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(Circulation. 1999;100:799-806.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Acute Platelet Inhibition With Abciximab Does Not Reduce In-Stent Restenosis (ERASER Study)
Correspondence to Stephen G. Ellis, MD, the Cleveland Clinic Foundation, 9500 Euclid Ave, F-25, Cleveland, OH 44195. E-mail elliss{at}cesmtp.ccf.org
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionAppendix 1References |
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Background—Although stents reduce restenosis compared with balloon angioplasty, their long-term efficacy is limited by neointimal hyperplasia. Platelet and
vß3 integrin receptor
inhibition limits neointimal proliferation in animal models
of arterial injury.
Methods and Results—We tested whether the dual ß3
integrin blocking agent abciximab, administered for 12 or 24 hours at
the same intravenous dose as that shown to reduce adverse
clinical events (death, infarction, and
revascularization) after angioplasty, would reduce
restenotic tissue volume, as measured by intravascular
ultrasound at 6 months. Two hundred twenty-five patients were randomly
allocated to placebo or abciximab before coronary intervention.
Of the 215 patients who received stents and study drug, 191 (88.8%)
returned for late (
4 months) coronary evaluation. Tissue
volume, expressed as a percentage of stent volume, did not differ:
25±15%, 27±15%, and 29±14% for the patients in the placebo and
the 12- and 24-hour abciximab groups, respectively. Lack of abciximab
benefit was confirmed by quantitative coronary angiography
(dichotomous restenosis: 11.6%, 18.9%, and 19.4%; loss
index: 0.33, 0.52, and 0.47, respectively, P=NS).
Conclusions—Potent platelet inhibition with abciximab, as administered in this study, does not reduce in-stent restenosis. The interrelationship between stents, platelets, and neointimal proliferation requires further study.
Key Words: angioplasty • stents • platelets • glycoproteins • vitronectin
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Intracoronary stents reduce the absolute incidence of restenosis compared with balloon angioplasty in selected patients and lesions by 10% to 15% and improve 6-month event-free survival by 10% to 19%.1 2 Stents reduce restenosis by an improvement in initial lesion cross-sectional area, but stenting aggravates the neointimal hyperplasia and the late lumen loss compared with that after angioplasty alone.1
Reduction of neointimal hyperplasia after stent
placement should greatly retard clinical restenosis. Schwartz
et al3 and Miller et al4 described the
chronology of in-stent restenosis in animal models as early
thrombosis, followed by thrombus endothelialization and
infiltration by lymphocytes and monocytes, and finally smooth muscle
cell migration into the resolving thrombus and proliferation. Ligand
binding to IIBß3
(glycoprotein IIb/IIIa) and
vß3
(vitronectin) receptors mediates platelet aggregation
and smooth muscle cell migration, respectively, both of which appear to
be involved in the restenosis process.5 Combined
inhibition of both integrins,6 specific inhibition of
vß3,7 8 9 10 11
and profound antibody-induced thrombocytopenia12 inhibit
neointimal thickening after arterial injury in
animal models. Abciximab inhibits both integrins and has been shown to
decrease the incidence of target lesion
revascularization (TLR) after
angioplasty.13 Abciximab also cross-reacts with the
leukocyte integrins Mac-1 and intracellular adhesion molecule-1, which
mediate inflammation after arterial injury and may be
involved in restenosis.14 15
We hypothesized that intravenous abciximab might diminish neointimal hyperplasia after intracoronary stenting in humans. This study was designed to test that hypothesis, determining neointimal hyperplasia by measuring in-stent volume obstruction by 3D arterial reconstruction of intravascular ultrasound (IVUS) images.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Study Design and Study Population
The Evaluation of ReoPro® And Stenting to Eliminate Restenosis (ERASER) study was a double-blind, placebo-controlled randomized trial carried out at 17 institutions. Patient enrollment began May 16, 1996, and was completed February 17, 1997. The protocol was approved by the institutional review board at all sites. Eligible patients provided written informed consent. Patients were required to have a de novo target coronary artery stenosis of
50% in a vessel of diameter 2.75 to 3.5 mm
and to be referred for intracoronary stent implantation with an
(expected single) 15-mm Palmaz-Schatz stent. Patients were excluded if
they had a myocardial infarction within 72 hours before randomization,
evident intracoronary thrombus, previous coronary
intervention on a nontarget lesion within the past 6 months, planned
debulking before stent placement, expected inability to access the
target lesion by IVUS (eg, calcified plaque, tortuous vessel), or
standard contraindications to the use of abciximab.13
Randomization and Drug Regimen
Patients were randomized after the target lesion had been
identified by angiography and before first device activation into 1 of
3 groups by sealed envelopes provided by the coordinating center. The
physicians involved with the procedure remained blinded to study drug.
