scholarly journals The “Edge Effect” After Implantation of β-Emitting (55Co) Stents with High Initial Activity

2004 ◽  
Vol 47 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Pavel Červinka ◽  
Josef Šťásek ◽  
Marco Aurelio Costa ◽  
Jan Štursa ◽  
Miloslav Fišer ◽  
...  

The aim of this study was to evaluate the incidence and the cause of “edge restenosis” after implantation of high activity 41.1 μCi±1.2 μCi=1520 kBq±44 kBq, β-emitting (55Co) stents. Proton bombarding in cyclotron has brought the radioactivity. Intravascular ultrasound (IVUS) investigation has been completed in 10 patients. The angiographies performed at 6 month revealed restenosis >50 % in 5 cases (50 %). The analysis of edges (5 mm distally and proximally to the last stent struts) showed no significant changes in TVV (187.3±62.60 mm3 and 176.9±53.5 mm3) but PMV increase significantly (i.e. neointimal proliferation) from 61.9±31.2 mm3 to 82.2±43.4 mm3 (p<0.04) and was the major contributor (from 66 %) to lumen volume loss (125.4±40.7 mm3 and 94.7±22.2 mm3, p<0.02). In conclusion, neither statistically significant positive nor negative remodelling at the “stent edges“, were present. Statistically significant increase in plaque+media volume (i.e. neointimal hyperplasia) and reduction in lumen volume were found. The cause of “edge restenosis” was especially (from 66 %) due to increase in plaque+media volume (i.e. neointimal hyperplasia). Probably, main reason for “edge effect”/neointimal hyperplasia was in this trial sharp fall-off in radiation at the edges of the stents.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Fusako Sera ◽  
Jun-ichi Kotani ◽  
Masaki Awata ◽  
Shinsuke Nanto ◽  
Masaaki Uematsu ◽  
...  

Background: Although sirolimus-eluting stent (SES) has significantly reduced in-stent restenosis by inhibiting neointimal hyperplasia, insufficient neointimal coverage after stenting may result in adverse outcomes. Determinants of neointimal coverage following SES, however, are poorly understood. Methods: We evaluated 28 SES lesions using both angioscopy and intravascular ultrasound (IVUS). Degree of neointimal coverage was judged by angioscopy at follow-up (11 ± 6 months): complete/incomplete coverage, based on whether the stent struts were embedded by the neointima. Minimal stent area (MSA), external elastic membrane (EEM), lumen cross-sectional area (CSA) and plaque burden (EEM minus lumen/EEM CSA) were measured by IVUS at stent implantation. Both proximal and distal references were used. Stent expansion was assessed by stent expansion index (SEI) as MSA/reference EEM CSA. Under-expansion was defined as SEI < 0.4. Incomplete apposition was defined as the lack of contact between any strut and the underlying vessel wall. Results: Complete coverage was identified in 10 (36%), and incomplete coverage in 18 (64%). Time from the stenting to angioscopy (10 ± 5 versus 11 ± 7 months, p=0.8) as well as the lesion and procedural characteristics was similar between the complete/incomplete coverage groups. IVUS parameters were also similar, except for the final MSA (7.0±1.8mm 2 in complete versus 5.3±1.9mm 2 in incomplete , p=0.02) and lumen CSA at the distal reference site (6.1±1.4mm 2 in complete versus 4.9 ±1.2mm 2 in incomplete , p= 0.02). The frequency of incomplete apposition was similar between the groups (20% in complete versus 39% in incomplete , P= 0.4); however, SEI was significantly larger in the complete coverage than in the incomplete coverage group (0.52 ± 0.11 versus 0.39 ± 0.09, p=0.002). Stent under-expansion was identified only in 2 (20%) of the complete coverage, as compared to 67% of the incomplete coverage group (P=0.046). By multivariate logistic regression analysis, large SEI was strongly associated with complete neointimal coverage (P=0.04). Conclusion: Optimal expansion of the stent is a major contributor to the complete neointimal coverage following sirolimus-eluting stent implantation.


