(Circulation. 1996;94:35-43.)
© 1996 American Heart Association, Inc.
Articles |
Arterial Remodeling After Coronary Angioplasty
A Serial Intravascular Ultrasound Study
From the Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, the Washington Hospital Center, Washington, DC.
Correspondence to Martin B. Leon, MD, 110 Irving St NW (4B-1), Washington, DC 20010.
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Abstract |
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Background Restenosis occurs after 30% to 50% of transcatheter coronary procedures; however, the natural history and pathophysiology of restenosis are still incompletely understood.
Methods and Results Serial (postintervention and
follow-up) intravascular ultrasound imaging was used to study 212
native coronary lesions in 209 patients after
percutaneous transluminal coronary angioplasty,
directional coronary atherectomy, rotational atherectomy, or
excimer laser angioplasty. The external elastic membrane (EEM) and
lumen cross-sectional areas (CSA) were measured; plaque plus media
(P+M) CSA was calculated as EEM minus lumen CSA. The anatomic slice
selected for serial analysis had an axial location within the
target lesion at the smallest follow-up lumen CSA. At
follow-up, 73% of the decrease in lumen (from 6.6±2.5 to 4.0±3.7
mm2, P<.0001) was due to a decrease in
EEM (from 20.1±6.4 to 18.2±6.4 mm2,
P<.0001); 27% was due to an increase in P+M (from
13.5±5.5 to 14.2±5.4 mm2, P<.0001).
Lumen CSA correlated more strongly with EEM CSA
(r=.751, P<.0001) than with P+M CSA
(r=.284, P<.0001). EEM was bidirectional; 47
lesions (22%) showed an increase in EEM. Despite a greater increase in
P+M (1.5±2.5 versus 0.5±2.0 mm2,
P=.0009), lesions exhibiting an increase in EEM had (1) no
change in lumen (-0.1±3.3 versus 3.6±2.3
mm2, P<.0001), (2) a reduced
restenosis rate (26% versus 62%, P<.0001),
and (3) a 49% frequency of late lumen gain (versus 1%,
P<.0001) compared with lesions with no increase in EEM.
Conclusions Restenosis appears to be
determined primarily by the direction and magnitude of vessel wall
remodeling (EEM). An increase in EEM is adaptive, whereas a decrease
in EEM contributes to restenosis.
Key Words: angioplasty • restenosis • ultrasonics • remodeling
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Restenosis occurs within the first 6 months after 30% to 50% of transcatheter procedures; it remains the major limitation to percutaneous coronary revascularization.1 2 3 4 5 Animal models,6 7 8 9 human necropsy studies,10 11 12 13 14 15 16 17 18 19 20 and analyses of retrieved atherectomy specimens21 22 23 24 25 26 27 originally suggested that an exaggeration of the normal reparative processes after angioplasty-induced local vessel trauma leads to uncontrolled smooth muscle cell proliferation and restenosis.28 29 30 However, no animal model completely simulates the vascular healing processes after catheter-induced trauma31 ; most animal models of restenosis occur in the absence of underlying chronic atherosclerosis with its associated pathobiology and flow abnormalities,31 and pharmacological strategies that prevent restenosis in animals have been strikingly ineffective in humans.31 32
One possible explanation for the failure of these treatment strategies is an incomplete understanding of the natural history and pathophysiology of restenosis.32 33 34 Recent animal and clinical studies have begun to question the predominant role of cellular proliferation, suggesting that remodeling with arterial constriction may result in lumen compromise and may be a major contributing factor to the development of restenosis.35 36 37 38 39 40 41 42 43 Furthermore, recent reexamination of original animal experiments (using different quantitative analyses) now indicate that arterial remodeling (which was once ignored) is, in fact, an important part of the restenosis process (D.P. Faxon, unpublished results, 1995, Los Angeles, Calif; with permission). In support of this hypothesis, endovascular stents, which merely scaffold the inner vascular lumen preventing recoil and remodeling without diminishing proliferative responses, have been shown to reduce restenosis in two randomized clinical trials.44 45
Importantly, arterial remodeling also represents an adaptive (or compensatory) response of blood vessels to hemodynamic stress, arterial injury, and cellular proliferation.6 31 46 47 48 49 50 51 52 53 Compensatory dilatation early in the coronary artery atherosclerotic disease process, as originally described by Glagov et al,54 55 delays the development of focal stenoses despite significant plaque accumulation.
IVUS allows transmural, tomographic imaging of coronary arteries in humans in vivo, providing unique insights into the pathology of coronary artery disease by defining vessel wall geometry and the major components of the atherosclerotic plaque. Sequential IVUS studies have been used to study mechanisms of angioplasty devices.56 57 58 59 The purpose of this study was to use serial IVUS imaging in human coronary arteries after successful angioplasty and at the time of late angiographic follow-up to define the relative contributions of the changes in plaque and arterial cross-sectional areas to late lumen loss.