The treatment regimens were (1) placebo bolus+2 consecutive 12-hour
placebo infusions; (2) abciximab 0.25 mg/kg bolus+0.125 µg ·
kg-1 · min-1 (up
to 10 µg/min maximum) continuous infusion for 12 hours followed by
12-hour placebo infusion; or (3) abciximab 0.25 mg/kg bolus+2
consecutive 12-hour 0.125 µg ·
kg-1 · min-1 (up
to 10 µg/min maximum) infusions. Patients received 200 mg oral
aspirin 2 hours before the procedure and intravenous
heparin titrated to an activated clotting time of 250 to 300
seconds. Aspirin was to be continued for 6 months. It was strongly
recommended that heparin be discontinued immediately on the completion
of the procedure to allow removal of arterial sheaths 4 to
6 hours later. When heparin was continued for clinical indications, it
was to be titrated to an activated partial thromboplastin time
between 50 and 70 seconds. Ticlopidine use was left to the
investigator's discretion. Patients received
nitroglycerin 100 to 300 µg IC immediately before
preintervention, postintervention, and follow-up angiograms and IVUS
interrogations.
Stent Implantation Procedure
Stent implantation was performed according to routine clinical
practice, aiming for an "optimal" result. To standardize the
measurements, a single 15-mm Palmaz-Schatz stent was planned in all
cases. If clinically indicated, a second stent could be placed in
series with the first. Postdilatation to 14 atm was strongly
recommended. IVUS guidance was used to confirm optimal placement or
suggest further dilatations. The MUSIC criteria (complete stent
apposition, symmetrical expansion, and adequate in-stent
cross-sectional dimension16 ) were used to define adequate
stent expansion.
Follow-Up Evaluation
Patients were discharged from hospital after completion of study
drug infusion and being deemed clinically stable. In-hospital testing
included electrocardiography before treatment,
at the completion of the stent procedure, and at hospital discharge;
platelet count before study drug infusion, at 2, 12, and 24 hours
after initiation of study drug, and at hospital discharge; and creatine
kinase with MB isoenzymes 
2 hours before study drug administration
and at 8, 16, and 24 hours.
Patients were asked to return for follow-up at 6 months for an assessment of clinical status, electrocardiography, angiography, and IVUS. If the patient required revascularization of the target lesion earlier, angiography and IVUS were to be performed at that time. These results were used as the 6-month results. If stent occlusion occurred within the first 30 days, the patient was excluded from evaluation for the primary efficacy end point. Coronary angiography performed earlier than 4 months was not used for end-point determination unless restenosis or TLR was documented.
Quantitative IVUS and Angiography
Three IVUS systems were used: Cardiovascular
Imaging Systems, Hewlett-Packard and Boston Scientific Corp, and
Endosonics. The same instrument type was used for poststent and
follow-up imaging. Results from the 3 instruments would be expected to
be similar.17 The IVUS examination was performed with
motorized pullback of the ultrasound catheter at 0.5 mm/s
beginning 1 cm distal and continuing to 1 cm proximal to the
stent(s) with videotape recording.
Ultrasound analysis was performed by the Cardialysis IVUS Core Laboratory by investigators blinded to clinical treatment. A maximum of 200 IVUS images were digitized at a user-defined digitization frame rate (maximum 20 images/s). A minimum-cost algorithm was applied for the automated contour detection of the intimal leading edge and the intracoronary stent boundary. Segments of 3 to 5 mm immediately proximal and distal to the stent were taken as reference diameter. In these segments, the intimal leading edge and external boundary contours (plaque-media) were determined by the algorithm.
