(Circulation. 1996;93:2161-2169.)
© 1996 American Heart Association, Inc.
Articles |
Paired Comparison of Vascular Wall Reactions to Palmaz Stents, Strecker Tantalum Stents, and Wallstents in Canine Iliac and Femoral Arteries
From the Vascular/Interventional Radiology Division, Georgetown University Medical Center (K.H.B., J.F., T.T., S.V.L., D.L.); the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology (R.V., R.J.); and the Georgetown University Research Resources Facility (J.N.), Washington, DC.
Correspondence to Klemens H. Barth, MD, Division of Vascular and Interventional Radiology, Georgetown University Hospital, Washington, DC 20007.
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Abstract |
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Background Palmaz stents, Strecker stents, and Wallstents, all used clinically, differ substantially in their physical characteristics, yet how differently the vascular wall reacts to them has not been demonstrated conclusively. We therefore undertook a side-by-side comparison.
Methods and Results One stent was implanted into each canine external iliac and/or the flexing portion of the proximal femoral artery. In 9 dogs, Palmaz stents were placed vis-à-vis Strecker stents, with follow-up of 2 and 4 months. In 7 dogs, Palmaz stents were placed vis-à-vis Wallstents, with 4 months of follow-up. Angiographic midstent luminal diameters immediately after placement and at follow-up as well as midstent cross-sectional areas of neointima were compared for significant differences. In addition, neointimal maturation, medial atrophy, and stent-related trauma were assessed. Angiographically, all arteries remained open. The degree of luminal narrowing by recoil and neointima never reached 50% and was modest for Palmaz stents and Wallstents (P=.33) but significantly higher for Strecker stents (P<.0001 compared with Palmaz stents). This corresponded histologically to a significantly thicker neointima (P=.003) over Strecker than over Palmaz stents but not between Palmaz stents and Wallstents (P=.18). Neointimal buildup was generally more pronounced in the femoral artery segments than in the iliac segments. Maturation of the neointima over Palmaz stents was much further advanced than over Strecker stents and slightly more advanced than over Wallstents. Pressure-related atrophy of the tunica media was least for Strecker stents and more pronounced but similar for Wallstents and Palmaz stents. Wallstent wire ends caused some wall trauma; several femoral Palmaz stent struts protruded through the media.
Conclusions The lower-hoop-strength, higher-profile tantalum Strecker stent is affected by vascular wall recoil and evokes a greater degree of neointima formation than the lower-profile, higher-hoop-strength Palmaz stent and Wallstent. Medial atrophy is pronounced outside the latter two stents. The rigid Palmaz stent can penetrate through the vascular wall in flexing arteries.
Key Words: stents • arteries
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Introduction |
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Metallic vascular endoprostheses have been introduced clinically to help retain or restore a patent vascular lumen after balloon angioplasty or mechanical or laser atherectomy and improve long-term patency by increasing early gain in vascular caliber, thus reducing late loss from neointimal buildup. To date, noncoronary Palmaz stents, Wallstents, and tantalum Strecker stents have been in clinical use for some time in the United States and/or in other countries.1 2 3 4 The three stents are distinctly different in design but are used for the same clinical indications.1 2 3 4 The Palmaz stent is the most rigid stent and resists higher compression forces in vitro than the Wallstent.5 The tantalum Strecker stent, having the lowest hoop strength of the three, is very flexible and easily maneuverable to the target lesion.6 Both the Wallstent and the Strecker stent have struts that may move against each other during stent flexion; the Wallstent is fully elastic, the Strecker stent is elastic to a lesser degree, and the Palmaz stent is nonelastic.5 7 Although these mechanical properties had no apparent impact on reported comparative clinical experience,2 anything but a gross difference in biological reactions may be difficult to discover, given the heterogeneity of atheromatous plaque and clinical parameters. However, if these stents are subjected to an identical biological environment in a controlled experimental setting, subtle differences should become apparent that may warrant consideration for choosing the optimal stent. For this purpose, we undertook a direct side-by-side comparison by implanting Palmaz stents vis-à-vis Strecker stents and Wallstents in the paired normal canine external iliac and proximal femoral arteries. Although induction of atherosclerotic lesions would have been desirable from the standpoint of clinical correlation, the composition and degree of the atherosclerotic plaque would have been uncontrollable and would have interfered with the primary aim of comparing biological response with only the stent itself as the variable.
