(Circulation. 2000;101:360.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Three-Year Clinical and Angiographic Follow-Up After Intracoronary Radiation
Results of a Randomized Clinical Trial
From the Division of Cardiovascular Diseases (P.S.T., R.J.R., R.A.S., E.M.G., S.S., K.S., D.A.C.) and Division of Radiation Oncology (V.M., S.J., P.T.), Scripps Clinic, La Jolla, Calif; Division of Cardiology, Brigham and Women’s Hospital (J.J.P.), Boston, Mass; and Division of Cardiology, Washington Hospital Center (M.B.L.), Washington, DC.
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Abstract |
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Background—Although several early trials indicate treatment of restenosis with radiation therapy is safe and effective, the long-term impact of this new technology has been questioned. The objective of this report is to document angiographic and clinical outcome 3 years after treatment of restenotic stented coronary arteries with catheter-based 192Ir.
Methods and Results—A double-blind, randomized trial compared 192Ir with placebo sources in patients with previous restenosis after coronary angioplasty. Over a 9-month period, 55 patients were enrolled; 26 were randomized to 192Ir and 29 to placebo. At 3-year follow-up, target-lesion revascularization was significantly lower in the 192Ir group (15.4% versus 48.3%; P<0.01). The dichotomous restenosis rate at 3-year follow-up was also significantly lower in 192Ir patients (33% versus 64%; P<0.05). In a subgroup of patients with 3-year angiographic follow-up not subjected to target-lesion revascularization by the 6-month angiogram, the mean minimal luminal diameter between 6 months and 3 years decreased from 2.49±0.81 to 2.12±0.73 mm in 192Ir patients but was unchanged in placebo patients.
Conclusions—The early clinical benefits observed after treatment of coronary restenosis with 192Ir appear durable at late follow-up. Angiographic restenosis continues to be significantly reduced in 192Ir-treated patients, but a small amount of late loss was observed between the 6-month and 3-year follow-up time points. No events occurred in the 192Ir group to suggest major untoward effects of vascular radiotherapy. At 3-year follow-up, vascular radiotherapy continues to be a promising new treatment for restenosis.
Key Words: radioisotopes • radiotherapy • stents • coronary disease • restenosis
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Introduction |
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Restenosis continues to be the major limitation of catheter-based vascular procedures. Early preclinical studies have demonstrated radiation therapy to be a uniquely efficacious treatment for restenosis.1 2 3 4 5 6 7 8 Although short-term clinical results have been promising, the long-term efficacy and, most importantly, safety of this technique are not known. The possibility of late adverse angiographic findings such as aneurysm formation, perforation, or accelerated vascular disease is of significant concern.2 3 The objective of this report is to document angiographic and clinical outcome 3 years after treatment of restenotic stented coronary arteries with catheter-based 192Ir.
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Methods |
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The Scripps Coronary Radiation to Inhibit Proliferation Post-Stenting (SCRIPPS) trial was a double-blind, randomized trial comparing 192Ir with placebo sources. The methods have been described previously.9 This clinical trial was approved by the institution’s human subjects and radiation safety committees. Patient inclusion criteria required a target lesion in a restenotic coronary artery that either already contained a stent or was a candidate for
stent placement. If the lesion was not already stented, single
or (if required) tandem coronary stenting (Johnson and Johnson
Interventional Systems) was performed. If stents had been placed
previously, redilation was undertaken, and often, additional stents
were placed within the original stent to optimize the angiographic
result. In all cases, high-pressure (
18 atm) balloon dilations were
performed in an attempt to achieve a 0% residual stenosis
within the stented segment. Patients were then randomly assigned to
receive a 0.76-mm (0.03-inch) ribbon (Best Industries) containing
sealed sources of either 192Ir or placebo. The
study ribbon was left in place for 20 to 45 minutes, as required to
administer the prescribed dose of 800 to 3000 cGy to the adventitial
border.9
All patients were requested to return for repeat coronary angiography at 6 months and again at 3 years. Revascularization was repeated after follow-up angiography only if the patient had recurrent symptoms or if functional tests demonstrated the presence of coronary ischemia. At 3-year follow-up, patients were queried regarding any hospitalizations or procedures occurring since their index procedure. Medical records were obtained from each patient’s primary treating physician along with copies of hospital records from all admissions and procedures. Where necessary, the county coroner’s office was contacted to obtain data regarding the cause and date of patient deaths. Several patients who initially appeared lost to follow-up were located by a commercial service (1–800-US-SEARCH).
