(Circulation. 1999;99:44-52.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Pathology of Acute and Chronic Coronary Stenting in Humans
From the Department of Cardiovascular Pathology (A.F., A.J.C., R.V.), Armed Forces Institute of Pathology, Washington, DC; the Mayo Clinic (G.S., W.D.E., R.S.S.), Rochester, Minn; and The University of Ottawa Heart Institute and Ottawa Civic Hospital (V.M.W.), Ottawa, Ontario, Canada.
Correspondence to Renu Virmani, MD, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000.
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Abstract |
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Background—Despite the increasing use of stents, few reports have described human coronary artery morphology early and late after stenting.
Methods and Results—Histology was performed on 55 stents in 35
coronary vessels (32 native arteries and 3 vein grafts) from 32
patients. The mean duration of stent placement was 39±82 days. Fibrin,
platelets, and neutrophils were associated with stent struts 
11
days after deployment. In stents implanted for 3 days, only 3% of
struts in contact with fibrous plaque had >20 associated inflammatory
cells compared with 44% of struts embedded in a lipid core and 36% of
struts in contact with damaged media (P<0.001).
Neointimal growth determined late
histological success, and increased
neointimal growth correlated with increased stent size
relative to the proximal reference lumen area. Neointimal
thickness was greater for struts associated with medial damage than
struts in contact with plaque (P<0.0001) or intact
media (P<0.0001). When matched for time since
treatment, neointimal cell density in stented arteries was
similar to that in unstented arteries that had undergone balloon
angioplasty and showed similar proteoglycan deposition.
Conclusions—Morphology after coronary stenting demonstrates early thrombus formation and acute inflammation followed by neointimal growth. Medial injury and lipid core penetration by struts result in increased inflammation. Neointima increases as the ratio of stent area to reference lumen area increases. Deployment strategies that reduce medial damage and avoid stent oversizing may lower the frequency of in-stent restenosis.
Key Words: stents • coronary disease • restenosis • angioplasty • pathology
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Intracoronary stent placement is being used increasingly for the treatment of atherosclerotic coronary disease. Emergency coronary artery stent placement for abrupt or threatened artery closure due to arterial dissection after PTCA has been a valuable treatment in maintaining lumen patency and reducing the need for urgent coronary bypass surgery.1 The use of stents as primary therapy for coronary atherosclerosis has gained widespread acceptance, with reports of reduced restenosis rates in selected lesions compared with PTCA.2 3 Currently, coronary stenting in acute myocardial infarction is under active investigation.4
Although stents reduce restenosis rates in carefully selected lesions,2 3 in-stent restenosis remains a recognized clinical problem5 and can be expected to increase in incidence as coronary stenting becomes more frequent and is used in less ideal lesions.6 Despite the tremendous expansion of the use of coronary stents, there have been few published data on the pathology of stents deployed in human coronary arteries.7 8 9 The pathology of human coronary stenting may provide insights into the biology of stent–vessel wall interaction and guide approaches to therapies to prevent or treat in-stent restenosis.
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Methods |
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In brief, human stented coronary arteries were either embedded whole in methylmethacrylate or cut transversely for paraffin embedding (complete details of the methods will be provided by the authors on request). Histological observations consisted of plaque-stent interaction, thrombus formation, inflammation, and the presence of a neointima. In native arteries, each stent strut was evaluated with respect to contact with plaque or media, and the media was determined to be damaged or intact. The extent of arterial injury at the site of stent struts was graded by the method of Schwartz et al.10 For arteries stented for
3 days, inflammation around each strut was assessed, and
the following scale for inflammatory cells adjacent to struts was used:
1+, 0 to 10 inflammatory cells/strut; 2+, 11 to 20 inflammatory
cells/strut; and 3+, >20 inflammatory cells/strut. Immunohistochemical
staining for detection of smooth muscle cells and macrophages
was performed in selected cases.
