Radioactive Stents Research Articles

Can angiotensin receptor antagonists prevent restenosis after stent placement?

Restenosis rates after coronary stent implantation in complex lesions are between 30 and 50%. Neointimal hyperplasia promoted by complex interaction between cellular and acellular elements, such as cytokines and growth factors, is thought to be the primary process responsible for restenosis. The risk of in-stent restenosis is increased in patients with a history of restenosis after percutaneous transluminal coronary angioplasty, in long lesions, in total occlusions, in patients with diabetes mellitus, in small vessels, in the proximal parts of the left anterior descending coronary artery and in cases of stent oversizing. In-stent restenosis represents a serious economic burden on society because treatment strategies include expensive approaches such as cutting-balloon angioplasty, rotational atherectomy and brachytherapy. A number of pharmacological agents, including ACE inhibitors, have been unsuccessful in preventing restenosis. Alternative procedures such as brachytherapy, radioactive stents and drug-eluting stents are under evaluation. Although sirolimus- or paclitaxel-eluting stents have been associated with very low restenosis rates over durations of 6 to 12 months, the long-term efficacy and tolerability of this approach is currently being investigated. Although ACE inhibitors have failed in reducing restenosis rates, the selective angiotensin II type 1 (AT(1)) receptor antagonist valsartan has shown encouraging results in the single-center Valsartan for Prevention of Restenosis after Stenting of Type B2/C lesions trial (ValPREST). The ValPREST trial is the first randomized, placebo-controlled study to have evaluated the effect of an angiotensin receptor antagonist on in-stent restenosis in a moderate number of patients. Compared with ACE inhibitors, angiotensin receptor blockers exert additional effects on the pathophysiological processes which lead to restenosis. Angiotensin receptor antagonists may affect several mechanisms involved in neointimal hyperplasia such as decreasing circulating cytokine and growth factor levels and reducing neutrophil activation, especially after stenting in acute coronary syndromes, but the results need to be confirmed in a large multicenter trial. The question whether long-term therapy, with an oral angiotensin receptor antagonist, is cost-effective and whether angiotensin receptor antagonists should be used as an add-on therapy to drug-eluting stents, requires clarification.

Effects of 32P radioactive stents on in-stent restenosis in a double stent injury model of the porcine coronary arteries

Background: The major limitation of coronary stenting remains in-stent restenosis, due to the development of neointimal proliferation. Radioactive stents have demonstrated the ability to reduce this proliferation in the healthy nonatherosclerotic porcine animal model. However, inhibition of tissue proliferation in the in-stent restenotic lesion in a porcine model is not well characterized. The objective of this study was to examine the efficacy and safety of the 32P radioactive stent for the treatment of in-stent restenosis in a double stent injury model of the porcine coronaries.Methods and Materials: Eighteen coronary arteries in 9 pigs underwent nonradioactive stent (8 mm in length) implantation. Thirty days after the initial stent implantation, a 32P radioactive stent (18 mm in length) with an activity of 0 and 18 μCi was implanted to cover the initial stent. The swine were killed 30 days after the second stent implantation. Histomorphometric analysis was performed for vessel area (VA), stent strut area (SSA), intimal area (IA), and lumen area (LA).Results: Injury scores, VA, SSA, and LA were similar among the control and radiated groups. Neointimal formation was significantly reduced after placement of radioactive stents as compared to control in both the overlapped (0.93 ± 0.12 vs. 1.31 ± 0.51 mm2, p < 0.05) and nonoverlapped segments (1.14 ± 0.21 vs. 1.91 ± 1.04 mm2, p < 0.05). The smooth muscle cell index in the neointima was reduced. Intimal fibrin was increased in the radiated group as compared to the control (p < 0.01 respectively).Conclusions: 32P radioactive stents may be safe and effective in reducing neointimal formation leading to in-stent restenosis. Longer follow-up will be required to examine whether these positive findings can be maintained.

