(Circulation. 1995;91:1533-1539.)
© 1995 American Heart Association, Inc.
Articles |
Endovascular Low-Dose Irradiation Inhibits Neointima Formation After Coronary Artery Balloon Injury in Swine
A Possible Role for Radiation Therapy in Restenosis Prevention
From the Andreas Gruentzig Cardiovascular Center, Department of Medicine, Division of Cardiology (R.W., K.A.R., G.D.C., S.B.K. III), Department of Radiation Oncology (I.R.C.), and Department of Pathology (M.B.G.), Emory University School of Medicine, Atlanta, Ga.
Correspondence to Spencer B. King III, MD, Andreas Gruentzig Cardiovascular Center, F606 Emory University Hospital, 1364 Clifton Rd NE, Atlanta, GA 30322.
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Abstract |
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Background Restenosis after percutaneous transluminal coronary angioplasty remains a major limitation of the long-term success of this procedure. Restenosis is a form of wound healing. Low-dose ionizing radiation has been effective in inhibiting exuberant wound healing responses in a variety of clinical situations.
Methods and Results Vascular neointimal lesions resembling human restenosis were created in the coronary arteries of normal pigs by overstretch balloon angioplasty injury. To test the effect of low-dose endovascular gamma radiation on lesion formation, a high-activity 192Ir source was introduced into one of the injured arteries in each animal and left in place for a period sufficient to deliver one of three doses: 350, 700, or 1400 cGy. To test potential benefits of delayed irradiation, 700 cGy was given in another group 2 days after injury. Animals were killed 14 days after balloon injury and the coronary vasculature was pressure-perfusion fixed. To test the late effect and safety of endovascular low-dose irradiation, 700 or 1400 cGy was given in miniswine coronary arteries after injury as well as in noninjured carotid arteries; this group was followed up for 6 months. Tissue sections were measured by computer-assisted planimetry. All arteries treated with radiation demonstrated significantly decreased neointima formation compared with control arteries. The ratio of intimal area–to–medial fracture length (IA/FL) was inversely correlated with the different radiation doses: control, 0.59; 350 cGy, 0.38; 700 cGy, 0.42; and 1400 cGy, 0.17 (r=-0.75, P<.0001). Delay of 700-cGy irradiation for 2 days after injury significantly decreased neointima formation compared with the same dose given immediately after injury. Analysis of long-term specimens showed reduction of IA/FL in the arteries irradiated with 700 cGy (0.3, P=.009) and 1400 cGy (0.31, P=.001) compared with control arteries (0.50). There was no excess fibrosis in the media, adventitia, or perivascular space of the coronary arteries or adjacent myocardium in pigs that received radiation compared with control animals.
Conclusions Low-dose intracoronary irradiation delivered to the site of coronary arterial overstretch balloon injury in pigs inhibited subsequent intimal thickening (hyperplasia). A dose-response relationship was demonstrated, and delay of treatment for 48 hours appeared to augment the inhibitory effect. Six months of follow-up without fibrosis or arteriosclerosis demonstrated the durability of the beneficial effect in the treated group. These data suggest that intracoronary irradiation therapy may aid in preventing clinical restenosis.
Key Words: restenosis • angioplasty • arteries • radiation
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Restenosis after successful percutaneous transluminal coronary angioplasty is the major limitation to long-term success of the procedure.1 It is mediated in part by an uncontrolled proliferation and extracellular matrix synthesis by modified smooth muscle cells that migrate to the site of balloon catheterization.2 The development of the neointimal component of the restenosis lesion is the end point of a healing process initiated by vascular injury, predominantly by injury to the nonatheromatous aspect of the dilated artery.2 Despite numerous trials of pharmacological agents, including antiplatelet drugs, anticoagulants, corticosteroids, calcium-channel blockers, fish oils, and others, the frequency of restenosis has not diminished.3 4 5 6 7 8
Gamma radiation affects self-renewing tissues by arresting cell division, and therefore limits proliferation by reducing the number of clonal progenitors.9 Vascular smooth muscle does not normally display actively dividing cell populations. However, mechanical injury or other stimuli can induce a response by smooth muscle cells characterized by migration, proliferation, and matrix synthesis. In this situation, radiation may effectively inhibit neointima formation by killing more rapidly dividing, synthetic smooth muscle cells. Ionizing radiation has been shown to inhibit thymidine uptake and collagen synthesis by cultured fibroblasts.10 11 12 13 Furthermore, the use of low doses of superficial x-rays after surgery has been effective in the prevention of hypertrophic scarring and keloid formation. This has been accomplished with fractionated doses in the range of 10 Gy (1000 rad) and does not interfere with normal wound repair processes.14 15 16 17
We have developed an animal model of restenosis based on oversized balloon catheter inflation in the coronary arteries of normal juvenile pigs.18 19 The acute injury to the tunica media and the subsequent healing process, analogous to hypertrophic scarring, bear a close resemblance to the histopathological responses of human coronary arteries after angioplasty as revealed by autopsy studies.19 20 21 The purposes of this study were to determine whether low-dose gamma radiation delivered intraluminally could reduce the extent of neointima formation after balloon injury in the swine model and, if it could, to define the minimum effective dose.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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All experiments and animal care conformed to National Institutes of Health and American Heart Association guidelines for the care and use of animals and were approved by the Emory University Animal Care and Use Committee.
