68 research outputs found
Radiation and the Stent: Results From Catheter - Based Radiation. And Radioactive Stenting
Angiographic restenosis occurs in up to 60% of cases after balloon angioplasty (BA).
Restenosis after BA occurs due to elastic recoil of the artery, vascular remodeling
with vessel shrinkage and neointimal hyperplasia. Neointimal hyperplasia develops by
migration and proliferation of smooth muscle cells (SMCs) and myofibroblasts after
balloon-induced trauma of the arterial wall and by deposition of an extracellular matrix
by the SMCs. By preventing elastic recoil and negative remodeling stent implantation
has resolved many of the problems created by balloon angioplasty. However, a new
problem has been created - that of in-stent restenosis, wh
Reference chart derived from post-stent-implantation intravascular ultrasound predictors of 6-month expected restenosis on quantitative coronary angiography
BACKGROUND: Intravascular ultrasound (IVUS)-guided stent implantation and
the availability of a reference chart to predict the expected in-stent
restenosis rate based on operator-dependent IVUS parameters ma
Late coronary occlusion after intracoronary brachytherapy
BACKGROUND: Intracoronary brachytherapy appears to be a promising
technology to prevent restenosis. Presently, limited data are available
regarding the late safety of this therapeutic modality. The aim of the
study was to determine the incidence of late (>1 month) thrombosis after
PTCA and radiotherapy. METHODS AND RESULTS: From April 1997 to March 1999,
we successfully treated 108 patients with PTCA followed by intracoronary
beta-radiation. Ninety-one patients have completed at least 2 months of
clinical follow-up. Of these patients, 6.6% (6 patients) presented with
sudden thrombotic events confirmed by angiography 2 to 15 months after
intervention (2 balloon angioplasty and 4 stent). Some factors
(overlapping stents, unhealed dissection) may have triggered the
thrombosis process, but the timing of the event is extremely unusual.
Therefore, the effect of radiation on delaying the healing process and
maintaining a thrombogenic coronary surface is proposed as the most
plausible mechanism to explain such late events. CONCLUSIONS: Late and
sudden thrombosis after PTCA followed by intracoronary radiotherapy is a
new phenomenon in interventional cardiology
Radioactive stents delay but do not prevent in-stent neointimal hyperplasia
BACKGROUND: Restenosis after conventional stenting is almost exclusively caused by neointimal hyperplasia. Beta-particle-emitting radioactive stents decrease in-stent neointimal hyperplasia at 6-month follow-up. The purpose of this study was to evaluate the 1-year outcome of (32)P radioactive stents with an initial activity of 6 to 12 microCi using serial quantitative coronary angiography and volumetric ECG-gated 3D intravascular ultrasound (IVUS). METHODS AND RESULTS: Of 40 patients undergoing initial stent implantation, 26 were event-free after the 6-month follow-up period and 22 underwent repeat catheterization and IVUS at 1 year; they comprised half of the study population. Significant luminal deterioration was observed within the stents between 6 months and 1 year, as evidenced by a decrease in the angiographic minimum lumen diameter (-0.43+/-0.56 mm; P:=0.028) and in the mean lumen diameter in the stent (-0.55+/-0. 63 mm; P:=0.001); a significant increase in in-stent neointimal hyperplasia by IVUS (18.16+/-12.59 mm(3) at 6 months to 27.75+/-11. 99 mm(3) at 1 year; P:=0.001) was also observed. Target vessel revascularization was performed in 5 patients (23%). No patient experienced late occlusion, myocardial infarction, or death. By 1 year, 21 of the initial 40 patients (65%) remained event-free. CONCLUSIONS: Neointimal proliferation is delayed rather than prevented by radioactive stent implantation. Clinical outcome 1 year after the implantation of stents with an initial activity of 6 to 12 microCi is not favorable when compared with conventional stenting
Geographic Miss
Background—A recognized limitation of endovascular ß-radiation therapy is the development of new stenosis at the edges of the irradiated area. The combination of injury and low-dose radiation may be the precursor of this phenomenon. We translated the radio-oncological concept of "geographic miss" to define cases in which the radiation source did not fully cover the injured area. The aims of the study were to determine the incidence and causes of geographic miss and evaluate the impact of this inadequate treatment on the outcome of patients treated with intracoronary ß-radiation.