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Methods |
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Patient Population
From July 1, 1991, to April 30, 1995, serial IVUS imaging was used to study 212 native coronary target lesions in 209 patients. This represents a consecutive series of patients imaged after intervention and at the time of follow-up angiography for recurrent symptoms or as part of clinical protocols. Reasons for study exclusion were stent implantation at the lesion site, ostial left main or ostial right coronary artery lesion location, target lesion calcification extensive enough to preclude accurate cross-sectional vessel quantification, and the inability to perform follow-up IVUS imaging because of clinical instability, patient refusal, or follow-up angiography performed at another institution.
There were 171 men and 38 women, ages 58±11 years. Lesion location was left main in 5, left anterior descending in 99, left circumflex in 31, and right coronary artery in 77. Interventional procedures performed included balloon angioplasty (n=29), DCA (n=114), high-speed rotational atherectomy (n=45), and excimer laser angioplasty (n=24). Adjunct balloon angioplasty was used in 138 lesions (65%) and adjunct DCA (after excimer laser angioplasty or rotational atherectomy) in 22 lesions (10%). Fifty-nine lesions (28%) were restenotic lesions.
Angiographic Analysis
All treatment and follow-up cineangiograms were
analyzed by an independent core angiographic laboratory using a
quantitative coronary angiographic automated edge detection
algorithm (ARTREK, Quantitative Cardiac Systems). The outer diameter of
the contrast-filled catheter was used for calibration. MLD,
reference diameter, and percent DS before and after intervention and on
follow-up were measured from multiple projections, and the
results from the "worst" view were recorded. Angiographic
restenosis was defined as a DS 
50%.60
IVUS Imaging Systems
IVUS studies were performed using one of two systems. The first
(InterTherapy Inc) incorporated a single-element, 25-MHz transducer
coupled to an angled mirror, mounted on the tip of a flexible shaft,
and rotated at 1800 rpm within a 3.9F short monorail polyethylene
imaging sheath to form cross-sectional images in real time. The
second (Cardiovascular Imaging Systems Inc)
incorporated a single-element, 30-MHz beveled transducer within
either a 2.9F long monorail imaging catheter having a common distal
lumen design (the distal lumen alternatively accommodated the imaging
core or the guidewire, but not both) or a 3.2F short monorail imaging
catheter. In all studies the transducer was withdrawn at 0.5 mm/s
within the stationary imaging sheath using a motorized pullback device.
At 0.5 mm/s, contiguous tomographic image slices were 16.7 µm apart.
This systematic approach facilitated comparative image analysis
of the serial ultrasound studies. Studies were recorded on
1/2-inch, high-resolution s-VHS taped for off-line
analysis.
Before angioplasty (as the first step in the procedure), after angioplasty (as the last step in the procedure), and on follow-up (before any subsequent intervention), 0.2 mg intracoronary nitroglycerin was administered and a complete ultrasound imaging run was performed from beyond the target lesion to the aortoostial junction.
Quantitative IVUS Measurements
Validation of cross-sectional measurements by IVUS has been
reported previously.61 62 63 64 65 66 67 By use of computerized
planimetry, the EEM and lumen CSA were measured at the lesion site; P+M
CSA was calculated as EEM CSA minus lumen CSA (Fig 1
).
The EEM CSA (which represents the area within the border
between the hypoechoic media and the echoreflective adventitia) has
been shown to be a reproducible measure of total arterial
CSA. Because ultrasound cannot measure media thickness accurately, P+M
CSA was used as a measure of plaque mass.68 When the
atherosclerotic plaque encompassed the catheter, the lumen was assumed
to be the physical size of the imaging catheter.
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The same anatomic image slice was analyzed before intervention, after intervention, and on follow-up, and the differences were compared. By using one or more reproducible axial landmarks (for example, the aortoostial junction, large proximal and/or distal side branches, or unusually shaped calcium deposits) and a known pullback speed, identical cross-sectional slices on serial studies could be identified for comparison. The anatomic slice selected for serial analysis had an axial location within the target lesion at the smallest follow-up lumen CSA (rather than at the smallest preintervention or postintervention lumen CSA).
In practice, the follow-up study was analyzed first to identify the anatomic slice with the smallest lumen; then, the distance from this anatomic slice to the closest identifiable axial landmark was measured (using seconds or frames of videotape); finally, this distance was used to identify the corresponding anatomic slice on the preintervention and postintervention studies. Vascular and perivascular markings (eg, small side branches, venous structures, calcific and fibrotic deposits) were used to confirm image slice identification. If necessary, the postintervention and follow-up studies were analyzed side by side and the imaging runs studied frame by frame to ensure that the same anatomic cross section was measured.
Assessment of Reproducibility
All cross-sectional measurements were made by the same
individual, who was blinded to the angiographic results. To assess
reproducibility and intraobserver variability of sequential IVUS
measurements, a consecutive series of 40 postintervention and
follow-up ultrasound studies were analyzed at least 3
months apart. This reanalysis began with the original
videotapes and therefore included the error involved in repeatedly
selecting the same image slice as well as the error involved in
performing the cross-sectional measurements. The differences in the
postintervention measurements were as follows: EEM CSA (0.05±1.01
mm2), lumen CSA (0.01±1.06 mm2), and P+M CSA
(0.03±1.05 mm2). The intraclass correlation
coefficient69 for repeated postintervention measurement of
the EEM CSA was 0.99, of lumen CSA was 0.92, and of P+M CSA was 0.98.
