(Circulation. 1996;93:340-348.)
© 1996 American Heart Association, Inc.
Articles |
Adventitial Remodeling After Coronary Arterial Injury
From the Department of Medicine (Cardiology), Thomas Jefferson University, Philadelphia, Pa.
Correspondence to Andrew Zalewski, MD, Thomas Jefferson University, 1025 Walnut St, Suite 410N, Philadelphia, PA 19107.
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Abstract |
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Background Intraluminal thrombus formation and medial smooth muscle (SM) cell proliferation are recognized responses of the arterial system to injury. In contrast to these well-characterized processes during vascular repair, changes involving the adventitia have been largely neglected in previous studies. Hence, the goal of this investigation was to assess the response of the adventitia to coronary arterial injury.
Methods and Results Adventitial changes in porcine
coronary arteries subjected to medial injury were characterized
by immunohistochemistry, histochemistry, and microscopic morphometry.
The rapid development of a hypercellular response in the adventitia was
evident 3 days after balloon-induced medial injury. Cell
proliferation, as assessed by proliferating cell nuclear antigen
immunostaining, reached the maximum level in the
adventitia at 3 days, whereas at 14 and 28 days, the number of
replicating cells reverted toward the baseline. The proliferating
activity in the adventitia exceeded that seen in the media at all times
after injury. To further define the changes in the phenotype of
adventitial cells, the expression of three cytoskeletal proteins
(vimentin, 
-SM actin, and desmin) was characterized. Fibroblasts in
normal adventitia expressed vimentin but no -SM actin or desmin.
After injury, these cells acquired characteristics of myofibroblasts
expressing -SM actin, which peaked at 7 and 14 days. Desmin
expression was patchy in the adventitia, as opposed to its
homogeneous distribution in medial SM cells. The modulation
of fibroblast phenotype was transient, inasmuch as -SM actin
immunostaining declined at 28 days after injury, when
dense, collagen-rich scar was evident within the adventitia. The
above-described changes involving hypercellularity of the
adventitia, myofibroblast formation, and fibrosis were associated with
a significant focal adventitial thickening at 3, 7, 14, and 28 days
after injury (P<.01 versus uninjured coronary
arteries).
Conclusions This study demonstrates the involvement of the adventitia in the vascular repair process after medial injury. The hypercellularity of the adventitial layer, proliferation of fibroblasts, and modulation of their phenotype to myofibroblasts are associated with the development of the thickened adventitia. It is postulated that these phenomena affect vascular remodeling and may provide an important insight into the mechanisms of vascular disorders.
Key Words: adventitia • remodeling • myofibroblasts • angioplasty • restenosis
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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T he vessel wall response to injury provides the pathophysiological basis for the development of a wide spectrum of cardiovascular disorders.1 Vascular insult triggers a cascade of events in which blood-borne cells and resident mesenchymal cells modulate their phenotype in response to locally released cytokines. In particular, SMC migration and proliferation, followed by extracellular matrix synthesis, have provided the overall sequence of cellular events that contribute to the development of atherosclerosis2 and vascular restenosis.3 4 5 These processes can lead to a dramatic change in microscopic composition and dimensions of the vessel wall.
Coronary angioplasty and other transcatheter procedures induce an acute form of vascular injury whose long-term revascularization benefit is limited by restenosis. Although the pathogenesis of this process is multifactorial, the formation of neointima is common after balloon injury.6 7 Recent experimental8 9 10 and clinical observations, however,11 have questioned prior assumptions that neointima correlates with luminal renarrowing. These studies suggest that geometric remodeling due to poorly defined mechanisms is most likely involved in the loss of patency after vascular injury. Since radial dimensions of the artery after injury may depend on the intactness of its outer layer, we sought to examine the changes in the adventitia of porcine coronary arteries after medial injury. This study demonstrated that vascular injury induces profound remodeling of the adventitia, including an increase in its thickness, a transient change in the phenotype of adventitial fibroblasts, and the accumulation of extracellular matrix proteins (collagens). These changes, which were not emphasized in prior studies of vascular response to injury, may have an important functional role in the overall remodeling of the arterial wall in pathological conditions.