Dosimetry of a 188rhenium-labeled self-expanding stent for endovascular brachytherapy in peripheral arteries

Purpose: Radioactive stents have been proposed as endovascular irradiation device to prevent in-stent restenosis by inhibiting neointimal proliferation. 32P-stents have been used in several studies so far, but require large-scale labeling procedures and endovascular barotrauma for stent expansion supporting the development of edge restenosis. Purpose of this study was to establish dosimetry of a self-expanding nitinol stent for peripheral vascular disease, which was radiolabeled with 188rhenium ( 188Re) by a dip coating technique. Methods and materials: The surface of nitinol Memotherm FLEXX stents was polymer-coated providing functional NH 2 groups for diethylenetriaminepentaacetic acid (DTPA) binding, providing the ligand for the complexation of 188Re onto the stent surface. Stability of radiolabeling was tested over 48 h using an in vitro blood circulation (Chandler Loop). Radial and longitudinal dose distributions of a radiolabeled stent were obtained with a plastic scintillator dosimetry system. Results: Stents with a length of 30 mm and a diameter of 8 mm were labeled with up to 33 MBq 188Re. A total of 69±4% of the labeled 188Re remained stable on the stent surface after 48 h. Ninety-five percent of the infinitely accumulated dose was supplied to the target tissue within 72 h. Including correction for radioactivity washout from the stent, the infinitely accumulated dose at 1 mm radial distance from the stent surface was 1.85±0.19 Gy/MBq 188Re/cm stent length. Conclusions: We developed a technique for radiolabeling of self-expanding nitinol stents with 188Re by dip coating and formation of 188Re chelate complexes. We provide dosimetry data useful for application of this β-emitting stent for endovascular brachytherapy in peripheral vascular occlusive disease.

Stent development and local drug delivery.

Stent implantation has become the new standard angioplasty procedure. In-stent re-stenosis remains the major limitation of coronary stenting. Re-stenosis is related to patient-, lesion- and procedure-specific factors. Patient-specific factors can not be influenced to any extent. Procedure-specific factors are affected by implantation technique and stent characteristics. Design and material influence vascular injury and humoral and cellular response. Radiation has been shown to have inhibitory effects on smooth muscle cell growth and neo-intima formation, but in clinical trials the outcome has been hampered by re-stenosis at the edges of the radioactive stent ('candy wrapper'). New approaches target pharmacological modulation of local vascular biology by local administration of drugs. This allows for drug application at the precise site and time of vessel injury. Systemic release is minimal and this may reduce the risk of toxicity. The drug and the delivery vehicle must fulfil pharmacological, pharmacokinetic and mechanical requirements and the application of eluting degradable matrices seems to be a possible solution. Numerous pharmacological agents with antiproliferative properties are currently under clinical investigation, e.g. actinomycin D, rapamycin or paclitaxel. Another approach is for stents to be made of biodegradable materials as an alternative to metallic stents. Their potential long-term complications, such as in-stent re-stenosis and the inaccessibility of the lesion site for surgical revascularization, needs to be assessed. Current investigational devices and the line of (pre)clinical investigation are discussed in detail. Currently, there is little experimental, and only preliminary clinical, understanding of the acute and long-term effects of drug-eluting or biodegradable stents in coronary arteries. The clinical benefit of these approaches still has to be proven.

Intravascular ultrasound assessment of the mechanisms and results of brachytherapy.

Serial intravascular ultrasound (IVUS) studies have shown that restenosis in nonstented lesions and late lumen loss in reference segments contiguous with both stented and nonstented lesions is a balance between arterial remodeling and neointimal hyperplasia. Conversely, in-stent restenosis (ISR) is neointimal hyperplasia.1,2 The present review focuses on lessons learned from IVUS about mechanisms of brachytherapy in preventing or treating restenosis. Most brachytherapy studies have included IVUS analyses, but to various degrees and with various methodologies. In some studies—eg, the Washington Radiation for In-stent Restenosis (WRIST) trials—serial (postirradiation and follow-up) IVUS was performed in the majority of patients. In other trials, IVUS was usually a site-specific substudy in small numbers of patients (Table 1). These studies assessed only the short-term (typically 6 to 9 months) effects of brachytherapy. View this table: Table 1095275. IVUS Analyses in Various Brachytherapy Trials IVUS should be performed with motorized transducer pullback, and volumetric as well as mean cross-sectional area (CSA) analysis should be reported. Because lesion lengths vary among trials, longer lesions may have larger stent, lumen, and neointimal volumes. Therefore, mean planar analysis (in which measured volumes are normalized for lesion length) may be a preferable way to compare different studies. Understanding lesion effects is more straightforward than understanding edge effects. (1) Edge analysis was not performed in all studies (Table 1). (2) Some studies combined proximal and distal edges and analyzed them together; others analyzed proximal and distal edges separately. (3) Edge analysis requires a larger sample size because of the wider range of possible responses. (4) It may be hard to determine the relationship between the source, the injured segment, and the IVUS images to assess geographical miss. Angiographic guidance may work in stented lesions; even in stented lesions (which are often radiolucent), however, meticulous comparison of IVUS and angiographic studies is necessary. (5) Some studies …

Proposal for a gamma-emitting stent for the prevention and treatment of coronary artery restenosis.