Experimental Protocol
The model of overstretch injury has
been described
previously.19 20 Forty-two female domestic pigs
(Sus scrofa, 23 to 25 kg) were given aspirin (325 mg) 1 day
before the procedure and the day of the procedure. They were sedated
with a combination of ketamine (25 mg/kg), acepromazine (1.1 mg), and
atropine (0.6 mg/kg) by intramuscular injection. An intravenous line
was established, and the animals were given methohexital (10 mg/kg) and
intubated. The pigs were ventilated with oxygen (2 L/min), nitrous
oxide (2 L/min), and isoflurane 1% (1.5 L/min) using a Harvard
respirator. Adequate anesthesia was confirmed by the absence of a limb
withdrawal reflex. Limb-lead ECG (Honeywell E for M) was performed
throughout the procedure.
After placement of an 8F introducer sheath in the right femoral artery by surgical cutdown, each animal received a single dose of heparin (200 U/kg) and bretylium tosylate (2.5 mg/kg). Under fluoroscopic guidance, an 8F hockey-stick guiding catheter was positioned in the left coronary ostium. After the intracoronary administration of nitroglycerin (200 µg), coronary angiography was performed in the 45° left anterior oblique and 45° right anterior oblique views and was recorded by cineradiography (Phillips Cardiodiagnost).
Coronary overstretch injury was performed with a 3.5-mm angioplasty balloon (USCI), which was positioned in the proximal segments of the left anterior descending and left circumflex arteries, inflated to 10 atm three times for 30 seconds in each artery. Inflation periods were separated by 1-minute deflation periods to restore coronary perfusion. After the completion of the third inflation, the angioplasty balloon was withdrawn, and additional nitroglycerin (200 µg) was administered to limit coronary spasm. Final angiography was then performed to assess vessel patency and degree of injury.
One of the injured coronary arteries in each swine was randomly assigned to receive radiation treatment. Over a flexible 0.014" wire, a 4F perfusion-delivery catheter (USCI) was introduced to the injury site of the assigned artery, the guide wire was withdrawn, and a 3-cm ribbon of 192Ir was positioned at the site of injury in the target vessel with the use of cinefluoroscopic visualization within the delivery catheter. It was left in place for a period sufficient to deliver the assigned dose to a depth of 2 mm (8 to 38 minutes, depending on dose and source activity).
Radiation dose was determined in a standard fashion by entering the activity and length of the 192Ir ribbon (Medi-Physics Inc) into a radiation treatment planning system (CMS Modulex). The dose rate at the prescribed point was then calculated by the system with standard brachytherapy dose algorithms. No in vivo dosimetry was performed; the dose rate calculations and subsequent determination of dose at a distance from the source were the product of this treatment planning system. Because the delivery catheter was not self-centered within the lumen, the potential variability in the dose delivered to the artery wall ranged from 2.9 to 0.6 times the prescribed dose, depending on whether the catheter was apposed to the ipsilateral or contralateral side, respectively.
After irradiation, the ribbon and the guiding catheters were removed and the femoral cutdown was repaired. Nitroglycerin ointment (1 in) was administered topically and the animals were returned to routine care.
The pigs were killed either 14 days or 6 months after the initial injury. The animals were heparinized, a lethal dose of barbiturate was given, the chest was opened, and the heart was rapidly excised. The left coronary system was perfusion-fixed at 100- to 110-mm Hg driving pressure with 10% formaldehyde for 15 minutes, stored overnight in the same fixative, then prepared for histopathological analysis.
Short-term Study Groups
There were four treatment groups:
three received radiation in
doses of 350 cGy (10 arteries), 700 cGy (12 arteries), or 1400 cGy (9
arteries), delivered immediately after injury, and one group received
700 cGy (10 arteries) 48 hours after injury.
Long-term Study Group
Seven miniature pigs with a mean weight
(±SD) of 23.3±4.0 kg
underwent overstretch balloon injury similar to that of the other
treated groups, with an additional injury in the right coronary artery
as an internal control, and were given 700 cGy (7 arteries) or 1400 cGy
(6 arteries) immediately after the injury in the left anterior
descending and left circumflex arteries. In addition, 5 noninjured
carotid arteries in this group were treated with 1400 cGy. Six months
later the animals underwent repeat angiograms of the carotid and
coronary arteries, and tissue was retrieved for morphometric
analysis.
Tissue Analysis
The injured segments of the left anterior
descending and left
circumflex arteries were located with the guidance of the coronary
angiograms, then dissected free from the heart. Serial 2- to 3-mm
transverse segments were processed and embedded in paraffin.
Cross-sections (4 µm) were stained with hematoxylin and eosin or
Verhoeff–van Gieson's elastin stain. Hematoxylin and
eosin–stained
sections were examined by an experienced observer blinded to the
treatment group. Each specimen was evaluated for the presence of
neointima formation, luminal encroachment, medial
dissection, alteration of the internal and external elastic lamina, and
morphological appearance of the cells within the media, adventitia, and
neointima. Sections were also evaluated for the presence of
intraluminal thrombus and inflammatory cell infiltrate.