The differences in the follow-up measurements were as follows: EEM
CSA (0.04±0.80 mm2), lumen CSA (0.13±0.36
mm2), and P+M CSA (0.17±0.63 mm2). The
intraclass correlation coefficient69 for repeated
follow-up measurement of the EEM CSA was 0.99, of the lumen CSA was
0.96, and of the P+M CSA was 0.99.
Statistics
Statistical analysis was performed using StatView 4.02
or BMDP.70 Quantitative data are presented as
mean±1 SD. Qualitative data are presented as frequencies. The
intraclass correlation coefficient, which considers both
between-lesion variability and within-lesion variability and is
widely used as a measure of interrater variability, was used to assess
reproducibility of repeated measures.69 An intraclass
correlation coefficient of 0.80 to 1.00 indicates almost perfect
agreement. Comparisons between groups were performed using Mann-Whitney
U test or Wilcoxon test for continuous variables
or 
2 statistics and Fisher's exact test for
categorical variables.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Serial Angiographic Results
Overall, the preintervention MLD measured 0.90±0.48 mm and the DS measured 68±16%. The postintervention MLD increased to 2.42±0.59 mm, and the DS decreased to 17±13%. The follow-up interval was 5.6±3.4 months (range, 1 to 22). At follow-up, there was attrition in MLD to 1.44±0.88 mm, with an associated increase in DS to 49±28%; 99 target lesions (47%) were classified as restenotic lesions. See Table 1
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Serial IVUS Measurements
After intervention, the improvement in lesion site lumen CSA
(1.7±0.9 to 6.6±2.5 mm2, P<.0001) was
due to a combination of vessel expansion (increase in EEM CSA from
18.5±6.3 to 20.1±6.4 mm2, P<.0001) and
tissue ablation (decrease in P+M CSA from 16.8±6.2 to 13.5±5.5
mm2, P<.0001). At follow-up, the
decrease in lumen CSA (to 4.0±3.7 mm2,
P<.0001) was due more to a decrease in EEM CSA (to
18.2±6.4 mm2, P<.0001) than to an
increase in P+M CSA (to 14.2±5.4 mm2,
P<.0001) (Fig 2). Thus, 73% of late lumen
loss was explained by the decrease in EEM CSA (Figs 3 and 4; also see Table 1
).
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Restenotic lesions had a greater decrease in EEM CSA
(3.1±3.0 mm2) and lumen CSA (4.1±2.1 mm2)
than nonrestenotic lesions (0.8±2.9 and 1.2±2.8
mm2, respectively, both P<.0001). Compared with
nonrestenotic lesions, restenotic lesions
showed a trend toward an increase in P+M CSA (1.0±2.3 versus 0.4±2.0
mm2, P=.0784; Table 2).
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The change in lumen CSA correlated more strongly with the change in EEM
CSA (r=.751, P<.0001; Fig 5A)
than with the change in P+M CSA (r=.284,
P<.0001; Fig 5B). The changes in EEM CSA and in P+M CSA
also were significantly correlated (r=.452,
P<.0001; Fig 6).
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The change in EEM CSA was bidirectional. Forty-seven lesions (22%)
showed an increase in EEM CSA (Figs 7 and 8). Despite a greater increase in P+M CSA (1.5±2.5
versus 0.5±2.0 mm2, P=.0009), lesions
exhibiting an increase in EEM CSA had (1) no change in lumen CSA
(-0.1±3.3 mm2 versus a decrease in lumen CSA of
3.6±2.3 mm2 for lesions with a decrease in EEM CSA,
P<.0001), (2) a reduced restenosis rate (26%
versus 62% for lesions with a decrease in EEM CSA,
P<.0001), and (3) a 49% incidence of late lumen gain
(versus 1% for lesions with no increase in EEM CSA,
P<.0001).
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There were no consistent clinical (eg, history of diabetes), lesion-related (eg, calcification or eccentricity), or procedural (eg, vessel expansion versus tissue ablation) predictors of the direction or magnitude of the change in EEM or P+M CSA.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The pathophysiology of restenosis is complex and incompletely understood.28 30 71 Catheter-induced vascular injury causes immediate and progressive release of thrombogenic, vasoactive, and mitogenic factors leading to platelet aggregation, thrombus formation, and inflammatory changes, with activation of macrophages and smooth muscle cells.72 73 74 75 These events induce the production and release of growth factors and cytokines, which in turn may promote their own synthesis and release from target cells.7 9 27 73 76 77 78 79 80 81 Thus, a self-perpetuating cascade82 is initiated that results in the migration of smooth muscle cells from their usual location in the media to the intima, where they undergo a phenotype change, produce extracellular matrix, and proliferate.29 72 76 77 78 83 84 85 The restenotic lesion is therefore thought to be a proliferative lesion, with both cellular and matrix components causing an increased tissue mass.9 16 17 20 22 28 30 79 83 84 86 87 As the understanding of this process has advanced, attempts have been made to attack restenosis by interfering with this cascade.88 Although the results in animal models have been impressive, pharmacological trials using antiproliferative agents in humans have been disappointing.5 32 89 90 91
Recently, data from various sources have begun to challenge the traditional injury-proliferation restenosis hypothesis.35 37 38 92 New studies of retrieved atherectomy specimens have shown only a low level of active cellular proliferation in restenotic coronary lesions.35 In addition, animal studies have suggested that cellular proliferation may be a universal response to the trauma of transcatheter therapy regardless of the development of restenosis; the presence or absence of compensatory arterial dilatation (accommodating the increase in tissue mass) was the greater determinant of restenosis.37 38 42 Furthermore, late arterial contraction has now been shown to cause restenosis in the absence of extensive cellular proliferation.38
In this study, IVUS data from human coronary arteries support the emerging new animal model data.35 37 38 42 92 93 The impact of a change in EEM CSA on lumen dimensions could be differentiated from the change in P+M CSA. Serial ultrasound imaging indicated that (1) a decrease in total arterial (EEM) CSA accounted for 70% to 75% of late lumen loss and (2) late lumen loss correlated better with a decrease in EEM CSA than with an increase in P+M CSA.