Radioactive stents have failed to prevent restenosis despite the demonstrated success of other radionuclide therapies using beta- or gamma-emitting radionuclides in the coronary arteries. This may be due to the rapid dose reduction at the end of the stent that occurs with a stent coated with 32P, which is a pure beta-emitter. A gamma-emitter will give a greater dose beyond the end of the stent and would therefore be expected to produce better results. However, it is essential that the gamma-emitter is not contaminated with beta particles of either sign nor with conversion electrons. This requirement generally demands the use of a high energy gamma-emitter, preferably with an energy greater than 500 keV. High energy gammas have other advantages, including a high radiation dose delivered per decay which reduces the total activity required and reduced dose near to the source due to electron disequilibrium. The ideal dose distribution is one that provides a uniform dose to the proliferating tissues and a reduced dose elsewhere. Although the target tissues are not well defined it is believed that the adventitia is the source of the proliferating cells. Hence the target tissue is between 0.5 and 2 mm depth into the artery. It is shown that 96Tc is a very suitable radionuclide for the production of radioactive stents giving a significantly greater dose compared with 32P both at depth and beyond the end of the stent for the same dose at the surface of the stent. Furthermore, 96Tc should be able to be made with a standard medical cyclotron and may be coated on to a stainless steel stent by a simple process that takes approximately 30 minutes to perform. Its half-life of 4.3 days will allow radioactive stents to be transported over significant distances and will result in a treatment time with a mean value of approximately 1 week. This will allow the rapid reestablishment of the endothelial layer which may be a further advantage of this radioactive stent.

Is the "candy-wrapper" effect of (32)P radioactive beta-emitting stents due to remodeling or neointimal hyperplasia? Insights from intravascular ultrasound.

A recognized limitation of radioactive stents is the development of restenosis at the stent edges, known as the "candy-wrapper" effect. The mechanisms of this effect remain incompletely understood and controversial. The aim of this study is to assess the effect of endovascular irradiation on neointima formation and vascular remodeling. (32)P Palmaz-Schatz stents (1.5-4 microCi) were implanted in 11 patients with restenosis after previous percutaneous transluminal coronary angioplasty (PTCA). Intravascular ultrasound (IVUS) images of target sites and adjunct vessel segments were acquired both during intervention and after 6 months. The angiographic restenosis rate was 54%, and the MLD decreased from 2.21 +/- 0.6 mm to 1.38 +/- 0.4 mm at follow-up (P < 0.01). IVUS analysis demonstrated that late lumen loss was the result of neointimal tissue proliferation, which was nonuniformly distributed and exaggerated at both the central articulation and the distal stent edges. Negative remodeling did not contribute to restenosis. In contrast, we found a linear relationship between increase of area stenosis and a positive remodeling index (r = 0.84, P < 0.0001). Restenosis after implantation of (32)P Palmaz-Schatz stents was mainly the result of neointimal tissue proliferation which tended to be nonuniformly distributed in the stent articulation and edges. Negative remodeling or stent recoil was not observed. Cathet Cardiovasc Intervent 2001;54:41-48.

The pattern of restenosis and vascular remodelling after cold-end radioactive stent implantation.

Edge restenosis is a major problem after radioactive stenting. The cold-end stent has a radioactive mid-segment (15.9 mm) and non-radioactive proximal and distal 5.7 mm segments. Conceptually this may negate the impact of negative vascular remodelling at the edge of the radiation. ECG-gated intravascular ultrasound with three-dimensional reconstruction was performed post-stent implantation and at the 6-month follow-up to assess restenosis within the margins of the stent and at the stent edges in 16 patients. Angiographic restenosis was witnessed in four patients, all in the proximal in-stent position. By intravascular ultrasound in-stent neointimal hyperplasia, with a >50% stented cross-sectional area, was seen in eight patients. This was witnessed proximally (n=2), distally (n=2) and in both segments (n=4). Echolucent tissue, dubbed the 'black hole' was seen as a significant component of neointimal hyperplasia in six out of the eight cases of restenosis. Neointimal hyperplasia was inhibited in the area of radiation: Delta neointimal hyperplasia=3.72 mm3 (8.6%); in-stent at the edges of radiation proximally and distally Delta neointimal hyperplasia was 7.9 mm3 (19.0%) and 11.4 mm3 (25.6%), respectively (P=0.017). At the stent edges there was no significant change in lumen volume. Cold-end stenting results in increased neointimal hyperplasia in in-stent non-radioactive segments.