In native coronary arteries stented for >30 days, intimal
thickness at each strut was measured and strut location recorded
(in contact with plaque, intact media, or damaged media). A long-term
histological success was defined as a percent area
stenosis 75% and failure as stenosis >75%. Native
coronary arteries stented for >30 days (5 stents) were
compared with coronary arteries with PTCA alone (10 arteries)
matched for duration of stent placement or PTCA. Staining with Alcian
blue was performed to identify proteoglycans in the
neointima and their component
glycosaminoglycans (hyaluronic acid, chondroitin
sulfate, dermatan sulfate, and heparan sulfate), and staining was
repeated after 3 hours of testicular hyalidase digestion.
Neointimal cell density and neointimal
thickness were determined.
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Results |
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Fifty-five stents in 35 coronary vessels (32 native coronary arteries and 3 saphenous vein bypass grafts) from 32 patients (mean age, 64±10 years; 17 men and 15 women) with stents were studied. Coronary artery stents were obtained at autopsy in 28 patients; stents in saphenous vein grafts were obtained at repeat bypass surgery in 3 patients, and a stent in a native coronary artery was obtained at the time of cardiac transplantation in 1 patient. In autopsy cases, the cause of death was acute myocardial infarction in 18 cases, sudden unexpected cardiac death in 7, and noncardiac death in 3. The mean number of stents per artery was 1.6±1.1 (range, 1 to 4 stents). The 32 native coronary stents were placed as follows: left main, n=3; left anterior descending, n=12; left circumflex, n=8; and right coronary, n=9. The indication for stenting was primary therapy in 18 and suboptimal result from PTCA or significant arterial dissection in 17. Adjunctive PTCA was performed in all cases, along with atherectomy in 4 cases. The clinical diagnoses at the time of stenting were unstable angina in 13 cases, acute myocardial infarction in 7, and stable angina in 12. Bailout stenting, defined as stenting for threatened or acute vessel closure after PTCA, was performed in 6 patients.
The mean duration of stent implantation for the 55 stents was 39±82
days (range, 0.5 to 390 days), with 25 stents (from 14 patients)
examined 3 days after implantation, 8 stents (4 patients) from 
4 to
11 days, 11 stents (4 patients) from 12 to 30 days, and 11 stents
(10 patients) after >30 days (mean, 175±105 days). A total of 142
arterial sections (137 native coronary arteries and
5 saphenous vein bypass grafts) containing stents were analyzed
(Table 1
).
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Plaque compression (Figure 1) by stent
struts was observed in 30 (94%) of 32 patients and 129 (91%) of 142
arterial sections and was seen in all stent designs. A
lipid core was present in the plaque in 66 sections (21 of 32
patients), and the core was focally penetrated by stent struts in 17
sections (26%; 11 patients; Figure 2):
14 of 44 sections containing a Palmaz-Schatz stent, 2 of 13 containing
a Gianturco-Roubin stent, 0 of 1 containing a Wiktor stent, and 1 of 8
containing a Gianturco-Roubin II stent.
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Platelet-rich thrombi were associated with stent struts (Figure 3A) in 65 of the 142 arterial
sections (19 of 32 patients) and were related to the duration of stent
implantation: 44 (72%) of 61 sections at 3 days (13 of 14 patients),
14 (78%) of 18 sections at 4 to 11 days (3 of 4 patients), 7 (24%) of
29 sections at 12 to 30 days (2 of 4 patients), and 0 of 34 sections at
>30 days (0 of 11 patients (P<0.0001). The presence of
platelet deposition around stent struts at 3 days was similar in
Palmaz-Schatz stents (33 [80%] of 41 sections) compared with
Gianturco-Roubin stents (8 [62%] of 13 sections; P=NS).
Fibrin-rich thrombi were also commonly seen around stent struts,
especially early after stenting (Figure 3B). All 79
arterial sections from stents at 11 days (in 18 of 18
patients) had fibrin associated with stent struts; conversely, 12
(19%) of 63 sections and 7 of 14 patients at 12 days had stent
fibrin (P<0.0001).