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Methods |
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Animal Model
Domestic crossbred pigs (Sus scrofa, n=27) weighing from 22 to 30 kg were premedicated with aspirin (650 mg PO), atropine (1 mg IM), and nifedipine (10 mg sublingual). Anesthetics consisted of intramuscular injection of ketamine (12 mg/kg) and xylazine (2 mg/kg) supplemented with intravenous infusion of diprivan (12 mg·kg-1·h-1) throughout the experiment. The right external carotid artery was surgically exposed, and heparin (10 000 U) was administered intra-arterially. With an 8F SAL 1 guiding catheter (Medtronic Interventional Vascular, Inc), the coronary ostia were cannulated under fluoroscopic guidance and intracoronary nitroglycerin was administered (100 µg). The coronary arteries were injured by use of an oversized balloon (4.0 mm) that was inflated three times (6 to 10 atm) for 30 seconds. The number of coronary arteries analyzed for each parameter is reported as "n" values in the "Results" section. Postsurgical therapy included aspirin 325 mg PO and ampicillin 250 mg IM for the next 2 days. The animals were euthanatized with an overdose of pentobarbital (100 mg/kg IV) at the times indicated in the text. All animal experiments conformed to the position of the American Heart Association on research animal use and were in accordance with institutional guidelines.
Tissue Preparation and Histochemistry
To preserve the
integrity of the adventitia and perivascular
tissues, porcine coronary arteries were carefully removed in a
block along with adjacent tissues (ie, the adipose tissue,
myocardium), rinsed with PBS, and then immersed in
HistoChoice tissue fixative (Ameresco). The arteries were sectioned
into 2- to 5-mm blocks, placed in individual cassettes, and fixed for
at least 5 hours in HistoChoice. Then the samples were processed in a
Tissue-Tek VIP processor (Miles Inc), embedded in paraffin, and cut
into 5-µm-thick sections. Next, they were placed on glass slides
previously coated with Vectabond (Vector Laboratories).
The tissue sections were deparaffinized; Verhoeff's stain for elastic tissues12 was used in the representative slides from each block to identify the site of the most severe medial injury, defined as a distinct disruption of the internal elastic lamina with preserved continuity of the external elastic lamina. The specimens devoid of these criteria were excluded from further studies. Hence, all analyses were carried out using sections exhibiting comparable degrees of medial injury. Adjacent sections were examined by histochemistry, immunohistochemistry, and morphometry. To determine the cellularity of vascular lesions, hematoxylin-eosin stain was used. To characterize components of the extracellular matrix, Sirius red and Alcian blue stains were used to identify collagens and proteoglycans, respectively.13
Immunohistochemistry
The Vectastain Elite ABC system (Vector
Laboratories) was used
for immunohistochemistry. Sections were deparaffinized, incubated with
0.6% hydrogen peroxide in methanol for 30 minutes, and blocked with
5% horse serum when mouse monoclonal antibody was used. After a
washing in PBS, sections were incubated with primary antibodies for 1
hour at room temperature or 24 hours at 4°C in a moisture chamber.
The following primary antibodies were used: monoclonal mouse 1A4
antibody recognizing -SM actin (1:100, Sigma
Diagnostics); monoclonal mouse DE-R-11 antibody,
recognizing intermediate filament desmin (1:50, Novocastra); monoclonal
mouse NCL-VIM-V9, recognizing intermediate filament vimentin (1:100,
Novocastra); and monoclonal mouse PC10 antibody, identifying PCNA
(1:200, DAKO). Next, the slides were washed and incubated with
biotinylated secondary horse anti-mouse antibodies (1:2000, Vector
Laboratories) for 1 hour. The sections were visualized with DAB
substrate (Vector Laboratories) followed by counterstain with Gill's
hematoxylin (Sigma Diagnostics). Negative controls were
carried out with nonimmune serum instead of primary antibody.