Local arterial responses to 32P β-emitting stents

Purpose: 32P β-emitting stents reduce neointimal growth in rabbit iliac arteries for at least 12 months after deployment but are associated with incomplete healing. The aim of this study was to quantitate arterial cellularity, with emphasis on the inflammatory response following radioactive stenting. Methods: 32P β-emitting stents were placed in rabbit iliac arteries and analyzed at 3 months (6 and 24 μCi), and 6 and 12 months (6, 24, and 48 μCi). Arterial cellular proliferation and cell densities of smooth muscle cells (SMC), mononuclear cells (macrophages and lymphocytes), and neutrophils (PMN) were determined. Results: Total intimal cell density was greatest in control stents at all three time points, composed mostly of SMCs. SMC density associated with radioactive stents increased from 3 to 12 months but was significantly less than control nonradioactive stents. There was a 4-fold increase in cellular proliferation in the 24 and 48 μCi group vs. control stents. In the media, SMC density of radioactive stent groups was significantly reduced vs. control stents at all three time points, for all three activities. At 3, 6 and 12 months, there was a dose-dependent increase in intimal inflammatory cell density, which consisted mostly of macrophages. For 6-μCi stents inflammation peaked at 3 months and decreased thereafter. Inflammation for 24-μCi stents peaked at 6 months and then decreased at 12 months. Inflammation associated with 48-μCi stents remained high at 6 and 12 months. Focal atherosclerotic change was seen in 11% of stents in the 24-μCi group, and 37% and 50% in the 48-μCi group at 6 and 12 months, respectively. Conclusion: Intimal SMC density remains suppressed out to 12 months after placement of 32P β-emitting stents. However, inflammation and cell proliferation remain increased and may potentially result in greater neointimal formation over time.

Dose–volume histograms based on serial intravascular ultrasound: a calculation model for radioactive stents

Background and purpose: Radioactive stents are under investigation for reduction of coronary restenosis. However, the actual dose delivered to specific parts of the coronary artery wall based on the individual vessel anatomy has not been determined so far. Dose–volume histograms (DVHs) permit an estimation of the actual dose absorbed by the target volume. We present a method to calculate DVHs based on intravascular ultrasound (IVUS) measurements to determine the dose distribution within the vessel wall.Materials and methods: Ten patients were studied by intravascular ultrasound after radioactive stenting (BX Stent, P-32, 15-mm length) to obtain tomographic cross-sections of the treated segments. We developed a computer algorithm using the actual dose distribution of the stent to calculate differential and cumulative DVHs. The minimal target dose, the mean target dose, the minimal doses delivered to 10 and 90% of the adventitia (DV10, DV90), and the percentage of volume receiving a reference dose at 0.5 mm from the stent surface cumulated over 28 days were derived from the DVH plots. Results were expressed as mean±SD.Results: The mean activity of the stents was 438±140 kBq at implantation. The mean reference dose was 111±35 Gy, whereas the calculated mean target dose within the adventitia along the stent was 68±20 Gy. On average, DV90 and DV10 were 33±9 Gy and 117±41 Gy, respectively. Expanding the target volume to include 2.5-mm-long segments at the proximal and distal ends of the stent, the calculated mean target dose decreased to 55±17 Gy, and DV 90 and DV 10 were 6.4±2.4 Gy and 107±36 Gy, respectively.Conclusions: The assessment of DVHs seems in principle to be a valuable tool for both prospective and retrospective analysis of dose-distribution of radioactive stents. It may provide the basis to adapt treatment planning in coronary brachytherapy to the common standards of radiotherapy.

Clinical and angiographical follow-up after implantation of a 6--12 microCi radioactive stent in patients with coronary artery disease.