Quantitative ultrasound measurements included diameter (mm)
and area (mm2) in both the stent and the
reference segments. Volumes of the stent, lumen, and intimal
hyperplasia are calculated as
 |
Angiographic Measurements
Off-line quantitative coronary angiographic (QCA)
analysis was performed at the Washington (DC) Hospital Center
Angiographic Core Laboratory by investigators blinded to clinical
treatment. Cineangiograms were acquired at the clinical
sites in multiple, matched projections before and after stent
placement and at 6-month follow-up. Standard morphological criteria
were used to characterize baseline lesion complexity22 and
angiographic complications.23
Cine frames were selected from the 2 "sharpest and most severe" projections of the stenosis before and after stent placement and at late follow-up; sequential cine frames were matched for their position within the cardiac cycle. QCA used the CMS-GFT algorithm.24 Binary restenosis was defined as a >50% diameter stenosis at follow-up.
Definitions and End Points
The primary efficacy criterion for the trial was defined as
percent in-stent volume obstruction of the target lesion, measured at 6
months by IVUS. Primary safety objectives were defined as major
bleeding25 not associated with bypass surgery through
discharge or 7 days, whichever occurred first, and mortality and
intracranial hemorrhage through 6 months. Secondary efficacy
objectives were defined as target lesion mean and minimum lumen
diameter (MLD), late loss and loss index by QCA at 6 months, and a
composite of death, myocardial infarction, and TLR within 6 months.
Myocardial infarction was defined as (1) new significant Q wave of
0.04 seconds or having a depth of 25% of the corresponding R wave
amplitude in 2 contiguous leads or (2) creatine kinase MB 3 times
the upper limit of normal.
Study Hypothesis and Statistical Analysis
The primary study hypothesis was that either abciximab dosing
regimen would diminish in-stent percent volume obstruction compared
with placebo. Previous observation suggested an expected in-stent
volume obstruction of 38±24% (Gary Mintz, MD, personal
communication). To obtain 80% power to detect an absolute 11%
difference between treatment groups, 60 patients per group were
required. Assuming that 80% of randomized patients would return for an
interpretable 6-month IVUS, the total sample size was 225 patients. The
study was not powered to show differences in clinical end points.
Patients randomized but not treated with 1 stents or study drug or
who did not return for angiographic or ultrasound follow-up were
excluded from the primary efficacy analysis. Intergroup
differences were assessed by ANOVA or 
2
techniques. Grouping of the 2 abciximab groups for analysis of
clinical end points was prespecified. A nominal value of
P<0.05 was considered significant. Subset analyses
were prespecified only for 3 subgroups: optimal versus suboptimal stent
deployment, study drug administration according to protocol or not, and
1 stent at the target lesions versus 2 stents.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Baseline Characteristics
Baseline patient and angiographic characteristics are shown in Tables 1
and 2. Patient flow through the study is
depicted in Figure 1. There were no
intragroup differences in any of the measured characteristics.
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Initial Treatment and Outcome
Initial treatments are described in Table 3. Two hundred twenty-two patients
(98.7%) received study drug, and 199 (88.4%) completed the study
infusion. The median activated clotting time before treatment
was 312 seconds. Two hundred seventeen patients (96.4%) received
coronary stents. Less than optimal stent deployment by the
MUSIC criteria was observed in 45%, 62%, and 67% of the placebo and
short and long abciximab groups, respectively (P=NS).
Angiographic complications were rare and were equally distributed among
the treatment groups.
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Clinical Outcomes
Clinical outcomes are described in Table 4. The composite in-hospital end point of
death, myocardial infarction, or TLR was seen in 11.3%, 5.1%, and
9.3% in the placebo, short abciximab infusion, and long abciximab
infusion groups, respectively. The composite end point of death,
myocardial infarction, or TLR at 6 months did not differ among the
groups (25.4% placebo versus 21.4% combined abciximab,
P=NS). TLR predominated in the composite primary clinical
end point and occurred in 15.5% of placebo-treated patients and 13.6%
of the combined abciximab-treated group (P=NS).
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IVUS and QCA
Data for IVUS and QCA are presented in Tables 5 and 6 and
are illustrated in Figures 2 and 3. At the completion of the stenting
procedure, the treatment groups were well balanced for angiographic
percent stenosis. At follow-up, there was no difference in
angiographic outcome, with MLDs of 2.7±0.6, 2.6±0.9, and
2.7±0.7 mm in the placebo, 12-hour, and 24-hour abciximab groups,
respectively. When measured by IVUS, with or without imputation
for target sites that were occluded or tightly stenosed and could not
be crossed by the device (placebo, n=5; 12-hour abciximab infusion,
n=5; 24-hour abciximab infusion, n=4), there was no difference in the
in-stent percent volume obstruction among the 3 groups (see Figure 3).