This study does not seek to address the reasons for a decrease in EEM
CSA. However, several mechanisms have been postulated including (1)
fibrosis of the vessel wall, especially of the adventitia in response
to deep wall injury,39 94 (2) programmed cell death
(apoptosis),95 (3) changes in the extracellular
matrix composition and structure,96 and (4) responses to
shear stress–induced changes in vasomotor tone.31 The
ultrasound data can be used to support any or all of these theories;
for example, the decrease in EEM CSA was often associated with a
decrease in P+M CSA (Fig 6), suggesting the presence of
apoptosis with subsequent plaque retraction. Importantly, these
findings cannot exclude a possible relationship between early cellular
proliferation and a disproportionate late decrease in EEM CSA resulting
in exaggerated late lumen loss and restenosis in some
patients.
The change in EEM CSA was, in fact, bidirectional. Approximately 20% of lesions showed a compensatory increase in EEM CSA. This resulted in a decreased incidence of restenosis and an increased incidence of late lumen gain despite an increase in plaque mass analogous to adaptive arterial remodeling and vasodilatation early in the atherosclerotic disease process.49 50 51 52 54 55 Adaptive arterial remodeling (an increase in EEM CSA) in noninstrumented arteries prevents the reduction in lumen dimensions until plaque occupies 40% to 50% of the CSA within the internal elastic membrane (40% to 50% cross-sectional narrowing or plaque burden).54 55 Although the process after intervention may be different, adaptive arterial remodeling (an increase in EEM CSA) is the probable explanation for the occasional improvement in lumen dimensions seen during the follow-up period after catheter-based interventions.
This study does not determine the time course of the decrease in EEM CSA. Thus, it cannot exclude the contribution of acute passive elastic recoil after intervention.97 98 However, data from the Serial Ultrasound Restenosis Study 99 indicate that the decrease in arterial CSA is a late event (occurring between 1 and 6 months after angioplasty) and therefore is distinct from early passive elastic recoil.
Restenosis thus appears to be determined primarily by the
direction and magnitude of the change in EEM CSA, in other words, by
arterial remodeling (Fig 9). An increase in
EEM CSA (compensatory arterial dilatation) is adaptive,
whereas a decrease in EEM CSA leads to lumen compromise and
restenosis.
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Study Limitations
Because this is a study of patients presenting for
follow-up largely as the result of symptomatic
recurrence, it may represent a skewed population with
an increased rate of restenosis because of the nature of
the "clinical" follow-up. Nevertheless, it is a consecutive
series of patients studied after intervention and at follow-up
using serial IVUS.
The results of this study were dependent on accurate identification of the same anatomic cross section on serial ultrasound studies; this precluded blinded analysis. The use of a motorized transducer pullback to a reproducibly recognizable axial landmark at a known pullback speed coupled with careful attention to lesional and perilesional markings (and, if necessary, side-by-side and frame-by-frame comparisons) helped ensure identification of the same anatomic cross section on repeated imaging. This is attested to by the high reproducibility and low variability of the serial measurements. In addition, three-dimensional quantitative analysis of the entire length of target lesion (rather than just the narrowest cross section) might further enhance our understanding of this process.
Differences in vascular tone could have contributed to measurements of arterial and lumen dimensions. However, all patients were studied only after administration of significant doses of intracoronary nitroglycerin, and differences in vascular tone should not have affected measurement of P+M CSA.
Serial ultrasound analysis can measure only net changes in P+M CSA. Therefore, it cannot isolate cellular proliferation, matrix deposition, atherosclerosis progression/regression, or plaque stabilization/apoptosis from overall quantitative changes in P+M CSA. For example, it cannot exclude the possible contribution of progressive media atrophy to the changes in EEM and P+M CSA. However, because plaque accumulation is usually accompanied by media atrophy, we expect that most of the lesions already had significant media atrophy before treatment; additional (especially rapid) media atrophy during the follow-up interval would have been unusual.100
This study involved a heterogeneous patient and lesion mix, including primary and restenotic lesions in all three vessels and patients with and without unstable angina or diabetes mellitus. Therefore, for example, the analysis presented was not able to identify device-related or vessel-related differences in restenosis mechanisms. The numbers of lesions treated with each device were relatively small, and devices were usually followed by adjunct PTCA or were used in various combinations, depending on lesion morphology.