This study is the contribution by the Thoraxcenter, Rotterdam, to the European(32)P Dose Response Trial, a non-randomized multicentre trial to evaluate the safety and efficacy of the radioactive Isostent in patients with single coronary artery disease. The radioactivity of the stent at implantation was 6--12 microCi. All patients received aspirin indefinitely and either ticlopidine or clopidogrel for 3 months. Quantitative coronary angiography measurements of both the stent area and the target lesion (stent area and up to 5 mm proximal and distal to the stent edges) were performed pre- and post-procedure and at the 5-month follow-up. Forty-two radioactive stents were implanted in 40 patients. Treated vessels were the left anterior descending coronary artery (n=20), right coronary artery (n=10) or left circumflex artery (n=10). Eight patients received additional non-radioactive stents. Lesion length measured 10+/-3 mm with a reference diameter of 3.07+/-0.69 mm. Minimal lumen diameter increased from 0.98+/-0.53 mm pre-procedure to 2.29+/-0.52 mm (target lesion) and 2.57+/-0.44 mm (stent area) post-procedure. There was one procedural non-Q wave myocardial infarction, due to transient thrombotic closure. Thirty-six patients returned for angiographical follow-up. Two patients had a total occlusion proximal to the radioactive stent. Of the patent vessels, none had in-stent restenosis. Edge restenosis was observed in 44%, occurring predominantly at the proximal edge. Target lesion revascularization was performed in 10 patients and target vessel revascularization in one patient. No additional clinical end-points occurred during follow-up. The minimal lumen diameter at follow-up averaged 1.66+/-0.71 mm (target lesion) and 2.12+/-0.72 (stent area); therefore late loss was 0.63+/-0.69 (target lesion) and 0.46+/-0.76 (stent area), resulting in a late loss index of 0.65+/-1.15 (target lesion) and 0.30+/-0.53 (stent area). These results indicate that the use of radioactive stents is safe and feasible, however, the high incidence of edge restenosis makes this technique currently clinically non-applicable.

Late arterial responses (6 and 12 months) after (32)P beta-emitting stent placement: sustained intimal suppression with incomplete healing.

Three-month studies of stent-delivered brachytherapy in the rabbit model show reduced neointimal growth. However, intimal healing is delayed, raising the possibility that intimal inhibition is merely delayed rather than prevented. The purpose of this study was to explore the long-term histological changes after placement of beta-emitting radioactive stents in normal rabbit iliac arteries. Three-millimeter beta-emitting (32)P stents (6, 24, and 48 microCi) were placed in normal rabbit iliac arteries with nonradioactive stents as controls. Animals were euthanatized at 6 and 12 months, and histological assessment, morphometry, and analysis of endothelialization were performed. Morphometric measurements demonstrated a >50% reduction in intimal growth and percent lumen stenosis within 24- and 48-microCi stents versus control nonradioactive stents at both 6 and 12 months. However, the 24- and 48-microCi stents also showed delayed healing of the intimal surface, characterized by persistent fibrin thrombus with nonconfluent areas of matrix, incomplete endothelialization, and increased intimal cellular proliferation. Stent edge stenosis was present at 12 months in the 24- and 48-microCi stent groups, characterized by both intimal thickening and negative arterial remodeling. Inhibition of intimal growth is maintained 6 and 12 months after (32)P beta-emitting stent placement. However, delayed arterial healing, incomplete endothelialization, and edge effects are present.

Self-Assembled Monolayers on Gold for the Fabrication of Radioactive Stents

Self-Assembled Monolayers on Gold for the Fabrication of Radioactive Stents

Self-Assembled Monolayers on Gold for the Fabrication of Radioactive Stents

An innovative and easily applicable method for the fabrication of radioactive stents, to be used for the treatment of restenosis, is presented. By incorporating the b-emitting radioisotopes 186Re, 188Re, 90Y, or 32P into sulfur-containing adsorbates, it becomes possible to cover a gold surface with a radioactive self-assembled monolayer (SAM). Two methods have been investigated. In the first, SAMs consisting of potentially radioactive rhenium-, yttrium-, and phosphorus-containing adsorbates have been assembled on 2D gold substrates, after which they have been studied by wettability measurements, electrochemistry, and X-ray photoelectron spectroscopy (XPS). The stability of these SAMs under simulated physiological conditions (phosphate buffered saline, PBS solution) for periods up to two months has been demonstrated. Alternatively, potentially radioactive monolayers have been prepared by exposure of SAMs of mono-, bi-, and tridentate ligands to a solution containing a radiometal (rhenium) in order to bind the metal to the monolayer. The polydentate ligands exhibit excellent binding capacity, leading to SAMs containing over 10±10 mol/cm2 of the radiometal, which is more than sufficient to make this system viable for the delivery of therapeutical dosages of radiation.