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Acute inflammatory cells (neutrophils) associated with stent struts
were present in 48 (79%) of 61 arterial sections and
12 of 14 patients in stents implanted for 3 days, 15 (83%) of 18 at
4 to 11 days (3 of 4 patients), 21 (72%) of 29 at 12 to 30 days (3 of
4 patients), and 0 of 34 at >30 days (P<0.0001 for all
time points versus >30 days). Chronic inflammatory cells (lymphocytes
and macrophages) around stent struts were also commonly seen at
all time points: 50 (82%) of 61 sections at 3 days (11 of 14
patients), 12 (67%) of 18 sections at 4 to 11 days (3 of 4 patients),
28 (97%) of 29 sections at 12 to 30 days (4 of 4 patients), and 29
(85%) of 34 sections at >30 days (9 of 10 patients).
Inflammation associated with stents 3 days after implant in native
coronary arteries was related to the underlying
arterial wall morphology (Figures 4 and 5);
71% of struts in contact with fibrous plaque had 10 associated
inflammatory cells (1+ inflammation) compared with 11% of struts
embedded in a lipid core and 19% of struts in contact with damaged
media. In contrast, only 3% of struts in contact with fibrous plaque
had 3+ inflammation (>20 associated inflammatory cells) compared with
44% of struts embedded in a lipid core and 36% of struts in contact
with damaged media (P<0.001).
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A neointima consisting of spindle-shaped mesenchymal cells
(
-actin positive smooth muscle cells) within a proteoglycan matrix
associated with stent struts was not present in any section in any
of the 18 patients with 11 days implant duration; 45% of sections (2
of 4 patients) at 12 to 30 days (Figure 6) and 100% of sections (all 10
patients) at >30 days had spindle-shaped cells in a proteoglycan-rich
matrix (P<0.0001). Multinucleated giant cells were
present in only 3 (10%) of 29 sections at 12 to 30 days and were
more frequently seen in older stents (10 [29%] of 34 sections at
>30 days; Figure 7).
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The findings in the 3 patients with stenting of saphenous vein grafts
were similar to those in the 32 patients with stenting in native
arteries. In a 3-day-old Palmaz-Schatz stent, the stent wires focally
penetrated the thin fibrous cap and were embedded in the large necrotic
core of the lipid-rich plaque, with the necrotic core prolapsing into
the lumen (Figure 8). A well-defined
neointima (smooth muscle cells in a proteoglycan-collagen
matrix), focal plaque compression, and chronic inflammatory cells
associated with stent struts were present in the 2 patients with
chronic (120 and 270 days) Palmaz-Schatz stents in vein bypass
grafts.
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Arterial Injury and Coronary Stenting
There were a total of 1036 stent strut sites identified in the 137
sections of native coronary arteries, of which 643 (62%) of
1036 struts were in direct contact with atherosclerotic plaque. Of the
remaining 393 struts (38%) in contact with the media, medial damage
was present at 120 struts (30%) and medial compression without
laceration of the internal elastic lamina (IEL) at 215 struts (55%);
the media was unremarkable at 58 struts (15%). The mean
arterial injury score (Schwartz scale10 ) for
the arterial sections in which focal medial damage was
present was 0.73±0.80. When medial damage was absent and stent
struts were associated with a normal or compressed media, the injury
score was 0.11±0.21.
Neointimal Growth in Long-Term Stenting
In stents implanted for >30 days (mean, 175±105 days),
neointimal thickness at stent strut sites was greater when
medial damage (medial laceration or rupture) was present
(0.69±0.29 mm) than when struts were in contact with plaque
(0.33±0.26 mm; P<0.0001) or struts in contact with an
intact media (0.29±0.23 mm, P<0.0001, Figure 9). Ultimate histological
success was dependent on lumen area and neointimal growth
within the stent (Table 2). The mean
neointimal area and neointima area/stent area
in successes were 2.2±1.1 and 0.39±0.12
mm2, respectively, versus 3.9±1.9 and
0.68±0.15 mm2 in failures, respectively
(P<0.006 and P<0.0001). There were no
differences between successes and failures with respect to areas of the
external elastic lamina, IEL, plaque, or stent (Table 2). There
was a significant linear correlation (P<0.0001,
R2=0.54) between increased
neointimal growth and increased stent size relative to the
proximal reference coronary artery lumen (Figure 10).