Clinical Implications
Treatment strategies to prevent restenosis have
focused on limitation of cellular proliferation. Although previous
trials may be criticized because of methodological problems, it may be
that the underlying premise (ie, limitation of cellular proliferation
will prevent restenosis) was overly simplistic. An increase
in P+M CSA cannot account for the majority of late lumen loss in
restenosis lesions, although cellular proliferation may be
the initial "trigger" for arterial remodeling. Future
investigation and treatment strategies, therefore, should emphasize
arterial remodeling as well as tissue proliferation.
The identification of a decrease in EEM CSA as a major contributor to restenosis may explain the success of stent implantation in reducing restenosis.44 45 Serial intravascular ultrasound results have indicated that stents do not recoil chronically.101 Thus, even though there may be a stent-related increase in neointimal tissue proliferation, stents appear to reduce restenosis by withstanding the remodeling forces that lead to restenosis after other types of interventions.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by the Cardiology Research Foundation and the Medlantic Research Institute, Washington, DC.
Received September 21, 1995; revision received December 19, 1995; accepted December 21, 1995.
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P. Hoppmann, W. Koch, A. Schomig, and A. Kastrati The 5A/6A polymorphism of the stromelysin-1 gene and restenosis after percutaneous coronary interventions Eur. Heart J., February 2, 2004; 25(4): 335 - 341. [Abstract] [Full Text] [PDF]
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I. Iakovou, G. S. Mintz, G. Dangas, A. Abizaid, R. Mehran, Y. Kobayashi, A. J. Lansky, E. D. Aymong, E. Nikolsky, G. W. Stone, et al. Increased CK-MB release is a "trade-off" for optimal stent implantation: an intravascular ultrasound study J. Am. Coll. Cardiol., December 3, 2003; 42(11): 1900 - 1905. [Abstract] [Full Text] [PDF]
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W. Koch, G. Ndrepepa, J. Mehilli, S. Braun, M. Burghartz, H. Lengnick, K. Kolling, A. Schomig, and A. Kastrati Homocysteine Status and Polymorphisms of Methylenetetrahydrofolate Reductase Are Not Associated With Restenosis After Stenting in Coronary Arteries Arterioscler Thromb Vasc Biol, December 1, 2003; 23(12): 2229 - 2234. [Abstract] [Full Text] [PDF]
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A. Schober, S. Knarren, M. Lietz, E. A. Lin, and C. Weber Crucial Role of Stromal Cell-Derived Factor-1{alpha} in Neointima Formation After Vascular Injury in Apolipoprotein E-Deficient Mice Circulation, November 18, 2003; 108(20): 2491 - 2497. [Abstract] [Full Text] [PDF]
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M. B Smeets, J. P.G Sluijter, M. M.P.C Donners, E. Velema, S. Heeneman, G. Pasterkamp, and D. P.V de Kleijn Increased arterial expression of a glycosylated haptoglobin isoform after balloon dilation Cardiovasc Res, June 1, 2003; 58(3): 689 - 695. [Abstract] [Full Text] [PDF]
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J. Ibrahim, J. K. Miyashiro, and B. C. Berk Shear Stress Is Differentially Regulated Among Inbred Rat Strains Circ. Res., May 16, 2003; 92(9): 1001 - 1009. [Abstract] [Full Text] [PDF]
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T. Wakeyama, H. Ogawa, H. Iida, A. Takaki, T. Iwami, M. Mochizuki, and T. Tanaka Intima-media thickening of the radial artery after transradial intervention: An intravascular ultrasound study J. Am. Coll. Cardiol., April 2, 2003; 41(7): 1109 - 1114. [Abstract] [Full Text] [PDF]
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M. R Bennett IN-STENT STENOSIS: PATHOLOGY AND IMPLICATIONS FOR THE DEVELOPMENT OF DRUG ELUTING STENTS Heart, February 1, 2003; 89(2): 218 - 224. [Full Text] [PDF]
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F. G.P. Welt and C. Rogers Inflammation and Restenosis in the Stent Era Arterioscler Thromb Vasc Biol, November 1, 2002; 22(11): 1769 - 1776. [Abstract] [Full Text] [PDF]
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V. M. Shah, G. S. Mintz, S. Apple, and N. J. Weissman Background Incidence of Late Malapposition After Bare-Metal Stent Implantation Circulation, October 1, 2002; 106(14): 1753 - 1755. [Abstract] [Full Text] [PDF]
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R. Seabra-Gomes Intracoronary brachytherapy for restenosis: an efficient technique in the struggle for survival? Eur. Heart J., September 1, 2002; 23(17): 1319 - 1321. [Full Text] [PDF]