Morphometric
analysis was performed on each segment with evidence
of medial fracture, 1-5 in each artery (Fig 1
). The
histopathological features were measured using a computerized IBM-based
system (Bioscan 2, Thomas Optical Measurement System, Inc). Sections
stained with Verhoeff–van Gieson's elastin stain were magnified at
26x, digitized, and stored in a frame-grabber board. The maximal
intimal thickness was determined by a radial line drawn from the lumen
to the external lamina at the point of greatest tissue growth. The arc
length of the medial fracture (FL), traced through the
neointima from one dissected medial end to the other, was
used as a measure of the extent of injury. Area measurements were
obtained by tracing the lumen perimeter (luminal area [LA]),
neointima perimeter (intimal area [IA], defined by the
borders of the internal elastic lamina, lumen, media, and external
elastic lamina), and external elastic lamina (vessel area).
Calculations of the residual lumen (RL=LA/[LA+IA]) and
the ratio of
IA-to-fracture length (IA/FL) were performed to correct for vessel size
and extent of injury, respectively. Measurements were made by an
experienced observer blinded to the treatment groups, and repeat
measurements were made on randomly selected samples and found to vary
by less than 10%.
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Statistical Analysis
Data are expressed as mean±SD. A
one-way ANOVA was used to test
for an overall treatment effect, with follow-up Bonferroni-corrected
t tests used to analyze specific group differences. Linear
regression analysis was used to test for a dose-response effect.
Significance was established at the 95% confidence level
(P<.05), except for Bonferroni-corrected t tests
(P<.01 [.05/5] for short-term study; P<.025
[.05/2] for long-term study).
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Short-term Experiments
Group Characteristics
There were no significant differences in body weight between groups at the time of balloon injury (Table 1
). Arterial
diameter was similar on angiogram between groups, and although the
balloon-to-artery ratio was therefore the same between groups, the
extent of medial injury (FL) was significantly higher in the 350-cGy
group compared with controls (3.53±2.2 mm versus 1.6±0.8 mm,
P=.0008, Table 2).
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Histological Analysis
Hematoxylin and
eosin–stained sections of all segments were
examined. As shown in Fig 2, in injured segments there
was rupture of the tunica media, creating a vessel wall defect, with
neointimal growth having replaced the disrupted media at 2
weeks and 6 months. The neointima of control arteries
consisted mostly of stellate and spindle-shaped cells in a loose
extracellular matrix; in similar previous studies these cells have been
identified as being primarily of smooth muscle origin by positive
immunostaining for 
-actin and by ultrastructural
analysis.18 19 Cells of the neointima from
irradiated arteries were morphologically similar. In all samples, there
was complete coverage of the luminal surface by a monolayer of
endothelial-like cells. Excluded from the morphometric analysis
were 7 arteries with organized thrombus (10%) and 10 arteries without
evidence of medial tear.
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Low-magnification micrographs of sections
treated with Verhoeff–van
Gieson's elastin stain from injured coronary arteries of pigs in 4 of
the 5 treatment groups (control and 350, 700, and 1400 cGy) are shown
in Fig 2
. High-magnification micrographs of the dissected
medial ends
from representative sections of control and 700 cGy–irradiated
arteries are shown in Fig 3. There was no evidence of
substantial regions of pyknosis or necrosis in the media or adventitia,
and in all sections there was coverage of the external elastic lamina
at the injury site by at least 1 to 2 cell layers.
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Morphometric Analysis
The effects of radiation dose
and timing in the short-term
experiment on four descriptors of the vessel response to injury are
shown in Table 2. By ANOVA, significant treatment effects of
irradiation on maximal intimal thickness (F=48.2, P<.0001),
IA (F=982.67, P<.0001), IA/FL (F=26.85,
P<.0001), and RL (F=9.33, P<.0001) were
observed (Table 2 and Fig 4). Post hoc analysis
by
t test showed that all dependent variables were
significantly reduced in each treatment group compared with the control
group, except for maximal intimal thickness and IA for the 350-cGy
group. In addition, there was a linear relationship between the dose
(control, 350, 700, or 1400 cGy) and the IA/FL ratio
(m=-0.0028, P<.0001,
r=-.75; Fig 5). There were also
significant reductions in the
indexes of neointima formation in the group that had
700-cGy irradiation delayed by 2 days compared with the group given the
same dose immediately after injury (Table 2 and Fig
6).
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Long-term Experiments
There were no differences between the
short-term group and the
long-term group in terms of artery size or extent of injury (Tables
1 and 3). Angiography prior to balloon injury
revealed
mean artery size of 2.5±0.3 mm. The balloon-to-artery ratio was 1.42.
There were 2 arteries (10%) without evidence of medial tear. There
were no substantial differences in the morphological appearance of
coronary arteries from animals killed at 6 months compared with those
from animals killed 2 weeks after injury, and there was no evidence of
excess fibrosis within the arterial wall, in the perivascular space, or
in the adjacent myocardium compared with 2-week or control arteries
(Fig 6). There were no differences in the morphological
appearance of
carotid arteries that were irradiated compared with the nonirradiated
control arteries (Fig 7). There was significant
inhibition of intimal thickening in arteries treated by 700- and
1400-cGy irradiation, as demonstrated by a reduction in the IA, maximal
intimal thickness, and IA/FL ratio (Table 3).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The major finding of this study is that low-dose radiation reduced the extent of neointima formation after oversized balloon injury in the pig model of coronary restenosis. The greatest decrease in neointima formation at 2 weeks postinjury was seen with the 1400-cGy dose of radiation.