Adverse edge effects are not prevented by 32P beta-emitting hot-ends radioactive stents Michael C. John, Andrew Farb, Renu Virmani. Armed Forces Institute of Pathology, Washington, DC

Adverse edge effects are not prevented by 32P beta-emitting hot-ends radioactive stents Michael C. John, Andrew Farb, Renu Virmani. Armed Forces Institute of Pathology, Washington, DC

Radioactive stents inhibit neointimal hyperplasia and induce expansive remodeling in a dose-dependent pattern Paul Wexberg, Christian Kirisits, Mariann Gyongyosi, Michael Gottsauner-Wolf, Boris Pokrajac, Richard Potter, Dietmar Glogar. Division of Cardiology, University of Vienna Medical Center, Vienna, Austria, Department of Radiotherapy and Radiobiology, University of Vienna Medical Center, Vienna, Austria

Radioactive stents inhibit neointimal hyperplasia and induce expansive remodeling in a dose-dependent pattern Paul Wexberg, Christian Kirisits, Mariann Gyongyosi, Michael Gottsauner-Wolf, Boris Pokrajac, Richard Potter, Dietmar Glogar. Division of Cardiology, University of Vienna Medical Center, Vienna, Austria, Department of Radiotherapy and Radiobiology, University of Vienna Medical Center, Vienna, Austria

"Edge Effect" of (32)p radioactive stents is caused by the combination of chronic stent injury and radioactive dose falloff.

Radioactive stents have been reported to reduce in-stent neointimal thickening. An unexpected increase in neointimal response was observed, however, at the stent-to-artery transitions, the so-called "edge effect." To investigate the factors involved in this edge effect, we studied stents with 1 radioactive half and 1 regular nonradioactive half, thereby creating a midstent radioactive dose-falloff zone next to a nonradioactive stent-artery transition at one side and a radioactive stent-artery transition at the other side. Half-radioactive stents (n=20) and nonradioactive control stents (n=10) were implanted in the coronary arteries of Yucatan micropigs. Animals received aspirin and clopidogrel as antithrombotics. After 4 weeks, a significant midstent stenosis was observed by angiography in the half-radioactive stents. Two animals died suddenly because of coronary occlusion at this mid zone at 8 and 10 weeks. At 12-week follow-up angiography, intravascular ultrasound and histomorphometry showed a significant neointimal thickening at the midstent dose-falloff zone of the half-radioactive stents, but not at the stent-to-artery transitions at both extremities. Such a midstent response (mean angiographic late loss 1.0 mm) was not observed in the nonradioactive stents (mean loss 0.4 to 0.6 mm; P< 0.01). The edge effect of high-dose radioactive stents in porcine coronary arteries is associated with the combination of stent injury and radioactive dose falloff.

Why and how to avoid stenting during brachytherapy

Intracoronary radiation is a promising therapy to reduce restenosis after percutaneous coronary intervention. It may be anticipated that radiation and intracoronary stents - the current standard coronary revascularization procedure - have a synergic antirestenosis effect. However, this potential benefit has not been proven in the clinical scenario. Indeed, this combined approach (stenting plus brachytherapy) may even be harmful. Delayed endothelialization and late stent malapposition are important drawbacks of implanting a metallic prosthesis in the setting of radiation therapy. Owing to the relatively high frequency of late thrombosis after stenting irradiated coronary arteries, the Food and Drug Administration required that the labeling of both gamma- and beta-radiation devices recently approved for clinical use explicitly advise avoidance of the placement of new stents. The pathophysiologic aspects as well as the clinical implications of the implantation of a new stent in association with radiation delivered by radioactive stents or catheter-based systems are discussed in this paper.

Stent Obstruction-Preventive Techniques

This article outlines the causes of stent obstruction and the uses of endovascular brachytherapy with different sources and radioactive stents. Above this temporary stenting, another practical method to minimize trauma to the vessel walls is described. Endovascular brachytherapy with iridium 192 HDR to prevent restenosis in peripheral arteries was first described by the authors in 1990. The results of a 9-year follow-up are encouraging and demonstrate the usefulness of intravascular irradiation. The use of radioactive stents is restricted to the coronary arteries; a potential disadvantage is the delayed epithelization. Temporary stenting is defined as stenting within a limited time period of 24 hours, but there are only a few clinical reports dealing with this method.

Stent and stent-edge remodeling after conventional and radioactive stent implantation

Stent and stent-edge remodeling after conventional and radioactive stent implantation