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P.W. Serruys, G. Sianos, W. van der Giessen, H.J.R.M. Bonnier, P. Urban, W. Wijns, E. Benit, M. Vandormael, R. Dorr, C. Disco, et al. Intracoronary {beta}-radiation to reduce restenosis after balloon angioplasty and stenting. The Beta Radiation In Europe (BRIE) study Eur. Heart J., September 1, 2002; 23(17): 1351 - 1359. [Abstract] [Full Text] [PDF]
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K. Krueger, P. Landwehr, M. Bendel, M. Nolte, H. Stuetzer, R. Bongartz, M. Zaehringer, G. Winnekendonk, A. Gossmann, R.-P. Mueller, et al. Endovascular Gamma Irradiation of Femoropopliteal de Novo Stenoses Immediately after PTA: Interim Results of Prospective Randomized Controlled Trial Radiology, August 1, 2002; 224(2): 519 - 528. [Abstract] [Full Text] [PDF]
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C. J. Sullivan and J. B. Hoying Flow-Dependent Remodeling in the Carotid Artery of Fibroblast Growth Factor-2 Knockout Mice Arterioscler Thromb Vasc Biol, July 1, 2002; 22(7): 1100 - 1105. [Abstract] [Full Text] [PDF]
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D. G. Kuhel, B. Zhu, D. P. Witte, and D. Y. Hui Distinction in Genetic Determinants for Injury-Induced Neointimal Hyperplasia and Diet-Induced Atherosclerosis in Inbred Mice Arterioscler Thromb Vasc Biol, June 1, 2002; 22(6): 955 - 960. [Abstract] [Full Text] [PDF]
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S. Humphries, C. Bauters, A. Meirhaeghe, L. Luong, M. Bertrand, and P. Amouyel The 5A6A polymorphism in the promoter of the stromelysin-1 (MMP3) gene as a risk factor for restenosis Eur. Heart J., May 1, 2002; 23(9): 721 - 725. [Abstract] [Full Text] [PDF]
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A. E. Ajani, R. Waksman, D.-H. Cha, L. Gruberg, L. F. Satler, A. D. Pichard, and K. M. Kent The impact of lesion length and reference vessel diameter on angiographic restenosis and target vessel revascularization in treating in-stent restenosis with radiation J. Am. Coll. Cardiol., April 17, 2002; 39(8): 1290 - 1296. [Abstract] [Full Text] [PDF]
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C. von Birgelen and R. Erbel The stent is here to stay: a note on stenting, ultrasound imaging, and the prevention of restenosis Eur. Heart J., April 2, 2002; 23(8): 595 - 597. [Full Text] [PDF]
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Z. S. Galis and J. J. Khatri Matrix Metalloproteinases in Vascular Remodeling and Atherogenesis: The Good, the Bad, and the Ugly Circ. Res., February 22, 2002; 90(3): 251 - 262. [Abstract] [Full Text] [PDF]
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H. C. Lowe, S. N. Oesterle, and L. M. Khachigian Coronary in-stent restenosis: Current status and future strategies J. Am. Coll. Cardiol., January 16, 2002; 39(2): 183 - 193. [Abstract] [Full Text] [PDF]
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G. S. Cherr, S. J. Motew, J. A. Travis, J. Fingerle, L. Fisher, M. Brandl, J. K. Williams, and R. L. Geary Metalloproteinase Inhibition and the Response to Angioplasty and Stenting in Atherosclerotic Primates Arterioscler Thromb Vasc Biol, January 1, 2002; 22(1): 161 - 166. [Abstract] [Full Text] [PDF]
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H. Okura, M. Hayase, S. Shimodozono, H. N. Bonneau, P. G. Yock, and P. J. Fitzgerald Impact of pre-interventional arterial remodeling on subsequent vessel behavior after balloon angioplasty: a serial intravascular ultrasound study J. Am. Coll. Cardiol., December 1, 2001; 38(7): 2001 - 2005. [Abstract] [Full Text] [PDF]
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H. V. Anderson, J. McNatt, F. J. Clubb, M. Herman, J.-P. Maffrand, F. DeClerck, C. Ahn, L. M. Buja, and J. T. Willerson Platelet Inhibition Reduces Cyclic Flow Variations and Neointimal Proliferation in Normal and Hypercholesterolemic-Atherosclerotic Canine Coronary Arteries Circulation, November 6, 2001; 104(19): 2331 - 2337. [Abstract] [Full Text] [PDF]
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W. R. P. Agema, J. W. Jukema, S. N. Pimstone, and J. J. P. Kastelein Genetic aspects of restenosis after percutaneous coronary interventions;towards more tailored therapy Eur. Heart J., November 2, 2001; 22(22): 2058 - 2074. [PDF]
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B.J Rensing, J Vos, P.C Smits, D.P Foley, M.J.B.M van den Brand, W.J van der Giessen, P.J de Feijter, and P.W Serruys Coronary restenosis elimination with a sirolimus eluting stent; First European human experience with 6-month angiographic and intravascular ultrasonic follow-up Eur. Heart J., November 2, 2001; 22(22): 2125 - 2130. [Abstract] [PDF]