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Chronic Stenting Versus PTCA: Neointimal Cellularity
and Proteoglycans
The number of neointimal
cells/mm2 in native coronary arteries
stented for >30 days was 3280±869, similar to that in PTCA arteries
(3260±851 cells/mm2; Figure 11, A1-A2, B1-B2) matched for time
since treatment (195±131 days for stents and 180±137 days for PTCA).
The neointimal area was greater in the stented segments
than in PTCA arteries (3.1±1.6 versus 1.9±1.2
mm2, respectively; P<0.05). However,
IEL area was larger (11.6±2.1 mm2) with
stent placement than with PTCA (7.9±2.1
mm2, P=0.0001), so that the
neointima corrected for artery size
(neointima/IEL) was similar in stents and PTCA (0.26±0.16
versus 0.26±0.10, respectively; P=NS). The mean
neointimal thickness in the stented arteries
(0.39±0.26 mm) was smaller than in PTCA vessels (0.51±0.24
mm), but this difference did not reach statistical significance.
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Alcian blue staining of stented and matched PTCA arteries
demonstrated similar patterns of neointimal proteoglycan
deposition. Alcian blue staining showed strong blue staining of the
neointima in stented and PTCA arteries (Figure 11
, A3 and B3). After testicular hyalidase digestion, there was similar
light staining for heparan and dermatan sulfate in stented and PTCA
arteries (Figure 11, A4 and B4). These data identify
chondroitin sulfate and hyaluronic acid as the predominant
neointimal proteoglycans in PTCA and stented arteries.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study demonstrates the time course of histological vascular responses to coronary stenting in humans. Early after stenting (
11 days), fibrin,
platelets, and acute inflammatory cells were nearly always
present in association with stent struts. The
stent–arterial wall interface influenced the severity of
associated inflammation; increased numbers of inflammatory cells were
seen when the stent strut was adjacent to injured media or lipid core
rather than fibrous plaque. Chronic inflammation was also commonly
observed adjacent to stent struts at all time points, especially 12
days after stenting. Plaque was compressed by stent struts (seen in
91% of vessel sections) in the present study. However, the concept
that stents provide a boundary that excludes the underlying plaque from
the lumen was not supported by the present study; penetration of
the stent struts into a lipid core was common (26% of
arterial sections with a lipid core had stent struts
embedded in the core). A neointima containing smooth muscle
cells was recognized beginning 
2 weeks after stenting. In longer-term stents (>30 days after implant), histological success or failure was determined by neointimal growth within the stent and was not influenced by artery or stent size. Neointimal thickness was increased when medial damage was present compared with struts in contact with atherosclerotic plaque or an intact media. Furthermore, increased intrastent neointimal growth was present in histological failures, and increased neointimal area correlated with increased stent size relative to the proximal reference artery lumen. Therefore, stent oversizing relative to the reference lumen appears to be an undesirable goal in deployment. Intravascular ultrasound may be particularly useful in determining proximal reference lumen area. A stenting strategy in which stents are expanded to a point at which no gradient exists from the proximal reference to the stent may be beneficial. The present study is the first to compare whole arterial sections and to show neointimal cell density and type of proteoglycan deposition in coronary stents similar to those in matched PTCA coronary vessels. In these arteries, the neointimal area was greater in stented arteries than in arteries with PTCA, but this difference was accounted for by the larger vessel size in the stent group.