Core laboratory quantitative angiography was performed at the Brigham
and Women’s Hospital Center by individuals blinded to the treatment
allocation, as previously described.9 10 Selected serial
cine frames, obtained from 2 unforeshortened projections and
matched for position within the cardiac cycle with the use of
side-by-side projectors, were digitized with a cine video
converter, with the contrast-filled catheter used as the calibration
standard. The reference vessel was defined as the vessel segment 5
mm proximal and distal to the radiation sources. Binary
restenosis was defined as stenosis 50% of the
luminal diameter of the stent and/or stent margin 5 mm proximal
and distal to the radiation sources at follow-up. The assessment of
binary restenosis at 3 years included only those patients with
angiographic follow-up beyond 27 months, unless a target-lesion
revascularization occurred earlier. Patients with
restenosis at the 6-month angiogram but no target-lesion
revascularization who lacked 3-year angiography (1
in each group) were excluded from the late binary restenosis
analysis because stenosis regression could not be ruled
out. An analysis of serial changes in minimal luminal diameter
and diameter stenosis (Figures 4
and 5) included
only those patients with 3-year angiograms who had not had a
target-lesion revascularization by the 6-month
angiogram.
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Target-lesion revascularization was defined as
coronary angioplasty or surgical bypass of the target vessel
due to the presence of 50% diameter stenosis of the target
lesion as measured by the core angiographic laboratory. The target
lesion was defined as the stented segment in addition to the stent
margins 5 mm proximal and distal to the radioactive or placebo
sources. Thus, target-lesion revascularization
included revascularization of both in-stent
restenosis and restenosis at the stent or source
margins due to "edge effect." Target-vessel
revascularization included
revascularization of the target lesion or a segment
outside the target lesion but within the same vessel.
Non–target-vessel revascularization was defined as
revascularization of an epicardial vessel that did
not contain the target lesion. Myocardial infarction was defined as an
elevation of the MB fraction of creatinine kinase to a
value 3 times the upper limit of the normal range.
For the analysis of continuous data, Mann-Whitney rank sum
tests were used to assess differences between the 2 treatment groups,
except for serial comparisons of luminal diameter and percent diameter
stenosis, which were done with a 2-way ANOVA. The results are
expressed as mean±SD. Categorical data were compared with the use of
2 or Fisher’s exact test except for the
composite clinical end point, which was analyzed by means of
Kaplan-Meier survival analysis, with differences between the 2
treatment groups compared with the use of a Mantel-Cox test of
significance.
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Results |
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Between March 24 and December 22, 1995, 55 patients were enrolled in this study; 26 were randomized to 192Ir and 29 to placebo. Baseline clinical and angiographic factors were similar in the 2 groups. In-stent restenosis was present in 62% of both treated and placebo groups (Table 1
).
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Clinical follow-up was obtained on or after the 3-year anniversary
following the index procedure in 100% of living patients (Table 2). The mean time from index study
procedure to clinical follow-up was similar in
192Ir and placebo groups (39.1±2.3 versus
39.6±2.8 months; P=NS). Follow-up times ranged from 36 to
44 months in 192Ir patients and 36 to 46 months
in placebo patients.
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At 3-year follow-up, target-lesion
revascularization occurred in 4 patients (15.4%)
in the 192Ir group compared with 14 (48.3%) in
the placebo group (P<0.01). One patient in each group
sustained a new target-lesion revascularization
after the 6-month follow-up angiogram: at 36 months for an
asymptomatic 192Ir patient and at 40
months for a symptomatic placebo patient (Figure 1). Both restenoses were focal
and occurred within the target segment (not margins) at sites with
<50% diameter stenosis on the 6-month angiogram.
Target-vessel revascularization was also lower in
192Ir patients, occurring in 8 (30.8%) treated
versus 17 (58.7%) placebo patients (P=0.04). Target-vessel
revascularization was higher than target-lesion
revascularization in both groups because 4 patients
in the treated group and 3 in the placebo group had
revascularization of disease that was located at a
significant distance (>5 mm) from the target lesion and believed
therefore to be unrelated to edge effect. Two of these
revascularization procedures in the treated group
and 1 in the placebo group occurred between the 6-month and 3-year
follow-up periods. Non–target-vessel
revascularization, with or without target-vessel
revascularization, was similar in both groups,
occurring in 7 (26.9%) treated and 8 (27.6%) placebo patients. In
both groups, revascularization of nontarget lesions
over the follow-up period was common. Eight (30.8%) treated and
7 (24.1%) placebo patients who did not need target-lesion
revascularization did require
revascularization of other, nontarget lesions.