The maximal intimal thickness and the absolute IA reflect the new tissue formation after vessel injury and serve as reliable indicators of the capacity of a potential therapy to inhibit neointima formation after injury. The ratio IA/FL is somewhat more sensitive because it provides an adjustment for the extent of medial fracture, to which IA is directly correlated.22 RL is a measurement describing overall vessel geometry after wound healing that may more closely parallel the clinical entity of restenosis. Substantial effects of irradiation on all these descriptors were observed. Our data suggest that low-dose radiation delivered locally into the coronary artery after angioplasty may inhibit restenosis in the clinical setting.
Radiation may inhibit cellular hyperplasia by either killing progenitor cells or limiting their replicative capacity, thus reducing the number of clonal populations. In all dose groups, neither the smooth muscle cells of the intact media nor the fibroblasts of the adventitia appeared morphologically different from these same cell populations in the control group, displaying no regions of substantial pyknosis or necrosis. The latter explanation for inhibition of cellular hyperplasia therefore seems more likely but requires further study for confirmation. Also, it appears that the cellular migratory component of the wound healing process was not substantially affected by irradiation, because in all sections there was evidence of at least 1 to 2 cell layers covering the external elastic lamina. Further studies are planned to examine potential radiation effects on cellular migratory and matrix synthesis responses in the injured arteries.
In previous studies, injury to rat carotid arteries by balloon catheter induced smooth muscle cell ornithine decarboxylase activity (indicating smooth muscle cell entry into the prereplicative G1 phase) that peaked at 6 hours with a rapid fall by 9 hours, whereas the 3H[thymidine] index (indicating the S phase) was maximal at 33 hours, with a rapid decline by 48 hours.23 24 Although these proliferative indexes have not been reported for the swine model, immunostaining for proliferating cell nuclear antigen has qualitatively demonstrated peak replicative activity at 2 to 3 days.25 This finding, and the possibility of potentiating the radiation effect by exposure during peak replicative activity, led us to test the efficacy of a 2-day delay in irradiation. The results of these experiments, showing that radiation's effect on neointima formation is more pronounced when it is administered 48 hours after the vessel injury, suggest that radiation given near the peak of mitotic activity may more effectively suppress subsequent neointima formation.
Other models of injury have shown that dividing cells are more susceptible to the effects of radiation during the G2/M phase of the cell cycle.9 12 13 It is not known precisely when the arterial wall cells in this injury model enter into the proliferative phase, and it seems likely that there is considerable overlap in cycling among cell subpopulations; however, ongoing studies using specific proliferative markers with quantitative serial time point analysis may identify the time of maximal radiosensitivity. Our data indicate that single doses of 350 or 700 cGy are effective in reducing neointima formation, but further reduction was observed in the 1400-cGy and delayed 700-cGy groups. Therefore, a dose-response relationship was demonstrated in the short-term study; the same trend was observed in the long-term study, supporting the efficacy of this treatment. The results of our study are in contrast to those of experiments with low-dose (400 to 800 cGy) external radiation treatment administered after coronary stent placement, which accentuated the development of neointimal hyperplasia.26 There are two major differences between the studies that may explain the observed discrepancies. First, the method of injury in the present study was balloon angioplasty, as opposed to stent injury. Second, in the present study the radiation was delivered precisely to the site of coronary injury, with much less dose to the surrounding tissues than with the external beam technique. Although we feel that the balloon injury response bears closer resemblance to human restenosis than the stent response,19 20 21 we are also proceeding with studies to examine the effect of our radiation delivery technique in stented pig coronary arteries.
There is the potential for coronary fibrosis with x-irradiation. The
low and high doses of radiation delivered in this study were 350 and
1400 cGy in a single fraction. These would approximately equate to
fractionated doses of 700 and 2800 cGy, respectively. The lower dose is
well below the threshold at which isolated case reports of coronary
fibrosis due to mediastinal radiation for Hodgkin's disease have been
documented, and the higher dose is only 400 cGy above that threshold
(2400 cGy). Generally, the proven instances of fibrosis have been
observed at much higher doses (
5000 cGy).27 No
statistically significant increase in coronary artery disease was
detected by Borvin in a large sample of patients irradiated for
Hodgkin's disease at 3500 to 4400 cGy.28
To specifically address the potential for coronary fibrosis or accelerated arteriosclerosis with endovascular irradiation, we administered the 700 and 1400 cGy doses in injured coronary arteries and the 1400 cGy dose in the uninjured carotid arteries of mature miniature pigs, and examined the arteries and adjacent tissues at 6 months after treatment. In no sample was there evidence of fibrosis in the media, adventitia, or perivascular space different from that observed in control injured but nonirradiated arteries. Myocardium adjacent to the irradiated arteries showed a normal appearance, without evidence of fibrosis in the interstitium or blood vessels. No histological abnormalities were seen in carotid arteries that were irradiated. Furthermore, the findings in the long-term irradiated arteries that also received balloon injury demonstrated that the inhibitory effect of endovascular irradiation on neointima formation was maintained. A trend towards maintenance of the dose-response effect was observed, but it did not attain statistical significance.