Cell Density, Proliferation Index, and Morphometric
Analysis
Cell density and cell proliferation were determined by
counting total cell nuclei and PCNA-positive nuclear staining,
respectively, in a minimum of 250 cells per vessel layer per field.
Cellularity was expressed as number of cells per square millimeter,
whereas the proliferation index reflected the percentage of
PCNA-positive cells. These measurements were performed in sections
demonstrating comparable degrees of medial injury.
Morphometric analyses were carried out with a computerized imaging system (Advanced Imaging Concepts, Inc). The adventitia was defined between the medial edge of the external elastic lamina (inner border) and either the edge of the adipose tissue or the myocardium surrounding coronary arteries (outer border). Since the outer border often demonstrated a smooth transition into surrounding tissues, all morphometric measurements were carried out on slides stained with Verhoeff's stain at the same magnification that provided the optimal demarcation of the adventitia. The minimal and maximal adventitial thicknesses (in micrometers) as well as medial and neointimal thicknesses were calculated. In the control vessels, measurements were carried out on multiple sections (three or four per vessel) to account for naturally occurring variability in medial and adventitial dimensions. In injured coronary arteries, morphometric measurements were carried out in the sections demonstrating the most severe signs of medial injury to capture the maximal response. To minimize error of measurements, each parameter was calculated three times, and the average value was reported. The intraobserver variability for repeat measurements was <10%.
Statistical Methods
All numerical data are presented as
mean±SEM.
One-way ANOVA was used to compare the time-dependent
variables. If the F test results were significant,
Bonferroni analysis was carried out to determine differences
among subgroups. A value of P<.05 was required to reject
the null hypothesis.
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Results |
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Adventitial Thickening After Injury
The thickness of the adventitia in normal porcine coronary arteries varied from 131±6 µm (minimum diameter) to 224±9 µm (maximum diameter) in individual sections, with mean values of 178±44 µm (n=9). To assess adventitial remodeling after vascular injury, the maximal adventitial diameter was measured at 3 (n=4), 7 (n=4), 14 (n=4), and 28 (n=6) days after balloon injury and was compared with the maximal adventitial diameter of normal coronary arteries. Adventitial thickness was significantly increased at all time points compared with normal vessels (P<.01, Fig 1
). As depicted in Fig
2, the most striking changes in adventitial dimensions
were present in the regions adjacent to the site of medial injury.
In contrast, the thickness of the adventitia opposite medial injury or
in other uninjured sections from the same vessels remained largely
unaffected.
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Cellular Response in the Adventitia After Injury
A deep
medial injury without disruption of the external
elastic lamina was associated with an increase in adventitial cell
density beginning at 3 days, which returned to baseline at 14 days. In
control (ie, uninjured) coronary arteries, adventitial cell
density was 3880±372 cells/mm2 (n=5), which increased
to
7094±576 cells/mm2 at 3 days (n=4, P<.01)
and
7218±256 cells/mm2 at 7 days (n=4, P<.01)
after injury. At 14 and 28 days, cell density in the adventitia was
4617±208 cells/mm2 (n=4, P=NS versus
controls)
and 4989±547 cells/mm2 (n=6, P=NS
versus
controls), respectively, returning toward baseline (Fig 3). The
segments of coronary arteries remote
from the site of vascular injury resembled uninjured vessels exhibiting
no hypercellular response at all time points.