Thus, by 3 years, a total of 12 (46.2%) treated and 21 (72.4%)
placebo patients had undergone subsequent
revascularization procedures (Table 2
).
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There were 3 deaths in each group. Two of the deaths in the placebo group were cardiac deaths (at 8 and 11 months) associated with myocardial infarction, and the third (at 30 months) occurred in the postoperative period after bypass surgery for a target-lesion restenosis. One death in the 192Ir group (at 23 months) occurred in the postoperative period after bypass surgery for a non–target-lesion stenosis. Another death in the 192Ir group occurred in a patient who had self-terminated ticlopidine on day 3 and sustained a stent thrombosis that resulted in acute myocardial infarction on day 18 after the index procedure. Angiography during the acute thrombotic event and again at 6-month follow-up demonstrated 100% occlusion of the target lesion. This patient died 18 months after the study procedure of complications of abdominal surgery for diverticulitis. The third death was sudden (at 39 months) in a 192Ir-treatment-failure patient who had a target-lesion revascularization at 8 months.
The composite end point of death, myocardial infarction, or
target-lesion revascularization was significantly
lower in 192Ir versus placebo patients (23.1%
versus 55.2%; P=0.01). Life-table analysis of this
composite end point is displayed in Figure 2. Differences in clinical events were
driven largely by differences in the need for target-lesion
revascularization and become apparent at 
3
months. The 2 curves continue to diverge until 10 months, after which
clinical events are infrequent. However, owing to the large number of
non–target-lesion revascularizations, differences
in the composite end point of death, myocardial infarction, and
target-vessel revascularization (38.5% versus
65.5%; P<0.05) and differences in death, myocardial
infarction, and any revascularization (50% versus
79.3%; P=0.02) were less pronounced.
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As previously reported, initial follow-up angiography was obtained at a mean of 6.7 months in 96.4% of patients.9 At the 6-month time point, restenosis rates were significantly reduced in the 192Ir group (17% versus 54%; P=0.01). For the present report, all patients were asked to return for a repeat angiogram at 36 months. The mean interval from index procedure to late follow-up angiography was 36.7±4.5 months in 192Ir patients compared with 39.1±2.6 months in placebo patients (P=0.05). This late angiogram was obtained in 19 (73.1%) of 192Ir and 18 (62.1%) of placebo patients (P=NS). This represents 82.6% of living 192Ir and 69.2% of living placebo patients (P=NS). None of the 4 living 192Ir and 8 living placebo patients who refused 3-year angiography had symptoms of angina. Each of these patients had undergone numerous catheterization procedures in the past, had now broken the cycle of repeated invasive procedures, and adamantly refused catheterization.
At the 3-year follow-up, angiographic restenosis (50%
stenosis of the luminal diameter) either within the stent or at
its border (outside the stent but spanned by the study ribbon) was
observed in 33.3% of 192Ir patients compared
with 63.6% of placebo patients (P<0.05). Thus, whereas
restenosis rates were reduced by 69% by the 6-month angiogram,
restenosis was only reduced by 48% by the 3-year angiogram.
However, at 3 years, this reduction in restenosis was still
significant (P<0.05) (Figure 3).
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To better characterize the late natural history after radiation
therapy, angiograms were analyzed in patients who were alive
and had not had a target-lesion revascularization
by the 6-month angiographic time point. This is an important subgroup
of patients, because these lesions were not subjected to interim
interventions, and therefore, they best represent the late
natural history after radiation therapy. Late follow-up angiography was
obtained in 17 (81%) of 21 eligible 192Ir and 10
(71.4%) of 14 eligible placebo patients in this subgroup. The mean
minimal luminal diameter between the 6-month and 3-year angiograms
decreased from 2.49±0.81 to 2.12±0.73 mm (P=0.15) in
192Ir patients but was unchanged in placebo
patients in this subgroup (Figure 4).