Follow-up IVUS and QCA measurements of mean luminal diameter
(r=0.83) and MLD (r=0.72) were closely
correlated. Because of heightened interest engendered by the EPISTENT
trial results in diabetics, we also present a post hoc
analysis of the primary end-point data, divided into subsets by
diabetic status. In-stent volume obstruction for diabetics randomized
to placebo was 35±22% (n=3), randomized to 12-hour infusion of
abciximab was 27±18% (n=10), and randomized to 24-hour infusion of
abciximab was 31±16 (n=13).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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This study shows that abciximab, given either at the same dose or for the same dose at a longer duration than that which decreased TLR at 6 months from 22.3% to 16.5% (P=0.007) after balloon angioplasty in the EPIC study,13 does not reduce neointimal volume after stenting.
This observation enhances our understanding of restenosis
after stenting by essentially eliminating 1 putative mechanism,
organization of platelet-rich thrombus, and improving our
understanding of the role of the
vß3 receptor in that
process. At the onset of this study, the abciximab dose used was
believed to be likely to inhibit the
vß3 receptor, whose
KD50 (11±3 nmol) is similar to the
platelet IIbß3
receptor.26 Reconciliation of these data suggests that the
dose used was too low or asynchronously timed with a maximal
vß3 receptor
expression, or that redundant pathways exist to, in a teleological
sense, "protect" the wound-healing process. In fact, recent data
suggest that vß3
receptor expression after arterial injury peaks at 7 to 14
days,27 after high-level receptor inhibition by abciximab,
as used in this study, it diminished.26 28 Unless
the late clinical benefit noted in EPIC was due to happenstance alone,
one would have to invoke a different set of mechanisms than those
tested in the present study.
This was the first clinical trial to use percent volume coronary obstruction assessed by IVUS as a primary study end point. Our results provide insight into the advantages and disadvantages of this end point instead of percent stenosis or MLD as judged by QCA, or instead of clinical events. IVUS-determined 3D neointimal volume was chosen because it most closely reflects the tissue mass of restenosis, it could be easily measured because of the visibility of the stent to IVUS, and its mean/SD ratio would allow a lower sample size with adequate power to detect a plausible biological difference.
Correlations between IVUS and QCA measurements were good. We did not anticipate the relatively large proportion of patients without follow-up IVUS because of the presence of a high-grade coronary stenosis that made passage of the ultrasound device unsafe or impossible (6.5%) or the relatively large proportion of patients with technically inadequate studies (5.6%). Were a therapeutic intervention to decrease restenosis, the imbalance in the number of lesions that could not be restudied because of failure to pass the ultrasound device would necessitate an acceptable method of imputation for this end point to be useful. Miniaturization of the IVUS probe and further clinical experience should diminish these problems in the future. One must question whether a measurement of the volume of neointima itself or one that on the basis of prior QCA studies (percent area stenosis or minimum cross-sectional area)29 30 may better correlate with adverse clinical events is better suited as a primary end point for such a trial. Notably, the coefficient of variation (SD/mean) for the QCA data was less than for the IVUS data, implying that on a purely statistical basis, QCA has greater power to detect differences in a given patient population than does IVUS. Finally, a sizable proportion of implanted stents did not meet criteria for "optimal" deployment by the MUSIC criteria. These criteria were infrequently achieved in that study also.16
Three other factors may influence the interpretation of this
study. First, the results should not necessarily be extrapolated to
balloon angioplasty because the mechanisms of restenosis
differ.31 32 Second, we cannot exclude a benefit of
larger, and possibly longer, infusion doses of abciximab or of a more
powerful or longer-lasting
vß3 receptor
inhibitor.33 Finally, the important reduction
in periprocedural myocardial infarction with abciximab noted in the
EPIC,13 EPILOG,34 and EPISTENT
studies,35 with which our data are consistent,
must be considered.
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Footnotes |
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1 The principal investigators and study coordinators of the ERASER Study Group are listed in the Appendix.
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Steering Committee
Stephen G. Ellis, MD; Mark B. Effron, MD; Herman K. Gold, MD; Martin B. Leon, MD; Jeffrey J. Popma, MD; and Patrick W.J.C. Serruys, MD.