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The increase in the
cellularity of the adventitia was
paralleled by high proliferative activity. With PCNA staining,
replicating cells were identified in 3±1% of adventitial cells in
control coronary arteries (n=4), whereas at 3 (n=3) and 7
(n=3)
days after injury, the proliferating index was significantly higher at
42±6% (P<.01) and 34±4% (P<.01),
respectively. As depicted in Fig 4, this proliferative
response in the adventitia exceeded values observed in the media after
balloon injury. At 14 (n=4) and 28 (n=3) days after medial
injury, the
adventitia was largely quiescent, with 2±1% of cells expressing PCNA
at each time (P=NS versus controls, Fig 4). As
illustrated
in Fig 5, at 3 days after injury, proliferating cells
were circumferentially distributed in the adventitia, with fewer
PCNA-positive cells present within the media. A similar
distribution of actively dividing cells was observed with
5-bromo-2'-deoxyuridine labeling (data not shown). At later time
points, PCNA-positive cells accumulated predominantly in the portion of
the adventitia in the vicinity of medial injury as well as in the newly
formed neointima.
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Cellular Composition in the Adventitia After Injury
To
identify the cellular composition in the adventitia,
vascular specimens were subjected to immunohistochemistry, with
monoclonal antibodies recognizing major cytoskeletal proteins of
mesenchymal cells (n=3 to 5 vessels per time point). In uninjured
coronary arteries, adventitial cells were uniformly positive
for vimentin but negative for -SM actin and desmin (V type, not
shown). In contrast, medial SMCs showed strong immunoreactivity, with
antibodies against all three cytoskeletal proteins (VAD type).
Coronary arterial injury did not alter vimentin
expression, but it did increase the -SM actin and desmin expression
in the adventitia. The adventitia containing hypercellular,
granulation-like tissue exhibited weakly positive staining with
-SM actin antibodies at 3 days. The immunostaining
for -SM actin became strongly positive within the adventitia at 7
and 14 days after injury (VA type, Fig 6). This change
in the phenotype of adventitial fibroblasts to myofibroblasts
(ie, containing -SM actin) was particularly evident in the areas
adjacent to medial injury, although circumferential localization of
these cells was occasionally noted at 7 days. There was no evidence for
-SM actin immunostaining in the adventitia beyond
the site of medial injury. As shown in Fig 6, the presence of
myofibroblasts appeared to decline at later times, with frequent
disappearance at 28 days.
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In general, the time course of
immunoreactivity with desmin
antibodies in the adventitia paralleled that of -SM actin
(VAD type). However, desmin-positive cells were less frequent, with
more patchy distribution in the adventitia after medial injury
(Fig 7).
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Extracellular Matrix Deposition in the Adventitia
The above
changes leading to myofibroblast formation were
associated with a striking accumulation of collagen-containing scar
in the thickened adventitia by Sirius red (Fig 8) and
Masson's trichrome (not shown) histochemical staining. In contrast,
proteoglycans were mostly confined to the neointima at 28
days after injury (Fig 8).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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This study indicates that adventitial fibroblasts/myofibroblasts are involved in the vascular repair process, resulting in significant cellular and structural changes affecting the adventitia of injured coronary arteries.
Proliferation of Adventitial Fibroblasts
Tissue response to
injury involves a cascade of adaptive phenomena
that were evolutionarily developed to close an open
wound.14 15 16 There are striking
similarities between the
process of wound healing and the response of the arterial
wall to injury.17 They involve the disruption of tissue
continuity as well as a chain of interconnected events allowing
cells to assume "new" functions according to microenvironmental
needs. Proliferation of medial SMCs has been considered a common event
shortly after vascular injury.3 4 18
However, as shown in
this study, adventitial rather than medial cell proliferation was
typical shortly after coronary arterial injury.
This process reached a maximum at 3 days, when few medial SMCs were
replicating. Hypercellular adventitia after coronary injury
contained vimentin, a known marker of mesenchymal cells,19
which identified these cells as fibroblasts. It is important to
emphasize that the initial paucity of -SM actin in the adventitia
distinguished these cells from medial SMCs. Notwithstanding the above,
macrophages are probably also present in injured adventitia
during an early phase of vascular repair, inasmuch as they may express
vimentin (as opposed to other blood-borne
cells).20
Phenotypic Modulation of Adventitial Fibroblasts
In normal
coronary arteries, vimentin-rich
adventitial fibroblasts (V type) can easily be distinguished from
medial SMCs, which exhibit positive staining not only with vimentin
antibodies but also with antibodies recognizing -SM actin and desmin
(VAD type).21 22 Shortly after medial injury (ie,
within 3
days), the adventitia becomes hypercellular with concomitant
significant proliferative activity that resembles the formation of
granulation tissue containing replicating fibroblasts in wound healing.
