of the entire artery, and endothelial regrowth in this model after 14 days has not been characterized. It is possible that stents of different configurations might differ in the extent to which they denude intact endothelium during deployment, and remnant endothelium within the stented artery might enhance regrowth and limit both thrombosis and neointimal hyperplasia. These issues are the focus of current investigation in our laboratory.
Stent Surface
To assess the effects of the stent surface
material on vascular
responses, we applied a thin coating of a biologically inert polymer
material to stent struts before implantation. Since all arteries were
stripped of endothelium before stent placement, and all stents
contained the same amount and surface area of metal, the only
difference between groups at the stent-vessel-blood interface was the
stent surface material itself. We found that complete thrombosis was
virtually eliminated by the polymer material coating and was reduced by
69% by reducing the number of strut-strut intersections included in
the stent.
Acute and subacute thrombosis occurred in up to 39% of coronary stents in early clinical trials,3 41 a rate similar to the 42% incidence of complete thrombosis observed in our model. Stimuli for such thrombosis within the blood stream may be the stent itself and/or the injured vessel wall. We have reported that release of heparin from the stent surface reduces thrombosis in vivo,13 and others have demonstrated that application of an inert polymer material to metal stents can reduce platelet deposition early after stent placement.42 43 Our data now demonstrate that stent thrombosis can be limited both by using innovative configuration design to reduce the amount of deep injury to the vessel and by applying a coating at the interface of the metal stent with the blood vessel wall. The polymer material coating might attenuate stent thrombosis by reducing the electronegativity and resultant corrosion of the metal, in turn limiting the hemodynamic and chemical stimuli for platelet adhesion and aggregation and enhancing endothelial cell recovery, among other effects.
Study Limitations
A few potential limitations need to be
considered with respect to
our study. First, although an important feature of endovascular stents
is that they may provide a scaffold for atherosclerotic arterial walls
that prevents mural dissection flaps from impinging on the arterial
lumen, the model used in our study could not address the relative
efficacies of the different stent configurations in this regard.
Second, this model uses elastic peripheral arteries rather than more
muscular coronary arteries, and although the relation that we noted
between vascular injury and neointimal growth has been
described in experimental coronary arteries as
well,36 40
confirmation in other normal or atherosclerotic arterial systems will
shed further light on the generalizability of our conclusions. Third,
we limited our study duration to 14 days, the experimental period most
often used in in vivo models of vascular repair. Although studies in
rabbit carotid arteries have shown that intimal smooth muscle cell
proliferation is somewhat more prolonged after stent placement than
after balloon injury,12 37 the peak rate of
proliferation
still occurs within the same time after either form of injury. Our
study focuses on biological mechanisms underlying this initial period
of accelerated arteriopathy, and it is unlikely in this model that a
later period of reacceleration would occur that would in turn modify
our conclusions.
Conclusions
In an experimental model, we examined how
arterial expansion,
stent configuration, and the material in contact with the blood vessel
wall each contribute to endovascular stent-induced vascular injury and
repair. Configuration-dependent interactions of stent struts with
vessel wall elements, to a greater extent than arterial enlargement or
stent surface material, determine vascular injury and
neointimal hyperplasia. Monocyte recruitment to these areas
may be important in this response. At the same time, the stent material
in contact with the vessel wall plays a greater role in thrombosis.
These findings suggest that stents may not fit into an overall
framework for other coronary interventions, whereby acute gains in
initial lumen size alone determine later luminal loss. Unlike other
interventions, leaving a stent behind within the artery may cause more
severe and prolonged vascular injury and provide a chronic stimulus for
smooth muscle cell proliferation and neointimal
hyperplasia. Stent deployment protocols may need to consider optimal
rather than maximal lumen diameters to limit vascular injury.
Exploration of mechanisms of stent-induced vascular injury may allow a
rational approach to novel stent design, reducing the need for
concomitant antithrombotic and antiproliferative drug treatment.
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Acknowledgments |
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This study was supported in part by grants from the National Institutes of Health (HL-17747, GM/HL49039, AG00294), the Burroughs Wellcome Fund for Experimental Therapeutics, and the Whitaker Foundation. We are grateful to Dr M.J. Karnovsky for critical review of the manuscript, to S. Lam and J. Callol of Advanced Cardiovascular Systems, Inc, for support, and W. Appel and A. Hassan for technical assistance.
Received September 22, 1994; revision received December 7, 1994; accepted December 27, 1994.
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