The results of our study have been corroborated by Wiedermann et al,29 who found that intraluminal irradiation prior to angioplasty in a similar pig model reduced neointima formation. We believe, however, that the immediate postangioplasty radiation delivery approach has a greater potential clinical relevance.
Clinical Implications
This technique of endovascular low-dose
irradiation will require
clinical testing to determine whether similar inhibition of
neointimal response is observed in patients. An experience
with 20 patients who had previously undergone stent implantation in
peripheral arteries and then developed restenosis was recently
reported.30 These patients then had balloon dilatation and
intraluminal low-dose irradiation with 1200 cGy. Follow-up at 18 months
showed suppression of restenosis.30
The finding that endovascular low-dose irradiation inhibited neointima formation after coronary balloon injury needs extension. Efforts are under way to develop an improved radiation delivery system and determine optimal dose and timing of radiation delivery.
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Acknowledgments |
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This work was supported in part by a grant from the University Research Committee of Emory University. We wish to thank Barbara Britt, AHT, for assistance with experimental procedures; Robert Santoianni, HT(ASCP), and Sherry West, HT(ASCP), for help with specimen preparation; and Tim Fox, PhD, and Chris Aguilera, MS, for assistance with dosimetry and radioactive source handling and monitoring.
Received October 3, 1994; accepted October 5, 1994.
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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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J. M. A. Meyer, B. Nowak, K. Schuermann, A. Buecker, F. Moltzahn, A. Kulisch, N. Heussen, T. Gorgen, U. Bull, and R. W. Gunther Inhibition of Neointimal Proliferation with 188Re-labeled Self-Expanding Nitinol Stent in a Sheep Model Radiology, December 1, 2003; 229(3): 847 - 854. [Abstract] [Full Text] [PDF]
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 C.-L. Hang, M. Fu, B.-T. Hsieh, S. W. Leung, C.-J. Wu, H.-K. Yip, and G. Ting Intracoronary {beta}-Irradiation With Liquid Rhenium-188: Results of the Taiwan Radiation in Prevention of Post-Pure Balloon Angioplasty Restenosis Study Chest, October 1, 2003; 124(4): 1284 - 1293. [Abstract] [Full Text] [PDF]
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 C. Bartels, A. Erasmi, F. Sayk, R. Eggers, A. Dendorfer, T. Feyerabend, W. Eichler, and Hans.-H. Sievers Prophylactic gamma radiation of unaffected vein grafts failed to prevent vein graft disease in a chronic hypercholesterolemic porcine model Eur. J. Cardiothorac. Surg., July 1, 2003; 24(1): 92 - 97. [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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M. Apple, R. Waksman, R. C. Chan, Y. Vodovotz, J. Fournadjiev, and B. G. Bass Radioactive 133-Xenon Gas-Filled Balloon to Prevent Restenosis: Dosimetry, Efficacy, and Safety Considerations Circulation, August 6, 2002; 106(6): 725 - 729. [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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 A. Maehara, N. S. Patel, L. B. Harrison, N. J. Weissman, A. B. Bui, H.-S. Kim, A. E. Ajani, M. T. Castagna, T. L. McMillan, N. Yang, et al. Dose heterogeneity may not affect the neointimal proliferation after gamma radiation for in-stent restenosis: A volumetric intravascular ultrasound dosimetric study J. Am. Coll. Cardiol., June 19, 2002; 39(12): 1937 - 1942. [Abstract] [Full Text] [PDF]
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A. Finkelstein, R. Makkar, T. M. Doherty, V. R. Vegesna, P. Tripathi, M. Liu, J. Bergman, M. Fishbein, J. Hausleiter, K. Takizawa, et al. Increased Expression of Macrophage Colony-Stimulating Factor After Coronary Artery Balloon Injury Is Inhibited by Intracoronary Brachytherapy Circulation, May 21, 2002; 105(20): 2411 - 2415. [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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K. Kozuma, M.A. Costa, W.J. van der Giessen, M. Sabate, J.M.R. Ligthart, V.L.M.A. Coen, I.P. Kay, A.J. Wardeh, A.H.M. Knook, P.J de Feyter, et al. Initial observation regarding changes in vessel dimensions after balloon angioplasty and stenting followed by catheter-based {beta}-radiation. Is stenting necessary in the setting of catheter-based radiotherapy? Eur. Heart J., April 2, 2002; 23(8): 641 - 649. [Abstract] [Full Text] [PDF]
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P. S. Teirstein and R. E. Kuntz New Frontiers in Interventional Cardiology: Intravascular Radiation to Prevent Restenosis Circulation, November 20, 2001; 104(21): 2620 - 2626. [Full Text] [PDF]