The change in the phenotype of adventitial fibroblasts to
myofibroblasts is reflected by the induction of -SM actin, reaching
a maximum at 7 and 14 days after injury (Fig 6
, VA type), with
some
myofibroblasts also acquiring desmin (Fig 7, VAD type). The
mechanism(s) underlying the above process of phenotypic modulation in
vascular tissue remains to be determined. However, it is noteworthy
that transforming growth factor-ß1 has been implicated in the
induction of -SM actin expression in wound
myofibroblasts.23 24
There are several
potential explanations for the disappearance of
myofibroblasts noted at later times after vascular injury (Fig
6). The
possibility of their migration to the luminal surface, which may
contribute to the formation of neointima, should be
considered.25 In fact, direct adventitial injury has been
demonstrated to produce neointimal lesions even without
endothelial denudation in several experimental
models.26 27 28 29 The
difficulty in ascertaining the
contribution of myofibroblasts to neointimal formation,
however, lies in the similarities between myofibroblasts (VA and VAD
types) and SMCs (VAD type) in regard to their morphology and the
spectrum of cytoskeletal protein expression. Although these cells
demonstrate opposite changes in -SM actin expression, with a
reversible switch from -SM actin to other actin isoforms in SMCs and
adventitial cells acquiring -SM actin after injury, -SM actin
never completely disappears in medial cells.30 The
apoptotic cell death may represent another mechanism
removing myofibroblasts from the adventitia, as it has been involved in
the elimination of mesenchymal cells in dermal wounds and in
restenotic lesions.16 31 The regression to
fibroblast phenotype is also possible, since the reactivation
of -SM actin expression can be elicited with vessel reinjury (data
not shown).
Role of Adventitial Injury
The transition of fibroblasts to
myofibroblasts (ie, positive
for -SM actin) is associated with several biological activities,
including enhanced collagen
synthesis32 33 34 and tissue
contraction/retraction, which is often associated with scar
formation.16 35 Accordingly, the formation of
hypercellular, myofibroblast-rich adventitia that is subsequently
replaced by dense, collagen-rich scar tissue may have important
implications with regard to early and late events in vascular repair.
The expression of contractile cytoskeletal proteins in myofibroblasts,
in particular -SM actin, has been a hallmark of collagen matrix gel
remodeling in vitro36 and various fibrocontractive
disorders in vivo.32 37 38 39
Hence, vascular tissue
contraction may represent a putative mechanism of vessel
constriction that has recently been reported to correlate with residual
stenosis after experimental angioplasty.10
Unfavorable geometric remodeling has been documented after balloon
injury in several models of experimental
angioplasty,8 9 10
although it has not been found by others.40
The deposition
of collagen in the adventitia, as demonstrated by
histochemical staining in this study (Fig 8), is consistent
with the reported transcriptional activation of fibrillar procollagen
genes after experimental angioplasty.41 Procollagen
1(I) and 1(III) mRNA levels increase
between 2 and 7 days after injury, with collagen becoming the most
abundant protein, constituting >50% of the arterial
proteins at 30 days.41 Accordingly, deposits of fibrillar
collagens may contribute to the formation of a stiff,
"collarlike" adventitia that prevents coronary arteries
from undergoing compensatory dilatation during neointimal
formation, typical of the adaptive changes during the slow growth of an
atherosclerotic plaque.42 43
Clinical Implications
Recent advances in interventional
cardiology
have led to more aggressive strategies to relieve coronary
obstruction and often to ablate the underlying atherosclerotic plaque.