Methods and Results—We analyzed 50 consecutive patients treated with ß-radiation after percutaneous coronary intervention. The prescribed dose ranged between 12 and 20 Gy at 2 mm from the source axis. By means of quantitative coronary angiography, the irradiated segment (IRS) and both edges were studied before and after intervention and at 6-month follow-up. Edges that were injured during the procedure constituted the geographic miss edges. Twenty-two edges were injured during the intervention, mainly because of procedural complications that extended the treatment beyond the margins of the IRS. Late loss was significantly higher in geographic miss edges than in IRSs and uninjured edges (0.84±0.6 versus 0.15±0.4 and 0.09±0.4 mm, respectively; P<0.0001). Similarly, restenosis rate was significantly higher in the injured edges (10% within IRS, 40.9% in geographic miss edges, and 1.9% in uninjured edges; P<0.001).
Conclusions—These data support the hypothesis that the combination of injury and low-dose ß-radiation induces deleterious outcome
Geographic miss: a cause of treatment failure in radio-oncology applied to intracoronary radiation therapy
BACKGROUND: A recognized limitation of endovascular beta-radiation therapy
is the development of new stenosis at the edges of the irradiated area.
The combination of injury and low-dose radiation may be the precursor of
this phenomenon. We translated the radio-oncological concept of
"geographic miss" to define cases in which the radiation source did not
fully cover the injured area. The aims of the study were to determine the
incidence and causes of geographic miss and evaluate the impact of this
inadequate treatment on the outcome of patients treated with intracoronary
beta-radiation. METHODS AND RESULTS: We analyzed 50 consecutive patients
treated with beta-radiation after percutaneous coronary intervention. The
prescribed dose ranged between 12 and 20 Gy at 2 mm from the source axis.
By means of quantitative coronary angiography, the irradiated segment
(IRS) and both edges were studied before and after intervention and at
6-month follow-up. Edges that were injured during the procedure
constituted the geographic miss edges. Twenty-two edges were injured
during the intervention, mainly because of procedural complications that
extended the treatment beyond the margins of the IRS. Late loss was
significantly higher in geographic miss edges than in IRSs and uninjured
edges (0.84+/-0.6 versus 0.15+/-0.4 and 0.09+/-0.4 mm, respectively;
P<0.0001). Similarly, restenosis rate was significantly higher in the
injured edges (10% within IRS, 40.9% in geographic miss edges, and 1.9% in
uninjured edges; P<0.001). CONCLUSIONS: These data support the hypothesis
that the combination of injury and low-dose beta-radiation induces
deleterious outcome
Coronary flow velocity reserve after percutaneous interventions is predictive of periprocedural outcome
BACKGROUND: Because heterogeneous results have been reported, we assessed coronary flow velocity changes in individuals who underwent percutaneous transluminal coronary angioplasty (PTCA) and examined their impact on clinical outcome. METHODS AND RESULTS: As part of the Doppler Endpoints Balloon Angioplasty Trial Europe (DEBATE) II study, 379 patients underwent Doppler flow-guided angioplasty. All patients were evaluated according to their coronary flow velocity reserve (CFVR) results (> or =2.5 or < 2.5) at the end of the procedure. A CFVR < 2.5 after angioplasty was associated with an elevated baseline blood flow velocity in both the target artery and reference artery. CFVR before PTCA and CFVR in the reference artery were independent predictors of an optimal CFVR after balloon angioplasty (CFVR before PTCA: odds ratio [OR], 2.26; 95% confidence interval [CI], 1.57 to 3.24; CFVR in reference artery: OR, 1.90; 95% CI, 1.21 to 2.98; both P<0.001) and stent implantation (before PTCA: OR, 2.54; 95% CI, 1.47 to 4.36; reference artery: OR, 1.97; 95% CI, 1.07 to 3.87; both P<0.05). A low CFVR at the end of the procedure was an independent p
Positive geometric vascular remodeling is seen after catheter-based radiation followed by conventional stent implantation but not after radioactive stent implantation
BACKGROUND: Recent reports demonstrate that intracoronary radiation
affects not only neointimal formation but also vascular remodeling.