Principal Investigators, Study Coordinators, and Sites
North America
Antonio Colombo, MD, and Nancy Cohen, RCVT, Lenox Hill Hospital,
New York, NY; Stephen G. Ellis, MD, and Nadine Juran, RN, The Cleveland
Clinic Foundation, Cleveland, Ohio; Herman K. Gold, MD, and Wendy
Werner, RN, Massachusetts General Hospital, Boston, Mass; Richard R.
Heuser, MD, and Sue Spooner, RN, Arizona Heart Institute, Phoenix,
Ariz; Charanjit S. Rihal, MD, and Robyn Fox, Mayo Clinic,
Rochester, Minn; Martin B. Leon, MD, and Jay Brennan, RN, Washington
Hospital Center, Washington, DC; Donald Ricci, MD, and Rebecca Fox, PA,
Vancouver Hospital and Health Science Center, Vancouver, BC; Paul S.
Teirstein, MD, Shela Norman, RN, and Nancy Morris, RN, Scripps Clinic
and Research Foundation, La Jolla, Calif; James Zidar, MD, and Michele
Rund, RN, Duke University Medical Center, Durham, NC.
International
Yaron Almagor, MD, and Astrid Rojansky, MHA, Shaare Zedek
Medical Center, Jerusalem, Israel; Antonio Colombo, MD; Carlo DiMario,
MD; Bernhard Reimers, MD; and Giovanni Martini, Clinica Columbus,
Milano, Italy; Michael Haude, MD, and Beate Eick, MD, University GHS
Essen, Germany; Thierry Lefevre, MD; Gaetan Karillon, MD; and
Marie-Claude Morice, MD, Clinique du Bois de Verrieres l'Angio,
Antony, France; Harald Mudra, MD; Karl Henneke, MD; and Frank
Werner, MD, University of Munich, Germany; Jan H. Piessens, MD, and
Sabine Van Roey, RN, University Hospital Gasthuisberg, Leuven,
Belgium; Martin Rothman, MD, and Melanie Preston, RN, London Chest
Hospital, London, UK; and Patrick W.J.C. Serruys, MD, and A. Gijzel,
MD, Academisch Ziekenhuis, Rotterdam, Netherlands.
Angiographic Core Laboratory
Alexandra L. Lansky, MD; Jeffrey J. Popma, MD.
Intravascular Ultrasound Core Laboratory
Pim de Feyter, MD; Gerrit-Anne van Es, PhD.
Received October 30, 1998; revision received May 24, 1999; accepted June 2, 1999.
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References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
1. Fischman DL, Leon MB, Baim DS, Schatz RA, Savage MP, Penn I, Detre K, Veltri L, Ricci D, Nobuyoshi M, Cleman M, Heuser R, Almond D, Teirstein PS, Fish RD, Colombo A, Brinker J, Moses J, Shaknovich A, Hirshfeld J, Bailey S, Ellis S, Rake R, Goldberg S, for the STRESS Investigators. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med. 1994;331:496–501.
2.
Serruys PW, de Jaegere P, Kiemeneij F, Macaya C,
Rutsch W, Heyndrickx G, Emanuelsson H, Marco J, Legrand V, Materne P,
Belardi J, Sigwart U, Colombo A, Goy JJ, van den Heuvel P, Delcan J,
Morel M-A, for the BENESTENT Study Group. A comparison of
balloon-expandable-stent implantation with balloon angioplasty in
patients with coronary artery disease. N Engl J
Med. 1994;331:489–495.
3. Schwartz RS, Edwards WD, Huber KC, Antoniades LC, Bailey KR, Camrud AR, Jorgenson MA, Holmes DR Jr. Coronary restenosis: prospects for solution and new perspectives from a porcine model. Mayo Clin Proc. 1993;68:54–62.[Medline] [Order article via Infotrieve]
4. Miller DD, Karim MA, Edwards WD, Schwartz RS. Relationship of vascular thrombosis and inflammatory leukocyte infiltration to neointimal growth following porcine coronary artery stent placement. Atherosclerosis. 1996;124:145–155.[Medline] [Order article via Infotrieve]
5. Jang Y, Lincoff AM, Plow EF, Topol EJ. Cell adhesion molecules in coronary artery disease. J Am Coll Cardiol. 1994;24:1591–1601.[Abstract]
6.
Matsuno H, Stassen JM, Vermylen J, Deckmyn H.
Inhibition of integrin function by a cyclic RGD-containing peptide
prevents neointima formation. Circulation. 1994;90:2203–2206.