Thus, when the analysis was confined only to lesions that were
"untouched by human hands" by the 6-month angiogram, a small
reduction in minimal luminal diameter was observed between 6 months and
3 years in the treated group that was not found in the placebo group.
Correspondingly, there was a small amount of late "catch up" in
percent diameter stenosis between 6 months and 3 years in
192Ir-treated patients that was not matched by
the placebo group. The percent diameter stenosis increased from
14±28% at 6 months to 26±28% (P=0.25) at 3 years in
192Ir-treated patients but only increased from
21±24% to 23±17% (P=0.75) in placebo patients (Figure 5).
Although our sample size was small, it is notable that only 24% of treated and 20% of placebo patients had a reduction in diameter stenosis of >15% between the 6-month and 3-year angiograms. Thus, most late serial changes in percent diameter stenosis were small. However, between the 6-month and 3-year angiograms, 4 patients in the treated group had an increase in diameter stenosis that brought the final luminal diameter to >50%, whereas only 1 patient in the placebo group crossed this 50% threshold. Of the 3 patients in the treated group who crossed over the 50% threshold but did not have a target-lesion revascularization, the absolute increases in diameter stenosis were small (14%, 15%, and 35%); however, this small amount of late catch up in the treated group did narrow the difference in dichotomous restenosis rates between the 2 groups. No aneurysms, pseudoaneurysms, or perforations were observed by the core angiographic laboratory on any follow-up angiograms of either the 192Ir group or the placebo group.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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After 3 years of clinical and angiographic follow-up, treatment with 192Ir continues to demonstrate improved clinical outcome compared with placebo. With 100% clinical follow-up and each living patient followed up for
36 months, the clinical
benefits initially observed at 6 and 24 months9 11 were
maintained, and no unexpected, radiation-related adverse events were
identified. Interestingly, in 192Ir-treated
patients, there were no clinically apparent restenoses after
the initial follow-up angiogram until protocol-mandated 3-year
angiography documented a high-grade target-lesion restenosis in
an asymptomatic treated patient. This lesion was located in
the proximal segment of a large-diameter left anterior descending
artery. Although the patient was asymptomatic, noninvasive
testing (performed after the follow-up diagnostic
angiogram) did demonstrate silent coronary ischemia,
which prompted a return to the catheterization
laboratory for repeat angioplasty. There was 1 late target-lesion
revascularization after the 6-month angiogram in
the placebo group. This patient, who initially resisted 3-year
angiography, underwent restudy owing to recurrence of symptoms
at 40 months, was found to have significant proximal right
coronary artery stenosis, and underwent repeat
angioplasty. Over the 3-year follow-up period, the composite clinical event rate (death, myocardial infarction, or target-lesion revascularization) in the treated group was lower than in the placebo group (23.1% versus 55.2%; P=0.01). The 3 deaths in the 192Ir group had clearly identified causes: 1 was a consequence of elective bypass surgery of a nontarget lesion, another was a sudden death in a treatment-failure patient, and another was due to complications following abdominal surgery 18 months after a stent thrombosis. Although it is possible that the stent thrombosis was related to radiation exposure (in the absence of ticlopidine), this vessel was documented to be 100% occluded on angiography 6 months after the index procedure and was therefore unlikely to be a site of sudden coronary closure, perforation, or other acute cardiac event.
Another important finding of the present study was the large number
of non–target-lesion revascularization procedures
in both the treated and placebo groups over the 3-year follow-up
period. Fully 30.7% of treated and 24.1% of placebo patients who did
not need target-lesion revascularization did
require revascularization of other nontarget
lesions (Table 2). Thus, by the end of the follow-up period,
50% of treated patients and 79.3% of placebo patients had sustained a
clinical event. It should be emphasized, therefore, that although
-radiation effectively reduced events associated with the target
lesion, this local therapy did not affect the development of disease
outside of the target segment. Late events were common, even in treated
patients.