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Methods |
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The comparison study was conducted on 21 conditioned mixed-breed dogs of both sexes weighing 20 to 34 kg (mean, 26 kg). One stent was placed in each of the paired external iliac (referred to as iliac) or proximal femoral (referred to as femoral) arteries or in both. Two series were performed: the first, a series of 11 dogs, compared tantalum Strecker stents with Palmaz stents (designated SP); the second, a series of 10 dogs, compared Wallstents with Palmaz stents (designated PW). In the first series, 9 dogs completed the study. Five had received paired stents only in the femoral and 4 in both the femoral and the iliac arteries. In the second series, 7 dogs completed the study; 6 had received both iliac and femoral stents and 1 only iliac stents. In the SP series, 4 dogs were followed for 2 months and 5 dogs for 4 months. In the PW series, all 7 were followed for 4 months. Among the 5 animals excluded were 3 with incomplete protocols and 2 that died of unrelated causes during follow-up.
Devices Used
All stents were supplied sterile. Clinical
"iliac-type" (8- to 12-mm diameter) Palmaz stents were used
in both series and were supplied courtesy of Johnson & Johnson
Interventional Systems Co. The study was started before the 4- to 9-mm
Palmaz stents became available for clinical use. For
consistency, we decided to continue the use of the 8- to
12-mm stent throughout both studies.
These stents were mounted on 5F, 6F, and 7F noncompliant angioplasty catheters from a variety of manufactures (Bard Inc, Cook Inc, Meditech Inc, Vascath Inc). The Strecker stents were supplied premounted on 5-, 6-, and 7-mm (expanded diameter), 4-cm-long polyethylene balloons with 5F catheter shafts, courtesy of Meditech Inc. The balloon calibers for each pair of Strecker stents and Palmaz stents were identical. The Wallstents (Schneider Europe AG) were purchased premounted in 7-mm diameter only.
Study Protocol
The study protocols for both series were approved by the
Georgetown University Animal Care and Use Committee, with
animal housing and care based on laboratory animal standards
established by the National Institutes of Health. The animals received
aspirin 82 mg/d PO for 2 days before and, starting with the first
feeding after the stent placements, for 3 weeks thereafter. For the
stent placement and for the 2- and 4-month follow-up procedures,
the dogs were fasted overnight and anesthetized with
acepromazine 0.5 mg/kg IM followed by 0.5% sodium thiopenthal, 25
mg/kg IV initially, with additional doses administered as needed. An
airway was provided. The stent placement procedure was carried out
under strictly sterile conditions. Access to the vascular system was
obtained after cutdown through the left common carotid artery, and a
10F introducer sheath was placed retrograde into the left common
carotid artery, followed by systemic heparinization with l00 U/kg and
an additional 50 U/kg if the procedure exceeded 90 minutes. A 5F
"calibrated" pigtail catheter (with marker distances of 20 or 25
mm) was positioned above the aortic bifurcation for dorsoventral
aortofemoral film arteriography in straight- and flexed-leg
positions. The arteriograms in the flexed-leg position were used to
determine the point of maximum flexion of the femoral artery, into
which the stent was to be centered. True iliac and femoral artery
diameters to determine stent sizes were obtained by correction of the
arteriographic diameter (measured under loupe magnification) for
magnification on the basis of catheter reference markers. Stent
diameters of the balloon-expanded Strecker and Palmaz stents were
chosen so that they exceeded the true vessel diameter by up to 1 mm.
The stents were placed under digital road-mapping guidance,
starting with the femoral stents. The balloon-expandable Strecker
and Palmaz stents were expanded by a single complete balloon inflation
to 6 atm pressure. If the proximal or distal or both ends of the stent
were not completely expanded, the deflated balloon was advanced or
retracted slightly and reexpanded with the lowest pressure necessary
for complete expansion; these pressures were always <6 atm. Wallstents
were positioned so that the distal end of the stent emerged distal to
the anticipated final position to allow for considerable shortening of
this stent during expansion. To accommodate some uncertainty during
positioning, Wallstents were always placed first, followed by the
Palmaz stents in matching positions. After stent placement, film
arteriography was repeated (Figs 1A
and 2A). Then the left common carotid artery was ligated,
and the neck wound was closed. The dogs were allowed to recover under a
thermal blanket. Intravenous fluids were continued until
dogs were able to drink water.