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R. J. Pettersen, Z. A. Muna, K. K.J. Kuiper, E. Svendsen, F. Muller, P. Aukrust, R. K. Berge, and J. Erik Nordrehaug Sustained retention of tetradecylthioacetic acid after local delivery reduces angioplasty-induced coronary stenosis in the minipig Cardiovasc Res, November 1, 2001; 52(2): 306 - 313. [Abstract] [Full Text] [PDF]
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E.-i. Okamoto, T. Couse, H. De Leon, J. Vinten-Johansen, R. B. Goodman, N. A. Scott, and J. N. Wilcox Perivascular Inflammation After Balloon Angioplasty of Porcine Coronary Arteries Circulation, October 30, 2001; 104(18): 2228 - 2235. [Abstract] [Full Text] [PDF]
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P. S. Teirstein Living the Dream of No Restenosis Circulation, October 23, 2001; 104(17): 1996 - 1998. [Full Text] [PDF]
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G. S. Mintz, N. J. Weissman, and P. J. Fitzgerald Intravascular Ultrasound Assessment of the Mechanisms and Results of Brachytherapy Circulation, September 11, 2001; 104(11): 1320 - 1325. [Full Text] [PDF]
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J.J Piek, E Boersma, M Voskuil, C di Mario, E Schroeder, C Vrints, P Probst, B de Bruyne, C Hanet, E Fleck, et al. The immediate and long-term effect of optimal balloon angioplasty on the absolute coronary blood flow velocity reserve. A subanalysis of the DEBATE study Eur. Heart J., September 2, 2001; 22(18): 1725 - 1732. [Abstract] [PDF]
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N. Mercado, E. Boersma, W. Wijns, B. J. Gersh, C. A. Morillo, V. de Valk, G.-A. van Es, D. E. Grobbee, and P. W. Serruys Clinical and quantitative coronary angiographic predictors of coronary restenosis: A comparative analysis from the balloon-to-stent era J. Am. Coll. Cardiol., September 1, 2001; 38(3): 645 - 652. [Abstract] [Full Text] [PDF]
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P. Schoenhagen, K. M. Ziada, D. G. Vince, S. E. Nissen, and E. M. Tuzcu Arterial remodeling and coronary artery disease: the concept of "dilated" versus "obstructive" coronary atherosclerosis J. Am. Coll. Cardiol., August 1, 2001; 38(2): 297 - 306. [Abstract] [Full Text] [PDF]
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G. Sianos, I. P. Kay, M. A. Costa, E. Regar, K. Kozuma, P. J. de Feyter, E. Boersma, C. Disco, and P. W. Serruys Geographical miss during catheter-based intracoronary beta-radiation: incidence and implications in the BRIE study J. Am. Coll. Cardiol., August 1, 2001; 38(2): 415 - 420. [Abstract] [Full Text] [PDF]
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M. R. Ward, P. Kanellakis, D. Ramsey, J. Funder, and A. Bobik Eplerenone Suppresses Constrictive Remodeling and Collagen Accumulation After Angioplasty in Porcine Coronary Arteries Circulation, July 24, 2001; 104(4): 467 - 472. [Abstract] [Full Text] [PDF]
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S. C. Smith Jr, J. T. Dove, A. K. Jacobs, J. Ward Kennedy, D. Kereiakes, M. J. Kern, R. E. Kuntz, J. J. Popma, H. V. Schaff, D. O. Williams, et al. ACC/AHA guidelines for percutaneous coronary intervention (revision of the 1993 PTCA guidelines): A report of the American College of Cardiology/ American Heart Association Task Force on practice guidelines (Committee to revise the 1993 guidelines for percutaneous transluminal coronary angioplasty) endorsed by the Society for Cardiac Angiography and Interventions J. Am. Coll. Cardiol., June 15, 2001; 37(8): 2239 - 2239. [Full Text] [PDF]
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T. Kosokabe, K. Okumura, T. Sone, J. Kondo, H. Tsuboi, H. Mukawa, T. Tomida, T. Suzuki, H. Kamiya, H. Matsui, et al. Relation of a Common Methylenetetrahydrofolate Reductase Mutation and Plasma Homocysteine With Intimal Hyperplasia After Coronary Stenting Circulation, April 24, 2001; 103(16): 2048 - 2054. [Abstract] [Full Text] [PDF]
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Y. Kobayashi, Y. Honda, L. G. Christie, P. S. Teirstein, S. R. Bailey, C. L. Brown III, R. V. Matthews, A. C. De Franco, R. S. Schwartz, S. Goldberg, et al. Long-term vessel response to a self-expanding coronary stent: a serial volumetric intravascular ultrasound analysis from the ASSURE trial J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1329 - 1334. [Abstract] [Full Text] [PDF]
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G. S. Mintz, S. E. Nissen, W. D. Anderson, S. R. Bailey, R. Erbel, P. J. Fitzgerald, F. J. Pinto, K. Rosenfield, R. J. Siegel, E. M. Tuzcu, et al. American College of Cardiology clinical expert consensus document on standards for acquisition, measurement and reporting of intravascular ultrasound studies (ivus): A report of the american college of cardiology task force on clinical expert consensus documents developed in collaboration with the european society of cardiology endorsed by the society of cardiac angiography and interventions J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1478 - 1492. [Full Text] [PDF]