Thus, a deep medial injury that may potentially affect the adventitia
appears to be common in clinical practice.44 The
possibility of myofibroblast formation and the deposition of
extracellular matrix in the adventitia after coronary
arterial injury in humans may lead to vascular tissue
retraction, with the possible exception of intracoronary
stenting. In fact, recent findings with intravascular ultrasound appear
to corroborate this possibility, inasmuch as patients with
coronary restenosis after angioplasty exhibit a
smaller vessel circumference along the external elastic lamina, which
delineates the adventitial border.11
The failure of many pharmacological approaches to reduce restenosis in clinical settings has stimulated considerable interest in a site-specific therapy after coronary angioplasty.45 The involvement of the adventitia in the vascular repair process may require the development of strategies allowing for the administration of potentially active compounds not only to the media but also to the outer layers of the vessel wall. This clearly increases the complexity of local drug delivery in diseased, atherosclerotic vessels, since the possibility of additional vascular trauma is of concern with more aggressive approaches.
Conclusions
This study demonstrates the involvement of the
adventitia in the
vascular repair process in the coronary vasculature in a
porcine model. The hypercellularity of the adventitial layer due to
proliferation of fibroblasts was seen early after coronary
arterial injury (3 to 7 days). The expression of -SM
actin was evident in abundant adventitial myofibroblasts at 7 and 14
days. This was followed by the accumulation of collagen-containing
scar tissue within the adventitia. These changes were accompanied by
focal thickening of the outer layer of the coronary arteries.
Hence, the adventitial response contributes to vascular remodeling
after arterial injury.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by a standard Grant-in-Aid from the American Heart Association, Florida and Delaware Affiliates, Inc. The authors gratefully acknowledge the technical assistance of Dian Wang and Carolyn Talbot.
Received July 18, 1995; revision received September 7, 1995; accepted September 11, 1995.
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 S. M. Arribas, C. Hillier, C. Gonzalez, S. McGrory, A. F. Dominiczak, and J. C. McGrath Cellular Aspects of Vascular Remodeling in Hypertension Revealed by Confocal Microscopy Hypertension, December 1, 1997; 30(6): 1455 - 1464. [Abstract] [Full Text]
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S.S. Srivatsa, L. A Fitzpatrick, P. W Tsao, T. M Reilly, D. R Holmes Jr, R. S Schwartz, and S. A Mousa Selective {alpha}v{beta}3 integrin blockade potently limits neointimal hyperplasia and lumen stenosis following deep coronary arterial stent injury:: Evidence for the functional importance of integrin {alpha}v{beta}3 and osteopontin expression during neointima formation Cardiovasc Res, December 1, 1997; 36(3): 408 - 428. [Abstract] [Full Text] [PDF]
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C. M. Shanahan, N. R. B. Cary, J. K. Osbourn, and P. L. Weissberg Identification of Osteoglycin as a Component of the Vascular Matrix : Differential Expression by Vascular Smooth Muscle Cells During Neointima Formation and in Atherosclerotic Plaques Arterioscler Thromb Vasc Biol, November 1, 1997; 17(11): 2437 - 2447. [Abstract] [Full Text]
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I. J. Kullo, G. Mozes, R. S. Schwartz, P. Gloviczki, T. B. Crotty, D. A. Barber, Z. S. Katusic, and T. O'Brien Adventitial Gene Transfer of Recombinant Endothelial Nitric Oxide Synthase to Rabbit Carotid Arteries Alters Vascular Reactivity Circulation, October 7, 1997; 96(7): 2254 - 2261. [Abstract] [Full Text]