At 3 years, the angiographic restenosis rate in the treated group was 48% lower than in the placebo group (33% versus 64%; P<0.05). In 192Ir patients who did not undergo target-lesion revascularization by the 6-month follow-up angiogram, the mean minimal luminal diameter decreased and the mean percent diameter stenosis increased by a small amount between the 6-month and 3-year angiograms. This reduction in diameter was not matched by the placebo group, whose mean minimal luminal diameter was unchanged over the late follow-up period. The number of patients with serial angiographic measurements was small, and standard deviations were large, and therefore, the possibility exists that the play of chance alone may account for these observations. Nevertheless, our findings may contradict the concept that radiation, in a stented artery, "freezes" the postprocedure angiographic result. The response of the vessel to radiation appeared to be somewhat dynamic over the 3-year follow-up period, and in some patients, there was continued late loss. This late loss was small, but in 4 treated patients, it was enough to cross the 50% diameter threshold, provoking an increase in the dichotomous restenosis rate. Although the increase in restenosis rate in treated patients from 17% to 33% over the 3-year period raises some concerns about the prognosis for an even longer follow-up period, it should be emphasized that all 4 patients were asymptomatic, and only 1 patient had a high-grade stenosis with evidence of ischemia that prompted revascularization. Also, this initial pilot trial intentionally prescribed a relatively low dose of radiation; higher radiation exposures may further improve long-term results. Importantly, late angiographic follow-up in the present study revealed no evidence of perforation, aneurysm, or pseudoaneurysm in 192Ir-treated patients. Thus, no safety issues unique to radiotherapy have been identified.
Our late results differ from the reported long-term follow-up after
stent implantation for de novo disease. In the only published study
examining 3-year angiographic outcome after initial stent implantation
(without radiation),12 the minimal luminal diameter
increased slightly but significantly between the 6-month and 3-year
angiograms. Several other clinical trials using vascular radiotherapy
have been published.13 14 15 16 17 In 1 study, 7-year follow-up
documented high patency rates after femoropopliteal arteries undergoing
angioplasty were exposed to intravascular
-radiation.14 15 16 Other reports evaluating the
long-term effects of coronary radiation are
pending.13
Study Limitations
The most important limitation of this study is its small sample
size. The distribution of baseline characteristics was not entirely
even, with a trend toward more diabetic patients in the placebo group.
Also, more asymptomatic patients in the placebo group
refused 3-year angiography, which may have increased the
restenosis rate documented in the placebo arm.
Conclusions
With 100% clinical follow-up 3 years after study entry, the
clinical efficacy of 192Ir appears durable. In
192Ir-treated patients, target-lesion
revascularization was reduced by 74% at 6 months
and 68% at 3 years. Angiographic restenosis was reduced by
69% at 6 months but only 48% at 3 years because of small reductions
in luminal diameter over the longer follow-up period. No perforations,
aneurysms, pseudoaneurysms, or other safety issues were
observed. At the 3-year time point, vascular radiotherapy continues to
be a promising treatment for restenosis.
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Acknowledgments |
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We wish to thank Mary Quinones, Mindy Fernandez, Ross Prpic, and Krishnan Suthanthiran of Best Industries for their assistance with this project.
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Footnotes |
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Reprint requests to Paul S. Teirstein, MD, Division of Cardiovascular Diseases, SW206, Scripps Clinic, 10666 N Torrey Pines Rd, La Jolla, CA 92037.
Dr Teirstein is a consultant for companies that manufacture vascular radiation products and owns patents and may receive royalties from the sale of vascular delivery systems.
Received September 7, 1999; revision received October 14, 1999; accepted November 1, 1999.