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Y. Yamasaki, K. Miyoshi, N. Oda, M. Watanabe, H. Miyake, J. Chan, X. Wang, L. Sun, C. Tang, G. McMahon, et al. Weekly Dosing With the Platelet-Derived Growth Factor Receptor Tyrosine Kinase Inhibitor SU9518 Significantly Inhibits Arterial Stenosis Circ. Res., March 30, 2001; 88(6): 630 - 636. [Abstract] [Full Text] [PDF]
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H. Okura, Y. Morino, A. Oshima, M. Hayase, M. R. Ward, J. J. Popma, R. E. Kuntz, H. N. Bonneau, P. G. Yock, and P. J. Fitzgerald Preintervention arterial remodeling affects clinical outcome following stenting: an intravascular ultrasound study J. Am. Coll. Cardiol., March 15, 2001; 37(4): 1031 - 1035. [Abstract] [Full Text] [PDF]
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F Schiele, M K Batur, M F Seronde, N Meneveau, P Sewoke, A Bassignot, G Couetdic, F Caulfield, and J-P Bassand Cytomegalovirus, Chlamydia pneumoniae, and Helicobacter pylori IgG antibodies and restenosis after stent implantation: an angiographic and intravascular ultrasound study Heart, March 1, 2001; 85(3): 304 - 311. [Abstract] [Full Text]
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J.-G. Bienvenu, J.-F. Tanguay, J.-F. Theoret, A. Kumar, R. G. Schaub, and Y. Merhi Recombinant Soluble P-Selectin Glycoprotein Ligand-1-Ig Reduces Restenosis Through Inhibition of Platelet-Neutrophil Adhesion After Double Angioplasty in Swine Circulation, February 27, 2001; 103(8): 1128 - 1134. [Abstract] [Full Text] [PDF]
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M. R. Ward, P. S. Tsao, A. Agrotis, R. J. Dilley, G. L. Jennings, and A. Bobik Low Blood Flow After Angioplasty Augments Mechanisms of Restenosis : Inward Vessel Remodeling, Cell Migration, and Activity of Genes Regulating Migration Arterioscler Thromb Vasc Biol, February 1, 2001; 21(2): 208 - 213. [Abstract] [Full Text] [PDF]
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S. E. Nissen and P. Yock Intravascular Ultrasound : Novel Pathophysiological Insights and Current Clinical Applications Circulation, January 30, 2001; 103(4): 604 - 616. [Abstract] [Full Text] [PDF]
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M. J. Sierevogel, G. Pasterkamp, E. Velema, P. P. T. de Jaegere, B. J. G. L. de Smet, J. H. Verheijen, D. P. V. de Kleijn, and C. Borst Oral Matrix Metalloproteinase Inhibition and Arterial Remodeling After Balloon Dilation : An Intravascular Ultrasound Study in the Pig Circulation, January 16, 2001; 103(2): 302 - 307. [Abstract] [Full Text] [PDF]
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A. Endo, H. Hirayama, O. Yoshida, T. Arakawa, T. Akima, T. Yamada, and M. Nanasato Arterial remodeling influences the development of intimal hyperplasia after stent implantation J. Am. Coll. Cardiol., January 1, 2001; 37(1): 70 - 75. [Abstract] [Full Text] [PDF]
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G. S. Mintz, N. J. Weissman, P. S. Teirstein, S. G. Ellis, R. Waksman, R. J. Russo, I. Moussa, P. Tripuraneni, S. Jani, Y. Kobayashi, et al. Effect of Intracoronary {{gamma}}-Radiation Therapy on In-Stent Restenosis : An Intravascular Ultrasound Analysis from the Gamma-1 Study Circulation, December 12, 2000; 102(24): 2915 - 2918. [Abstract] [Full Text] [PDF]
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D. Godin, E. Ivan, C. Johnson, R. Magid, and Z. S. Galis Remodeling of Carotid Artery Is Associated With Increased Expression of Matrix Metalloproteinases in Mouse Blood Flow Cessation Model Circulation, December 5, 2000; 102(23): 2861 - 2866. [Abstract] [Full Text] [PDF]
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C Hehrlein, A Kovacs, G.K Wolf, N Yue, and R Nath A novel balloon angioplasty catheter impregnated with beta-particle emitting radioisotopes for vascular brachytherapy to prevent restenosis. First in vivo results Eur. Heart J., December 2, 2000; 21(24): 2056 - 2062. [Abstract] [PDF]
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S. K. Parikh, D. Nori, A. Osian, and P. Tripuraneni Practical Considerations in Setting Up an Intracoronary Brachytherapy Program: Results of a Multicenter Survey Radiology, December 1, 2000; 217(3): 723 - 728. [Abstract] [Full Text]
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S. L. Meyerson, C. L. Skelly, M. A. Curi, and L. B. Schwartz Gene Therapy for Cardiovascular Disease Seminars in Cardiothoracic and Vascular Anesthesia, November 1, 2000; 4(4): 289 - 300. [Abstract] [PDF]
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