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M. W. Liu, P. G. Anderson, J. F. Luo, and G. S. Roubin Local Delivery of Ethanol Inhibits Intimal Hyperplasia in Pig Coronary Arteries After Balloon Injury Circulation, October 7, 1997; 96(7): 2295 - 2301. [Abstract] [Full Text]
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M. E. Staab, R. D. Simari, S. S. Srivatsa, D. Hasdai, V. J. Pompili, D. R. Holmes, R. S. Schwartz, and R. S. Schwartz Enhanced Angiogenesis and Unfavorable Remodeling in Injured Porcine Coronary Artery Lesions: Effects of Local Basic Fibroblast Growth Factor Delivery Angiology, September 1, 1997; 48(9): 753 - 760. [Abstract] [PDF]
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L. J Feldman and G. Steg Optimal techniques for arterial gene transfer Cardiovasc Res, September 1, 1997; 35(3): 391 - 404. [Abstract] [Full Text] [PDF]
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M. R Garvin, M. Labinaz, K. Pels, V. M Walley, H. F Mizgala, and E. R O'Brien Arterial expression of the plasminogen activator system early after cardiac transplantation Cardiovasc Res, August 1, 1997; 35(2): 241 - 249. [Abstract] [Full Text] [PDF]
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Y. Shi, J. E. O'Brien Jr, J. D. Mannion, R. C. Morrison, W. Chung, A. Fard, and A. Zalewski Remodeling of Autologous Saphenous Vein Grafts : The Role of Perivascular Myofibroblasts Circulation, June 17, 1997; 95(12): 2684 - 2693. [Abstract] [Full Text]
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D. P. Faxon Identifying the Predictors of Restenosis: Do We Need New Glasses? Circulation, May 6, 1997; 95(9): 2244 - 2246. [Full Text]
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V. Verin, P. Urban, Y. Popowski, M. Schwager, P. Nouet, P. A. Dorsaz, P. Chatelain, J. M. Kurtz, and W. Rutishauser Feasibility of Intracoronary ß-Irradiation to Reduce Restenosis After Balloon Angioplasty: A Clinical Pilot Study Circulation, March 4, 1997; 95(5): 1138 - 1144. [Abstract] [Full Text]
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W. D. Coats, P. Whittaker, D. T. Cheung, J. W. Currier, B. Han, and D. P. Faxon Collagen Content Is Significantly Lower in Restenotic Versus Nonrestenotic Vessels After Balloon Angioplasty in the Atherosclerotic Rabbit Model Circulation, March 4, 1997; 95(5): 1293 - 1300. [Abstract] [Full Text]
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A. Zalewski and Y. Shi Vascular Myofibroblasts : Lessons From Coronary Repair and Remodeling Arterioscler Thromb Vasc Biol, March 1, 1997; 17(3): 417 - 422. [Full Text]
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Y. Shi, J. E. O'Brien, L. Ala-Kokko, W. Chung, J. D. Mannion, and A. Zalewski Origin of Extracellular Matrix Synthesis During Coronary Repair Circulation, February 18, 1997; 95(4): 997 - 1006. [Abstract] [Full Text]
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O. Tahlil, M. Brami, L. J Feldman, D. Branellec, and Ph.G. Steg The DispatchTM catheter as a delivery tool for arterial gene transfer Cardiovasc Res, January 1, 1997; 33(1): 181 - 187. [Abstract] [Full Text] [PDF]
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Y. Shi, J. E. O'Brien, A. Fard, and A. Zalewski Transforming Growth Factor-ß1 Expression and Myofibroblast Formation During Arterial Repair Arterioscler Thromb Vasc Biol, October 1, 1996; 16(10): 1298 - 1305. [Abstract] [Full Text]
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Y. Shi, J. E. O'Brien, A. Fard, J. D. Mannion, D. Wang, and A. Zalewski Adventitial Myofibroblasts Contribute to Neointimal Formation in Injured Porcine Coronary Arteries Circulation, October 1, 1996; 94(7): 1655 - 1664. [Abstract] [Full Text]
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C. A. J. Schulze-Bauer, P. Regitnig, and G. A. Holzapfel Mechanics of the human femoral adventitia including the high-pressure response Am J Physiol Heart Circ Physiol, June 1, 2002; 282(6): H2427 - H2440. [Abstract] [Full Text] [PDF]
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