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J. Aoki, A. Colombo, D. Dudek, A. P. Banning, J. Drzewiecki, K. Zmudka, F. Schiele, M. E. Russell, J. Koglin, P. W. Serruys, et al. Peristent Remodeling and Neointimal Suppression 2 Years After Polymer-Based, Paclitaxel-Eluting Stent Implantation: Insights From Serial Intravascular Ultrasound Analysis in the TAXUS II Study Circulation, December 20, 2005; 112(25): 3876 - 3883. [Abstract] [Full Text] [PDF]
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G Sianos, A Hoye, F Saia, W van der Giessen, P Lemos, P J de Feyter, P C Levendag, R van Domburg, and P W Serruys Long term outcome after intracoronary {beta} radiation therapy Heart, July 1, 2005; 91(7): 942 - 947. [Abstract] [Full Text] [PDF]
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M. A. Costa and D. I. Simon Molecular Basis of Restenosis and Drug-Eluting Stents Circulation, May 3, 2005; 111(17): 2257 - 2273. [Full Text] [PDF]
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Authors/Task Force Members, S. Silber, P. Albertsson, F. F. Aviles, P. G. Camici, A. Colombo, C. Hamm, E. Jorgensen, J. Marco, J.-E. Nordrehaug, et al. Guidelines for Percutaneous Coronary Interventions: The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology Eur. Heart J., April 2, 2005; 26(8): 804 - 847. [Full Text] [PDF]
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D. H. Walter, M. Cejna, L. Diaz-Sandoval, S. Willis, L. Kirkwood, P. W. Stratford, A. B. Tietz, R. Kirchmair, M. Silver, C. Curry, et al. Local Gene Transfer of phVEGF-2 Plasmid by Gene-Eluting Stents: An Alternative Strategy for Inhibition of Restenosis Circulation, July 6, 2004; 110(1): 36 - 45. [Abstract] [Full Text] [PDF]
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K. Krueger, M. Zaehringer, M. Bendel, H. Stuetzer, D. Strohe, M. Nolte, D. Wittig, R.-P. Mueller, and K. Lackner De Novo Femoropopliteal Stenoses: Endovascular Gamma Irradiation Following Angioplasty--Angiographic and Clinical Follow-up in a Prospective Randomized Controlled Trial Radiology, May 1, 2004; 231(2): 546 - 554. [Abstract] [Full Text] [PDF]
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R. Waksman, A. E. Ajani, R. L. White, R. Chan, B. Bass, A. D. Pichard, L. F. Satler, K. M. Kent, R. Torguson, R. Deible, et al. Five-Year Follow-Up After Intracoronary Gamma Radiation Therapy for In-Stent Restenosis Circulation, January 27, 2004; 109(3): 340 - 344. [Abstract] [Full Text] [PDF]
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M. Degertekin, P. A. Lemos, C. H. Lee, K. Tanabe, J.E. Sousa, A. Abizaid, E. Regar, G. Sianos, W. J. van der Giessen, P. J. de Feyter, et al. Intravascular ultrasound evaluation after sirolimus eluting stent implantation for de novo and in-stent restenosis lesions Eur. Heart J., January 1, 2004; 25(1): 32 - 38. [Abstract] [Full Text] [PDF]
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H.-J. Cho, H.-S. Kim, M.-M. Lee, D.-H. Kim, H.-J. Yang, J. Hur, K.-K. Hwang, S. Oh, Y.-J. Choi, I.-H. Chae, et al. Mobilized Endothelial Progenitor Cells by Granulocyte-Macrophage Colony-Stimulating Factor Accelerate Reendothelialization and Reduce Vascular Inflammation After Intravascular Radiation Circulation, December 9, 2003; 108(23): 2918 - 2925. [Abstract] [Full Text] [PDF]
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M. Hoher, J. Wohrle, M. Wohlfrom, J. Kamenz, T. Nusser, O. C. Grebe, H. Hanke, M. Kochs, S. N. Reske, V. Hombach, et al. Intracoronary {beta}-Irradiation With a Rhenium-188-Filled Balloon Catheter: A Randomized Trial in Patients With De Novo and Restenotic Lesions Circulation, June 24, 2003; 107(24): 3022 - 3027. [Abstract] [Full Text] [PDF]
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D. W. Losordo, J. M. Isner, and L. J. Diaz-Sandoval Endothelial Recovery: The Next Target in Restenosis Prevention Circulation, June 3, 2003; 107(21): 2635 - 2637. [Full Text] [PDF]
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A. E. Ajani, R. Waksman, E. Cheneau, D.-H. Cha, S. McGlynn, M. Castagna, R. C. Chan, L. F. Satler, K. M. Kent, A. D. Pichard, et al. The outcome of percutaneous coronary intervention in patients with In-Stentrestenosis who failed intracoronary radiation therapy J. Am. Coll. Cardiol., February 19, 2003; 41(4): 551 - 556. [Abstract] [Full Text] [PDF]
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K. Tanabe, P. W. Serruys, E. Grube, P. C. Smits, G. Selbach, W. J. van der Giessen, M. Staberock, P. de Feyter, R. Muller, E. Regar, et al. TAXUS III Trial: In-Stent Restenosis Treated With Stent-Based Delivery of Paclitaxel Incorporated in a Slow-Release Polymer Formulation Circulation, February 4, 2003; 107(4): 559 - 564. [Abstract] [Full Text] [PDF]
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