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At the end of follow-up, the dogs first underwent arteriography similar to the preplacement and postplacement studies via the right common carotid artery under systemic heparinization. After arteriography, the dogs received a 10 000-U heparin bolus and were euthanatized with 100 mg/kg sodium pentobarbital IV. Immediately thereafter, Ringer's lactate solution was infused into the distal aorta under 100 mm Hg pressure for 5 minutes, followed by in situ fixation with a solution of 4 parts 10% buffered formalin/1 part 3% glutaraldehyde at the same infusion pressure for about 15 minutes until hard fixation of the leg muscles was evident. The aorta-to-bifemoral arterial segment was then removed en bloc and the right side marked by suture. After further fixation in Trump's solution, the specimens were prepared for histological workup. From each stented segment, a 5-mm central block was removed, and the remaining proximal and distal halves were bisected longitudinally. Histological cross sections of the central stent segment and longitudinal sections of the proximal and distal quarters were obtained either after removal of stent struts and paraffin embedding or with the struts left in place and embedding in methyl methacrylate. Hematoxylin-eosin stains were made from all plastic-embedded and Movat stains from paraffin-embedded specimens.
Histology
The cross sections were used for quantitative digitized
morphometry under x15 magnification, after the section with the
greatest intimal proliferation was selected from 8 to 10 central stent
cross sections. After the luminal surface of the neointima,
the internal elastic lamina immediately beneath the stent struts, and
the external elastic lamina had been traced, the areas in between were
calculated. The means for all areas of neointima and media
in each series were compared for statistical significance by paired
Student's t test, with a significance level of
P<.05. The prevalence of neovascularity,
hemosiderin, and macrophages was assessed
semiquantitatively on cross sections as an indicator for maturation of
the neointima on a scale of 0 to 3+, with 0 being absent,
1+ minimal, 2+ moderate, and 3+ extensive. The ratios of collagen and
proteoglycan matrix to smooth muscle cells (SMCs) in the
neointima and of SMCs to collagen in the media were used as
an indicator for the degree of neointimal maturation and
for the degree of atrophy of the tunica media, respectively.
The longitudinal sections were reviewed for the transition of the neointima to the normal intima outside the stent and possible stent-related trauma.
Angiography
Film arteriograms were magnified by loupe, and the stented
midlumen diameters were measured and corrected for magnification by use
of catheter calibration markers. Diameters immediately after stent
placement were compared with those at 2 and 4 months. Changes in
diameters between the stent pairs were compared for significant
differences by the two-tailed t test.
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Results |
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Angiography
Before stent placement, angiography showed normal aortoiliac and femoral arteries in all animals. Iliac artery lumen diameters varied from 5.3 to 6.7 mm (mean, 6.l mm) at the level of stent placement and those of the femoral arteries from 4.4 to 6.2 mm (mean, 5.2 mm). Deployed stent lengths of Strecker stents ranged from 30 to 38 mm (mean, 35 mm), of Palmaz stents from 28 to 33 mm (mean, 30 mm), and of Wallstents from 28 to 49 mm (mean, 36 mm). The immediate poststent luminal diameters, initially identical to the inner stent diameters, are listed in Tables 1
and 2. The lumina
inside Strecker stents were always narrower than those inside Palmaz
stents (P=.0002), despite equal balloon size and pressure at
placement (Fig 1A
). This effect is accounted for by Strecker stent
recoil, not seen in Palmaz stents (Table 1; Fig 1A). At 2 and 4 months,
the lumina inside the Strecker stents had narrowed further to a
significantly larger degree than those inside Palmaz stents (Table 1;
Fig 1B and 1C). This effect is accounted for by the greater thickness
of neointima (Table 3). The PW series showed
all Wallstent diameters to be initially smaller than the designated
stent diameters of 7 mm and significantly less than the Palmaz stents
(P=.0064), which were expanded between 5 and 7 mm, depending
on the caliber of the arteries (Table 2). The differences were more
pronounced in the larger-caliber iliac arteries than in the femoral
arteries, in which Wallstents were more generously sized (Fig 2A).