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P. K. Coussement, H. de Leon, T. Ueno, M. Y. Salame, S. B. King III, N. A.F. Chronos, and K. A. Robinson Intracoronary {beta}-Radiation Exacerbates Long-Term Neointima Formation in Balloon-Injured Pig Coronary Arteries Circulation, November 13, 2001; 104(20): 2459 - 2464. [Abstract] [Full Text] [PDF]
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R. M. Wolfram, B. Pokrajac, R. Ahmadi, C. Fellner, M. Gyongyosi, M. Haumer, R. Bucek, R. Potter, and E. Minar Endovascular Brachytherapy for Prophylaxis against Restenosis after Long-Segment Femoropopliteal Placement of Stents: Initial Results Radiology, September 1, 2001; 220(3): 724 - 729. [Abstract] [Full Text] [PDF]
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G. L. Kaluza, A. E. Raizner, W. Mazur, D. G. Schulz, J. M. Buergler, L. F. Fajardo, F. O. Tio, and N. M. Ali Long-Term Effects of Intracoronary {beta}-Radiation in Balloon- and Stent-Injured Porcine Coronary Arteries Circulation, April 24, 2001; 103(16): 2108 - 2113. [Abstract] [Full Text] [PDF]
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M.Y Salame, S Verheye, I.R Crocker, N.A.F Chronos, K.A Robinson, and S.B King III Intracoronary radiation therapy Eur. Heart J., April 2, 2001; 22(8): 629 - 647. [PDF]
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S. Parikh, D. Nori, P. Tripuraneni, M. Sabate, M. A. Costa, K. Kozuma, I. P. Kay, W. J. van der Giessen, V. L.M.A. Coen, J. M.R. Ligthart, et al. Geographic Miss: A Cause of Treatment Failure in Radio-Oncology Applied to Intracoronary Radiation Therapy Response Circulation, March 27, 2001; 103 (12): e65 - e66. [Full Text] [PDF]
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 M. Wohlfrom, J. Kotzerke, J. Kamenz, M. Eble, B. Hess, J. Wohrle, S. N Reske, V. Hombach, H. Hanke, and M. Hoher Endovascular irradiation with the liquid {beta}-emitter Rhenium-188 to reduce restenosis after experimental wall injury Cardiovasc Res, January 1, 2001; 49(1): 169 - 176. [Abstract] [Full Text] [PDF]
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R. Makkar, J. Whiting, A. Li, H. Honda, M. C. Fishbein, F.F. Knapp, J. Hausleiter, F. Litvack, and N. L. Eigler Effects of {beta}--Emitting 188Re Balloon in Stented Porcine Coronary Arteries : An Angiographic, Intravascular Ultrasound, and Histomorphometric Study Circulation, December 19, 2000; 102(25): 3117 - 3123. [Abstract] [Full Text] [PDF]
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K Kozuma, M.A Costa, M Sabate, C.J Slager, E Boersma, I.P Kay, J.P.A Marijnissen, S.G Carlier, J.J Wentzel, A Thury, et al. Relationship between tensile stress and plaque growth after balloon angioplasty treated with and without intracoronary beta-brachytherapy Eur. Heart J., December 2, 2000; 21(24): 2063 - 2070. [Abstract] [PDF]
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E. Minar, B. Pokrajac, T. Maca, R. Ahmadi, C. Fellner, M. Mittlbock, W. Seitz, R. Wolfram, and R. Potter Endovascular Brachytherapy for Prophylaxis of Restenosis After Femoropopliteal Angioplasty : Results of a Prospective Randomized Study Circulation, November 28, 2000; 102(22): 2694 - 2699. [Abstract] [Full Text] [PDF]
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Y. Cottin, M. Kollum, R. Chan, B. Bhargava, Y. Vodovotz, and R. Waksman Vascular repair after balloon overstretch injury in porcine model effects of intracoronary radiation J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1389 - 1395. [Abstract] [Full Text] [PDF]
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 V. Z. Erzurum, U. O. Hafeli, M. K. Hirko, S. P. Schmidt, and J. R. Rubin Local Application of Beta-Particle Radiation to Reduce Venous Anastomotic Intimal Hyperplasia in Polytetrafluoroethylene Arteriovenous Fistulas Vascular and Endovascular Surgery, September 1, 2000; 34(5): 377 - 383. [Abstract] [PDF]
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A. E. Raizner, S. N. Oesterle, R. Waksman, P. W. Serruys, A. Colombo, Y.-L. Lim, A. C. Yeung, W. J. van der Giessen, L. Vandertie, J. K. Chiu, et al. Inhibition of Restenosis With {beta}-Emitting Radiotherapy : Report of the Proliferation Reduction With Vascular Energy Trial (PREVENT) Circulation, August 29, 2000; 102(9): 951 - 958. [Abstract] [Full Text] [PDF]
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R. Waksman, B. Bhargava, G. S. Mintz, R. Mehran, A. J. Lansky, L. F. Satler, A. D. Pichard, K. M. Kent, and M. B. Leon Late total occlusion after intracoronary brachytherapy for patients with in-stent restenosis J. Am. Coll. Cardiol., July 1, 2000; 36(1): 65 - 68. [Abstract] [Full Text] [PDF]
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M. Hoher, J. Wohrle, M. Wohlfrom, H. Hanke, R. Voisard, H. H. Osterhues, M. Kochs, S. N. Reske, V. Hombach, and J. Kotzerke Intracoronary {beta}-Irradiation With a Liquid 188Re-Filled Balloon : Six-Month Results From a Clinical Safety and Feasibility Study Circulation, May 23, 2000; 101(20): 2355 - 2360. [Abstract] [Full Text] [PDF]