Radioactive stents and catheter-based techniques deliver radiation in
different ways, suggesting that different patterns of remodeling after
each technique may be expected. METHODS AND RESULTS: We analyzed
remodeling in 18 patients after conventional stent implantation, 16
patients after low-activity radioactive stent implantation, 16 patients
after higher activity radioactive stent implantation, and, finally, 17
patients who underwent catheter-based radiation followed by conventional
stent implantation. Intravascular ultrasound with 3D reconstruction was
used after stent implantation and at the 6-month follow-up to assess
remodeling within the stent margins and at its edges. Preprocedural
characteristics were similar between groups. In-stent neointimal
hyperplasia (NIH) was inhibited by high-activity radioactive stent
implantation (NIH 9.0 mm(3)) and by catheter-based radiation followed by
conventional stent implantation (NIH 6.9 mm(3)) compared with low-activity
radioactive stent implantation (NIH 21.2 mm(3)) and conventional stent
implantation (NIH 20.8 mm(3)) (P:=0.008). No difference in plaque or total
vessel volume was seen behind the stent in the conventional, low-activity,
or high-activity stent implantation groups. However, significant increases
in plaque behind the stent (15%) and in total vessel volume (8%) were seen
in the group that underwent catheter-based radiation followed by
conventional stent implantation. All 4 groups demonstrated significant
late lumen loss at the stent edges; however, edge restenosis was seen only
in the group subjected to high-activity stent implantation and appeared to
be due to an increase in plaque and, to a lesser degree, to negative
remodeling. CONCLUSIONS: Distinct differences in the patterns of
remodeling exist between conventional, radioactive, and catheter-based
radiotherapy with stenting
Three dimensional intravascular ultrasonic assessment of the local mechanism of restenosis after balloon angioplasty
OBJECTIVE: To assess the mechanism of restenosis after balloon angioplasty. DESIGN: Prospective study. PATIENTS: 13 patients treated with balloon angioplasty. INTERVENTIONS: 111 coronary subsegments (2 mm each) were analysed after balloon angioplasty and at a six month follow up using three dimensional intravascular ultrasound (IVUS). MAIN OUTCOME MEASURES: Qualitative and quantitative IVUS analysis. Total vessel (external elastic membrane), plaque, and lumen volume were measured in each 2 mm subsegment. Delta values were calculated (follow up - postprocedure). Remodelling was defined as any (positive or negative) change in total vessel volume. RESULTS: Positive remodelling was observed in 52 subsegments while negative remodelling occurred in 44. Remodelling, plaque type, and dissection were heterogeneously distributed along the coronary segments. Plaque composition was not associated with changes in IVUS indices, whereas dissected subsegments had a greater increase in total vessel volume than those without dissection (1.7 mm(3) v -0.33 mm(3), p = 0.04). Change in total vessel volume was correlated with changes in lumen (p < 0.05, r = 0.56) and plaque volumes (p < 0.05, r = 0.64). The site with maximum lumen loss was not the same site as the minimum lumen area at follow up in the majority (n = 10) of the vessels. In the multivariate model, residual plaque burden had an influence on negative remodelling (p = 0.001, 95% confidence interval (CI) -0.391 to -0.108), whereas dissection had an effect on total vessel increase (p = 0.002, 95% CI 1.168 to 4.969). CONCLUSIONS: The mechanism of lumen renarrowing after balloon angioplasty appears to be determined by unfavourable remodelling. However, different patterns of remodelling may occur in individual injured coronary segments, which highlights the complexity and influence of local factors in the restenotic process
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