Vascular wall tonus kept the self-expanding Wallstents constrained
initially, but the elastic force of the stents compensated over time
for the expected further loss in diameter by neointima
(Table 4) to produce virtually no net loss of the
luminal diameter at follow-up angiography (Table 2; Fig 2B and 2C).
Luminal diameter losses inside Palmaz stents were similar in the PW and
the SP series (Tables 1 and 2). The luminal diameters did not differ
perceptibly between the ends and the center of the stents, a finding
confirmed by histological analysis of the
longitudinal sections of stent ends (see below).
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Several femoral Palmaz stents were seen protruding outside the
opacified femoral artery lumen, without corresponding lumen narrowing.
This correlated with histological evidence of stent
strut penetration and was particularly evident on the arteriograms in
the flexed-leg position (Fig 1B).
Histology
The areas of neointima measured on cross sections are
compiled in Tables 3 and 4. They show a statistically significant
difference (P=.003) between the Palmaz and the Strecker
stents for iliac and femoral stents (Fig 3A and 3B).
Although the relatively small number of iliac stents (four pairs) does
not reach a significant difference, the femoral stents do. There was
virtually no difference in the neointimal buildup over the
Wallstents compared with the Palmaz stents (P=.18).
Comparison of the cross-sectional area of media outside the
Strecker stents vis-à-vis the Palmaz stents in the femoral
arteries showed significantly less thinning or better preservation of
the muscular layer beneath the Strecker stents (P=.04)
(Table 5). The PW series and cross-comparison with
the SP series showed that the Palmaz stent and the Wallstent caused
similar degrees of pressure-induced medial thinning (Fig 3A, 3B, and 3C).
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The cellular and matrix contents of the neointima are
listed in Tables 6 and 7 and show the
highest proportion of neovascularity, hemosiderin, and
macrophages in the neointima covering the Strecker
stents and the least over the Palmaz stents, with the Wallstent showing
changes somewhere between the other two under cross-comparison of
the SP and PW series (Fig 3). The percentage of collagen to SMCs was
higher at 4 months than at 2 months for both stents of the first (SP)
series, indicating ongoing neointimal maturation (Table 6).
At the same intervals, the percentage of preserved SMCs in the media
was higher for Strecker than for Palmaz stents. Replacement of SMCs by
collagen in the media as an indicator of pressure-related atrophy
was about equal for Palmaz stents and Wallstents but was less expressed
for the Strecker stents, the latter corresponding to the lesser degree
of medial thinning outside the Strecker stents (Tables 6 and 7).
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Longitudinal sections revealed a smooth transition, with no evidence of
heaped-up neointima over the stent ends in the iliac
and femoral sites, at both the ventral and dorsal aspects. There was,
however, evidence of increased reparative activity (neovascularity,
macrophages, and hemosiderin) around the stent
ends (Fig 4). Several of the Palmaz stents showed
protrusion of stent struts through the media into the adventitia.
However, there was no evidence of false aneurysm formation, but
hemorrhage surrounding the stent end was seen at times (Fig 4A and 4B). The neointima covered those areas smoothly, with a
relatively short taper to the normal intima (Fig 4).
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Wallstent wire ends also penetrated into the media in some animals at
both the iliac and femoral levels (Fig 4C and 4D), but protrusion into
the adventitia as in femoral Palmaz stents was rarely seen.
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Discussion |
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Neointima formation is a ubiquitous response of the vascular wall to a variety of injuries, including iatrogenic trauma, such as surgical graft anastomosis, balloon angioplasty, and stent placement with or without balloon expansion.8 9 10 The degree of reparative reaction remains a potential variable among stents of different materials, surface areas, profiles, and other physical characteristics, such as high or low hoop strength, flexibility, and elasticity and the mode of expansion: by balloon (Palmaz and Strecker stents) or self-expanding (Wallstent).