7. van der Zee R, Passeri J, Barry JJ, Cheresh DA, Isner JM. A neutralizing antibody to the alpha v beta 3 integrin reduces neointimal thickening in a balloon-injured rabbit iliac artery. Circulation. 1996;94(suppl I):I-257. Abstract.
8. Wajih N, Sane DC. Mutants of vitronectin at the Arg-Gly-Asp cell recognition sequence have reduced haptotactic capacity for smooth muscle cells. Circulation. 1997;96(suppl I):I-668. Abstract.
9. Yue T-L, Louden C, Gu J-L, Vickery LM, Johanson K, Stadel JM. Sk&F107260, a cyclic RGD peptide, inhibits integrin avß3-mediated vascular smooth muscle cell migration and reduces neointima formation following balloon injury to the rat carotid artery. Circulation. 1997;96(suppl I):I-668. Abstract.
10. Racanelli AL, Flint SK, Schlingmann KL, Corjay MH, Stoltenborg JK, Diamond SM, Slee AM, Reilly TM. Inhibition of neointimal formation by a nonpeptide avß3 antagonist in a rabbit model. Circulation. 1997;96(suppl I):I-668. Abstract.
11.
Choi ET, Engel L, Callow AD, Sun S, Trachtenberg
J, Santoro S, Ryan US. Inhibition of neointimal hyperplasia
by blocking vß3
integrin with a small peptide antagonist
GpenGRGDSPCA. J Vasc Surg. 1994;19:125–134.[Medline]
[Order article via Infotrieve]
12. Friedman RJ, Stemerman MB, Wenz B, Moore S, Gauldie J, Gent M, Tiell ML, Spaet TH. The effect of thrombocytopenia on experimental arteriosclerotic lesion formation in rabbits. J Clin Invest. 1977;60:1191–1201.
13. Topol EJ, Califf RM, Weisman HF, Ellis SG, Tcheng JE, Worley S, Ivanhoe R, George BS, Fintel D, Weston M, Sigmon K, Anderson KM, Lee KL, Willerson JT, on behalf of the EPIC Investigators. Randomised trial of coronary intervention with antibody against platelet IIb/IIIa integrin for reduction of clinical restenosis: results at six months. Lancet. 1994;343:881–886.[Medline] [Order article via Infotrieve]
14.
Simon DI, Xu H, Ortlepp S, Rogers C, Rao NK. 7E3
monoclonal antibody directed against the platelet
glycoprotein IIb/IIIa cross-reacts with the leukocyte
integrin Mac-1 and blocks adhesion to fibrinogen and ICAM-1.
Arterioscler Thromb Vasc Biol. 1997;17:528–535.
15. Campbell R, Edelman ER, Simon DI. Blockade of the leukocyte integrin Mac-1 reduces experimental restenosis. Circulation. 1997;96(suppl I):I-667. Abstract.
16. de Jaegere P, Mudra H, Almagor Y, Figulla H, Penn I, Doucet S, Bartorelli A, Hamm C, for the Music Study Investigators. In-hospital and 1-month clinical results of an international study testing the concept of IVUS guided optimized stent expansion alleviating the need of systemic anticoagulation. Presented at the American College of Cardiology Scientific Sessions, Anaheim, Calif, March 26, 1996.
17. Tardif JC, Bilodeau L, Doucet S, Bonan R, Côté G. Comparison between mechanical and phased-array designs for intravascular ultrasound in stented and non-stented coronary arteries: animal studies. Circulation. 1995;92(suppl I):I-600. Abstract.
18. von Birgelen C, Di Mario C, Li W, Schuurbiers JC, Slager CJ, de Feyter PJ, Roelandt JR, Serruys PW. Morphometric analysis in three-dimensional intracoronary ultrasound: an in-vitro and in-vivo study using a novel system for the contour detection of lumen and plaque. Am Heart J. 1996;132:516–527.[Medline] [Order article via Infotrieve]
19. von Birgelen C, Mintz GS, Nicosia A, Foley DP, van der Giessen WJ, Bruining N, Airiian SG, Roelandt JRTC, de Feyter PJ, Serruys PW. Electrocardiogram-gated intravascular ultrasound image acquisition after coronary stent deployment facilitates on-line three-dimensional reconstruction and automated lumen quantification. J Am Coll Cardiol. 1997;30:436–443.[Abstract]
20. Li W, von Birgelen C, DiMario C, Boersma E, Gussenhoven EJ, van der Patten N, Bom N. Semi-automatic contour detection for volumetric quantification of intracoronary ultrasound. In: Computers in Cardiology 1994. Los Alamitos, Calif: IEEE Computer Society Press; 1994:277–280.