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R. Waksman, R. L. White, R. C. Chan, B. G. Bass, L. Geirlach, G. S. Mintz, L. F. Satler, R. Mehran, P. W. Serruys, A. J. Lansky, et al. Intracoronary {gamma}-Radiation Therapy After Angioplasty Inhibits Recurrence in Patients With In-Stent Restenosis Circulation, May 9, 2000; 101(18): 2165 - 2171. [Abstract] [Full Text] [PDF]
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C. Schulz, C. Niederer, C. Andres, R. A. Herrmann, X. Lin, R. Henkelmann, W. Panzer, C. Herrmann, D. F. Regulla, I. Wolf, et al. Endovascular Irradiation From {beta}-Particle-Emitting Gold Stents Results in Increased Neointima Formation in a Porcine Restenosis Model Circulation, April 25, 2000; 101(16): 1970 - 1975. [Abstract] [Full Text] [PDF]
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S. Ishiwata, S. Verheye, K. A. Robinson, M. Y. Salame, H. de Leon, S. B. King III, and N. A. F. Chronos Inhibition of neointima formation by tranilast in pig coronary arteries after balloon angioplasty and stent implantation J. Am. Coll. Cardiol., April 1, 2000; 35(5): 1331 - 1337. [Abstract] [Full Text] [PDF]
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E. Thorin, D. Meerkin, O. F. Bertrand, P. Paiement, M. Joyal, and R. Bonan Influence of Postangioplasty {beta}-Irradiation on Endothelial Function in Porcine Coronary Arteries Circulation, March 28, 2000; 101(12): 1430 - 1435. [Abstract] [Full Text] [PDF]
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P. S. Teirstein, V. Massullo, S. Jani, J. J. Popma, R. J. Russo, R. A. Schatz, E. M. Guarneri, S. Steuterman, K. Sirkin, D. A. Cloutier, et al. Three-Year Clinical and Angiographic Follow-Up After Intracoronary Radiation : Results of a Randomized Clinical Trial Circulation, February 1, 2000; 101(4): 360 - 365. [Abstract] [Full Text] [PDF]
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R. Albiero, M. Adamian, N. Kobayashi, A. Amato, M. Vaghetti, C. Di Mario, and A. Colombo Short- and Intermediate-Term Results of 32P Radioactive {beta}-Emitting Stent Implantation in Patients With Coronary Artery Disease : The Milan Dose-Response Study Circulation, January 4, 2000; 101(1): 18 - 26. [Abstract] [Full Text] [PDF]
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Y. Vodovotz, R. Waksman, W.-H. Kim, B. Bhargava, R. C. Chan, and M. Leon Effects of Intracoronary Radiation on Thrombosis After Balloon Overstretch Injury in the Porcine Model Circulation, December 21, 1999; 100(25): 2527 - 2533. [Abstract] [Full Text] [PDF]
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O F Bertrand, S Lehnert, R Mongrain, and M G Bourassa Early and late effects of radiation treatment for prevention of coronary restenosis: a critical appraisal Heart, December 1, 1999; 82(6): 658 - 662. [Full Text]
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 D. P Lee, S. Lo, K. Forster, A. C Yeung, and S. N Oesterle Clinical applications of brachytherapy for the prevention of restenosis Vascular Medicine, November 1, 1999; 4(4): 257 - 268. [Abstract] [PDF]
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A. J. Wardeh, I. P. Kay, M. Sabate, V. L. M. A. Coen, A. L. Gijzel, J. M. R. Ligthart, A. den Boer, P. C. Levendag, W. J. van der Giessen, and P. W. Serruys {beta}-Particle-Emitting Radioactive Stent Implantation : A Safety and Feasibility Study Circulation, October 19, 1999; 100(16): 1684 - 1689. [Abstract] [Full Text] [PDF]
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S. O. Trerotola, T. J. Carmody, R. D. Timmerman, K. A. Bergan, R. G. Dreesen, S. V. Frost, and M. Forney Brachytherapy for the Prevention of Stenosis in a Canine Hemodialysis Graft Model: Preliminary Observations Radiology, September 1, 1999; 212(3): 748 - 754. [Abstract] [Full Text]
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C. Hehrlein, S. Kaiser, R. Riessen, J.u. Metz, P. Fritz, and W. Kubler External beam radiation after stent implantation increases neointimal hyperplasia by augmenting smooth muscle cell proliferation and extracellular matrix accumulation J. Am. Coll. Cardiol., August 1, 1999; 34(2): 561 - 566. [Abstract] [Full Text] [PDF]
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D. Meerkin, J.-C. Tardif, I. R. Crocker, A. Arsenault, M. Joyal, G. Lucier, S. B. King III, D. O. Williams, P. W. Serruys, and R. Bonan Effects of Intracoronary ß-Radiation Therapy After Coronary Angioplasty : An Intravascular Ultrasound Study Circulation, April 6, 1999; 99(13): 1660 - 1665. [Abstract] [Full Text] [PDF]
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J. Fareh, R. Martel, P. Kermani, and G. Leclerc Cellular Effects of ß-Particle Delivery on Vascular Smooth Muscle Cells and Endothelial Cells : A Dose-Response Study Circulation, March 23, 1999; 99(11): 1477 - 1484. [Abstract] [Full Text] [PDF]