Previous Pathological Studies of Stenting in Humans
Few pathological observations of coronary stenting
in humans have been reported. Anderson et al8
reported pathological findings in 4 cases of Gianturco-Roubin stenting
in coronary vessels: 2 native coronary arteries and 2
coronary bypass vein grafts. At 21 days, stent
endothelialization was present, and a thin
neointima containing smooth muscle cells was
seen.8 In vein grafts at 19 weeks and 6 months, a smooth
muscle cell–rich neointima and occasional chronic
inflammatory cells were seen.8 In a study of 11 human
coronary stents, 4 of which were placed for restenosis
after PTCA, Komatsu et al9 showed actin-positive intimal
smooth muscle cells 30 days after stenting. Van Beusekom et
al7 studied saphenous vein coronary bypass grafts
with Wallstents (21 stents in 10 patients). At 3 days, leukocytes,
platelets, and fibrin were evident, and at 3 months, there was
complete endothelial stent coverage and a smooth muscle
cell–rich neointima. At 6 to 10 months, atherosclerotic
plaque, foam cells, and cholesterol crystals were observed;
it was suggested that stent- induced atheroma formation
may occur.7 In the present study, the
neointima was composed of smooth muscle cells in a
proteoglycan-rich matrix. The presence of atherosclerotic plaque within
the stent is likely due to penetration of struts into the necrotic core
and prolapse of plaque between stent wires rather than stent-induced
accelerated atherosclerosis.
Comparison to Stenting in Experimental Animal Models
In the porcine restenosis model, thrombus adjacent
to stent struts composed of fibrin and trapped erythrocytes with acute
inflammatory cells is seen at 24 hours.11 At 7 days, there
is organization of the thrombus associated with macrophages;
however, neutrophils are still observed.11 From 14 to 28
days after stenting, smooth muscle cells are the predominant cell type,
with occasional chronic inflammatory cells present.11
These data in the pig model regarding inflammation and thrombus
closely reflect the findings observed in human coronary
stenting early after implantation (with a relatively longer duration of
healing in humans).
The type of vascular injury in stented normal arteries in experimental animals differs considerably from that in human atherosclerotic arteries. In normal pig arteries, for example, stent oversizing to produce a proliferative neointimal lesion results in direct medial injury (compression or laceration) by stent struts. In contrast, in humans, we observed that 62% of stent struts were in direct contact with atherosclerotic plaque, not media; medial compression by stent struts or medial damage associated with struts was present at 32% of struts.
Arterial Inflammation and Injury: Clinical
Implications
Experimental studies suggest important relationships among
inflammation, vascular injury, and neointimal growth. In
stented, nonatherosclerotic, balloon-injured rabbit iliac arteries,
peak monocyte adherence was observed 3 days after stenting, with
maximal proliferation seen at 7 days.12 There was a linear
correlation (R2=0.82 to 0.92) between
monocyte adherence and neointima at 14 days.12
Furthermore, increased vascular injury correlated with increased
neointimal growth, inflammation, and thrombus
formation.13 In the porcine double-artery injury model,
neointimal thickness was smaller at strut sites adjacent to
an intact IEL and media than at areas of medial loss.14
The observations from experimental work showing correlations among
arterial injury, inflammation, and neointima
and data from the present study demonstrating increased
inflammation associated with stent struts in the vicinity of damaged
media and increased neointimal thickness at struts
associated with medial damage suggest that avoidance of severe
arterial injury during catheter-based interventions with
stents may have a beneficial effect on late neointimal
growth. Data from the present study showing the positive
association of neointimal growth and increased stent sizing
relative to the proximal reference lumen (a reflection of probable
increased arterial injury) are supportive of
stent-deployment techniques that can reduce arterial
injury. Novel devices that do not require very high balloon inflations
to accomplish close apposition of the stent to the arterial
wall (eg, self-expanding stents) are currently under clinical
trial.
Limitations
The findings in the present study are derived from descriptive
pathology. Because most of the tissues analyzed were obtained
at autopsy, the results presented may not be
representative of persons who receive stents and
survive. However, the present study is the first to report
histological findings from a large series of stents
placed in native human coronary arteries, and a majority of
segments with stents in place for >30 days demonstrated
histological success.
Conclusions
Morphology after coronary stent placement demonstrates the
following sequence of events: thrombus formation and acute inflammation
early after deployment, with subsequent neointimal growth.
Increased inflammation early after stenting is associated with medial
injury and lipid core penetration by stent struts. Medial damage and
stent oversizing relative to the reference arterial lumen
are associated with increased neointimal growth.
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Footnotes |
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The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.
Received May 13, 1998; revision received September 1, 1998; accepted September 16, 1998.
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