Our study examined the degree of neointima formation and other histological and angiographic parameters characterizing vascular wall response to three clinically used stents that have substantially different mechanical characteristics but were subjected to essentially identical biological conditions in paired arteries. The Palmaz stent is a rigid slotted stainless steel tube with rectangular strut profiles. The type we used had struts 80 µm high and about 230 µm wide. The Wallstent consists of a braided mesh of a round, cobalt-based-alloy wire. The type we used was made of 100-µm-caliber wire. Larger-diameter Wallstents are fabricated of heavier-gauge wire.7 Wire crossing points double the stent profile. The Strecker stent is knitted from a single round, 100-µm-caliber wire of elemental tantalum. The interlocking loops double the stent profile, and there is a tendency of the wire loops to rise slightly over a flat surface.6
The modulus of elasticity of the 8- to 12-mm Palmaz stents as an
indirect measure of hoop strength and resistance to external
compression is about 1.5 times greater than that of a
similar-caliber Wallstent and about 7 times greater than that of a
Strecker tantalum stent when subjected to about 1 mm of
strain.5 Since the Palmaz stent has virtually no
elasticity, higher strain results in plastic deformity, whereas both
the Wallstent and the Strecker stent remain elastic. The hoop strength
of the 8.5-mm Palmaz stent, the type used in the present study, was
found to be lower when the stent was only partially
expanded.5 The hoop strength of the 5- to 9-mm Palmaz
stent was actually found to be slightly higher than that of the 8- to
12-mm stent after both types of stents had been expanded to the same
8-mm diameter. This would mean a reduction in the difference in hoop
strength from the Wallstent in our experimental setting. Because no
comparative measurements are available at the 6- to 7-mm Palmaz stent
expansion levels, this difference remains speculative but should be of
limited interest for the present results, since the amount of
neointima found over either stent was similar. The Strecker
stent, with its severalfold lower hoop strength than either of the two
other stents, indeed showed a significantly higher
neointimal buildup. The low hoop strength also explains the
immediate loss of stent diameter after placement compared with the
Palmaz stents after both stents had been balloon-expanded to the
same diameter. Adding neointima to caliber loss by recoil
resulted in some instances in diameter narrowing of 
40%. Delayed
expansion of Wallstents after deployment by elastic forces almost
completely compensated for neointima, showing virtually no
net loss of luminal diameter at 4 months vis-à-vis an average
net loss of 12% inside Palmaz stents. Given the same degree of
neointima formation, Wallstents should otherwise have shown
the same net loss in luminal diameter. In recognition of this property,
the manufacturer actually recommends choosing Wallstents about 1 mm
larger than the vessel lumen to be restored (see package label). For
the Strecker stent, such a recommendation should perhaps call for an
even larger size. Contrary to our initial expectation, the Strecker
stent offered no advantage on the basis of its excellent flexibility
with regard to preserving the lumen of the flexing femoral arteries; in
fact, the neointimal buildup there was the highest.
To consider hoop strength the sole factor responsible for the observed biological differences would probably be too simplistic, because experimental results conflict. In a recently published study, the same stent design with high hoop strength (rigid) produced a significantly thicker neointima in swine iliac arteries than the lower-hoop-strength (flexible) stent after 5 weeks.11 However, another study showed no statistical difference in neointimal thickness in canine femoral arteries between the regular braid Wallstent and the "less-shortening" Wallstent, the latter having a lower hoop strength.12 Although the hoop strength of the regular braid Wallstent, the type we used in the present study, is two to three times greater than the less-shortening types, both types have considerably higher hoop strength than the Strecker stent.5
Stent profile also has an effect on neointimal thickness. The Strecker stent, because of its knitted loop design, has the highest profile in the area of the interlocking wire loops. As seen best under scanning electron microscopy, the neointimal "blanket" attempts to smooth the wall surface by leveling the "valleys" between the "hills" caused by the stent struts rising over the luminal surface.6 When the hills are higher, the valley floors are raised as well, leading to an overall thicker blanket. The Wallstent has crossing struts, too, but with a lower profile.
Experimental balloon angioplasty showed that elastic recoil of the vessel wall is associated with increased neointima formation.13 14 This factor also deserves consideration for low-hoop-strength stents, as alluded to above. Our findings correlate with another study of the thickness over Strecker stents of neointima deposited in femoral arteries of sheep.15 Certain metal properties or coatings also play a role in the degree of neointima formation as well as the type of cellular response16 ; however, none of the three stents used here have been shown to evoke foreign-body reactions.6 17 18
Finally, mesh size influences neointimal growth. For a given design, the tighter the mesh or the more metal per unit area, the higher the expected neointimal growth.19 However, the open surface areas of the three stents in our study are rather similar. Increased neointimal buildup related to balloon expansion of a stent was alleged in an experimental comparison between self-expanding Gianturco "Z" stents and balloon-expanded Gianturco-Roubin "bookbinder" stents in atherosclerotic miniature swine.20 According to our results, the differences are better explained by the lower hoop strength of the bookbinder stent than by the fact that it is balloon-expanded. To evaluate the influence of balloon expansion, we deliberately abstained from balloon-dilating the Wallstent initially, as may be done in clinical practice. In the latter situation, inadequacy of the immediate poststent lumen triggers this action; that was not an issue in our study.