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S. B. King III Radiation for Restenosis : Watchful Waiting Circulation, January 19, 1999; 99(2): 192 - 194. [Full Text] [PDF]
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P. S. Teirstein, V. Massullo, S. Jani, R. J. Russo, D. A. Cloutier, R. A. Schatz, E. M. Guarneri, S. Steuterman, K. Sirkin, S. Norman, et al. Two-Year Follow-Up After Catheter-Based Radiotherapy to Inhibit Coronary Restenosis Circulation, January 19, 1999; 99(2): 243 - 247. [Abstract] [Full Text] [PDF]
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H. I. Amols, F. Trichter, and J. Weinberger Intracoronary Radiation for Prevention of Restenosis : Dose Perturbations Caused by Stents Circulation, November 10, 1998; 98(19): 2024 - 2029. [Abstract] [Full Text] [PDF]
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S. B. King, D. O. Williams, P. Chougule, J. L. Klein, R. Waksman, R. Hilstead, J. Macdonald, K. Anderberg, and I. R. Crocker Endovascular ß-Radiation to Reduce Restenosis After Coronary Balloon Angioplasty : Results of the Beta Energy Restenosis Trial (BERT) Circulation, May 26, 1998; 97(20): 2025 - 2030. [Abstract] [Full Text] [PDF]
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R. Waksman, J. C. Rodriguez, K. A. Robinson, G. D. Cipolla, I. R. Crocker, N. A. Scott, S. B. King III, and J. N. Wilcox Effect of Intravascular Irradiation on Cell Proliferation, Apoptosis, and Vascular Remodeling After Balloon Overstretch Injury of Porcine Coronary Arteries Circulation, September 16, 1997; 96(6): 1944 - 1952. [Abstract] [Full Text]
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D. Brieger and E. Topol Local drug delivery systems and prevention of restenosis Cardiovasc Res, September 1, 1997; 35(3): 405 - 413. [Full Text] [PDF]
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 P. S. Teirstein, V. Massullo, S. Jani, J. J. Popma, G. S. Mintz, R. J. Russo, R. A. Schatz, E. M. Guarneri, S. Steuterman, N. B. Morris, et al. Catheter-Based Radiotherapy to Inhibit Restenosis after Coronary Stenting N. Engl. J. Med., June 12, 1997; 336(24): 1697 - 1703. [Abstract] [Full Text] [PDF]
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P. Teirstein ß-Radiation to Reduce Restenosis: Too Little, Too Soon? Circulation, March 4, 1997; 95(5): 1095 - 1097. [Full Text]
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V. Verin, P. Urban, Y. Popowski, M. Schwager, P. Nouet, P. A. Dorsaz, P. Chatelain, J. M. Kurtz, and W. Rutishauser Feasibility of Intracoronary ß-Irradiation to Reduce Restenosis After Balloon Angioplasty: A Clinical Pilot Study Circulation, March 4, 1997; 95(5): 1138 - 1144. [Abstract] [Full Text]
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W. J. van der Giessen and P. W. Serruys ß-Particle–Emitting Stents Radiate Enthusiasm in the Search for Effective Prevention of Restenosis Circulation, November 15, 1996; 94(10): 2358 - 2360. [Full Text]
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H. Rud Andersen, M. Mæng, M. Thorwest, and E. Falk Remodeling Rather Than Neointimal Formation Explains Luminal Narrowing After Deep Vessel Wall Injury : Insights From a Porcine Coronary (Re)stenosis Model Circulation, May 1, 1996; 93(9): 1716 - 1724. [Abstract] [Full Text]
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 R. R. Makkar, N. Eigler, F. Litvack, and J. S. Forrester Prevention of Restenosis by Local Drug Delivery Journal of Cardiovascular Pharmacology and Therapeutics, April 1, 1996; 1(2): 177 - 188. [Abstract] [PDF]
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C. Hehrlein, M. Stintz, R. Kinscherf, K. Schlosser, E. Huttel, L. Friedrich, P. Fehsenfeld, and W. Kubler Pure ß-ParticleEmitting Stents Inhibit Neointima Formation in Rabbits Circulation, February 15, 1996; 93(4): 641 - 645. [Abstract] [Full Text]
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J. R. Laird, A. J. Carter, W. M. Kufs, T. G. Hoopes, A. Farb, S. H. Nott, R. E. Fischell, D. R. Fischell, R. Virmani, and T. A. Fischell Inhibition of Neointimal Proliferation With Low-Dose Irradiation From a ß-Particle–Emitting Stent Circulation, February 1, 1996; 93(3): 529 - 536. [Abstract] [Full Text]
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R. Waksman, K. A. Robinson, I. R. Crocker, C. Wang, M. B. Gravanis, G. D. Cipolla, R. A. Hillstead, and S. B. King III Intracoronary Low-Dose ß-Irradiation Inhibits Neointima Formation After Coronary Artery Balloon Injury in the Swine Restenosis Model Circulation, November 15, 1995; 92(10): 3025 - 3031. [Abstract] [Full Text]
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V. Verin, Y. Popowski, P. Urban, J. Belenger, M. Redard, M. Costa, M.-C. Widmer, M. Rouzaud, P. Nouet, E. Grob, et al. Intra-arterial Beta Irradiation Prevents Neointimal Hyperplasia in a Hypercholesterolemic Rabbit Restenosis Model Circulation, October 15, 1995; 92(8): 2284 - 2290. [Abstract] [Full Text]
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