21.
von Birgelen C, de Vrey EA, Mintz GS, Nicosia A,
Bruining N, Li W, Slager CJ, Roelandt JRTC, Serruys PW, de Feyter PJ.
ECG-gated three-dimensional intravascular ultrasound: feasibility and
reproducibility of the automated analysis of coronary
lumen and atherosclerotic plaque dimensions in humans.
Circulation. 1997;96:2944–2952.
22.
Ellis SG, Vandormael MG, Cowley MJ. Coronary
morphologic and clinical determinants of procedural outcome with
angioplasty for multivessel coronary disease.
Circulation. 1990;82:1193–1202.
23. Popma JJ, Bashore T. Qualitative and quantitative angiography. In: Topol E, ed. Interventional Cardiology. Philadelphia, Pa: WB Saunders; 1993.
24. van der Zwet PM, Reiber JH. A new approach for the quantification of complex lesion morphology: the gradient field transform: basic principles and validation results. J Am Coll Cardiol. 1994;24:216–224.[Abstract]
25.
Antman EM, for the TIMI 9a Investigators. Hirudin in
acute myocardial infarction: safety report from the
Thrombolysis and Thrombin Inhibition in Myocardial
Infarction (TIMI) 9A Trial. Circulation. 1994;90:1624–1630.
26.
Tam SH, Sassoli PM, Jordan RE, Nakada MT. Abciximab
(ReoPro, chimeric 7E3 Fab) demonstrates equivalent affinity and
functional blockade of glycoprotein IIb/IIIa and
vß3 integrins.
Circulation. 1998;98:1085–1091.
27. Srivatsa SS, Tsao P, Holmes DR Jr, Schwartz RS, Mousa SA. Temporal and spatial variation in alpha v beta 3 integrin expression following deep arterial injury in the porcine coronary restenosis model. J Am Coll Cardiol. 1997;29:153A. Abstract.
28.
Mascelli MA, Lance ET, Damaraju L, Wagner CL, Weisman
HF, Jordan RE. Pharmacodynamic profile of short-term abciximab
treatment demonstrates prolonged platelet inhibition with gradual
recovery from GP IIb/IIIa receptor blockade. Circulation. 1998;97:1680–1688.
29.
Di Carli M, Czernin J, Hoh CK, Gerbaudo VH, Brunken RC,
Huang S-C, Phelps ME, Schelbert HR. Relation among stenosis
severity, myocardial blood flow, and flow reserve in patients with
coronary artery disease. Circulation. 1995;91:1944–1951.
30.
Wilson RF, Marcus ML, White CW. Prediction of the
physiologic significance of coronary arterial
lesions by quantitative lesion geometry in patients with limited
coronary artery disease. Circulation. 1987;75:723–732.
31.
Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler
LF, Wong C, Hong MK, Kovach JA, Leon MB. Arterial
remodeling after coronary angioplasty: a serial intravascular
ultrasound study. Circulation. 1996;94:35–43.
32.
Hoffmann R, Mintz GS, Dussaillant GR, Popma JJ, Pichard
AD, Satler LF, Kent KM, Griffin J, Leon MB. Patterns and mechanisms of
in-stent restenosis: a serial intravascular ultrasound study.
Circulation. 1996;94:1247–1254.
33. Marjinanowski MM, Nakada MT, Sundell BI, Kelly AB, Jordan RE, Jakubowski JA, Chronos NAF, Hanson SR. Abciximab reduces vascular lesion formation in non-human primates. J Am Coll Cardiol. 1999;33:69A. Abstract.
34.
EPILOG Investigators. Platelet
glycoprotein IIb/IIIa receptor blockade and low-dose
heparin during percutaneous coronary
revascularization. N Engl J
Med. 1997;336:1689–1697.
35. The EPISTENT Investigators. Randomised placebo-controlled and balloon-angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein-IIb/IIIa blockade. Lancet. 1998;352:87–92.[Medline] [Order article via Infotrieve]
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|
|
|
|
 |
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
 |
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
 |
|
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