Examination of the cellular and matrix composition of the neointima showed a striking difference between the maturation of the neointima between the three stents, particularly between the Palmaz and Strecker stents, for which results at 2 and 4 months were available. In an earlier study with Strecker stents in canine aortas, we found the stents to be completely covered with endothelium within 3 weeks.6 The neointimal growth phase differs among experimental animal species and lasts roughly 1 to 2 months in dogs, followed by a maturation phase.6 17 21 22 Ultimately, what starts as a richly cellular vascularized tissue becomes largely collagenous.6 17 22 At 2 months and definitely at 4 months, virtually all Palmaz stents were covered with a collagenous neointima, whereas considerable amounts of phagocytes, SMCs, and blood vessels were still present over the highly flexible Strecker stents, particularly in the flexing femoral arteries, and to a lesser degree over the Wallstents. Because we ended our observation at 4 months, we can only speculate about the additional time required for intima maturation over Strecker stents and Wallstents compared with Palmaz stents. What causes the differences in maturation remains speculative; motion of the stent struts must be considered a factor, particularly for the Strecker stent. This motion increases shear forces on platelets, which in turn can provide a sustained stimulus for microthrombi. Organization of such thrombi may contribute to the overall neointimal thickness. There is experimental evidence that immobilized artery segments are less susceptible to intimal hyperplasia.23 It is not known how long the ingrowing tissue allows the struts of Strecker stents to move; however, experimental studies with Wallstents have shown that stented arteries lost their wall compliance after 2 weeks, and the vessels became stiff.24
Histological changes outside the stent have generally not been the focus of studies on stent-related vascular reactions; however, thinning of the media has been observed by others studying stent-related histology.25 Our finding that the higher-hoop-strength Palmaz stents and Wallstents were associated with a greater degree of atrophy of the media than the Strecker stent is no surprise. Earlier experimental evidence gained from embolized detachable balloons shows that chronic pressure exerted on the vascular wall leads to medial thinning.26 If Wallstents and Palmaz stents lead to such wall transformation, would we then have to expect arterial aneurysms to evolve over the years in stented arteries, or does the stent itself protect against such late events? The answer may hinge, in part, on the strength of the transition between the atrophic media under the stent and the normal media adjacent to the stent.
In the flexing femoral arteries, we found trauma to the arterial wall, particularly by the Palmaz stents and to a lesser degree by the Wallstents. We did not observe perforation; therefore, it is apparent that the trauma by these stents occurs over time and not acutely. Interestingly, this degree of chronic trauma to the media and adventitia occurred beneath a smooth transition of the neointima to the normal intima. Use of more completely expanded 4- to 9-mm Palmaz stents, which would be expected to be more rigid, might have increased this type of chronic trauma.
With respect to clinical relevance of the experimental results, it is obvious that none of the stents occluded the artery or produced what would be considered a hemodynamically significant stenosis, although the Strecker stent came close at times. The information provided by this study should help to achieve a more rational choice of stents for a particular clinical application, considering the need for maneuverability to the target, when flexibility may be critical; hardness of plaque, when stent rigidity may be decisive; or deployment in an artery subject to extensive motion, such as coronary arteries and flexing common femoral or popliteal arteries, when a rigid stent may cause wall trauma.
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Acknowledgments |
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This work was funded in part by the Edward Bennett-Williams Memorial Grant for Radiological Research at Georgetown University Hospital. Material grants (vascular devices) were received from Meditech Inc, Division of Boston Scientific, Inc, Watertown, Mass, and Johnson & Johnson Interventional Systems Co, Warren, NJ. We acknowledge the technical support by Ann Wright, LATG, CVT, and Rafi Khallili, CVRT, as well as Linda Albertson's help in typing and editing this manuscript.
Received July 18, 1995; revision received November 29, 1995; accepted December 13, 1995.
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