2010 ◽  
Vol 145 (1) ◽  
pp. 125-126 ◽  
Author(s):  
Hiromasa Otake ◽  
Junya Ako ◽  
Katsuhisa Waseda ◽  
Ryota Sakurai ◽  
Atsushi Hirohata ◽  
...  

2002 ◽  
Vol 39 ◽  
pp. 70-71
Author(s):  
Andrea S. Abizaid ◽  
J.Eduardo Sousa ◽  
Pim de Feyter ◽  
Alexandre Abizald ◽  
Egon Wuelfert ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Sebastian Philipp ◽  
Dirk Böse ◽  
Igor Kordish ◽  
Johannes Brachmann ◽  
Klinikum Coburg ◽  
...  

Background: Although the use of drug-eluting stents has been shown to limit neointimal hyperplasia, currently available DES may adversely affect re-endothelialization, possibly precipitating late cardiac events. The aim of this study was to evaluate the efficacy and safety of a microbubble delivery of c-myc antisense peptide in preventing restenosis after coronary stenting in de novo stenosis with intravascular ultrasound. Methods: A BMS was implanted in de novo coronary artery lesions (RD ≥ 2.5- ≤4.0mm; TL ≥ 15- ≤ 30mm in length). Serial intravascular ultrasound analysis were performed in 25 lesions. A dose of 16mg RESTEN-MPTM (AVI BioPharma/Global Therapeutics LLC) was intravenously administered after stenting and again 24 hours later. Results: A total of 50 patients were enrolled, 34 in Essen, 13 in Coburg and 3 in Heidelberg. Before stenting, the MLD and length of stenosis was determined by QCA. 18 Patients had a LAD lesion, 21 LCX, 12 RCA. 84% (43/51) of the lesions were either Type B2 or C lesions. At six month follow-up, angiography with a QCA was performed. Generally the neointimal proliferation was minor and open vessel lumen could be demonstrated during follow-up. Of the 30 patients currently studied at six-months in the IVUS sub-study, six patients required TLR. Late lumen loss by QCA was 0.47±0.09mm. Volume stenosis by IVUS was 26 ± 4 %. Generally the neointima proliferation was minor and open vessel lumen could be demonstrated during follow-up. Summary: Microbubble delivery of c-myc antisense seems to be effective in reducing neointimal tissue proliferation without the problem of late stent thrombosis, because the proliferation seems to be attenuated but not fully blocked.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Cori A Cason ◽  
Thomas M Kuntz ◽  
Neil Gottel ◽  
Liqun Xiong ◽  
Qun Jiang ◽  
...  

Neointimal hyperplasia is a major contributor to restenosis after arterial interventions. The genetic and environmental mechanisms underlying the variable propensity for neointimal hyperplasia between individuals are not well understood. One possible modulator could be commensal gut microbes. To address whether microbes mediate neointimal hyperplasia, we cohoused genetically different rats (Lewis [LE] and Sprague-Dawley [SD]) which harbor different commensal microbes and compared neointimal hyperplasia 2 weeks after carotid angioplasty in the cohoused and non-cohoused cohorts. Cohousing is a means of microbial transfer between cage inhabitants. We observed that differences in neointimal hyperplasia between non-cohoused LE and SD rats (median intima+media [I+M] area 0.12 mm 2 LE vs. 0.26 mm 2 SD, P<.0001;Mann-Whitney) were mitigated when rats are cohoused for 1 month (Figure 1A), suggesting an environmental effect that outweighs the genetic influence. Specifically, I+M area decreased by 23% in SD rats that were cohoused with LE rats (P<.0001;Mann-Whitney), and there was a trend towards a 10% increase in I+M area in cohoused LE rats. To identify specific bacteria associated with the change in neointimal hyperplasia, we monitored fecal bacteria over time using 16S rRNA sequencing. Principal component analysis revealed that fecal samples from cohoused rats diverged from non-cohoused rats in both strains (P<.001 SD, P=.008 LE;PERMANOVA) (Figure 1B). The greatest change was cohoused SD samples becoming similar to non-cohoused LE samples over time, which correlates with the carotid morphometric data. Comparative analysis showed that abundance of the bacterial genera Peptococcus and Blautia negatively correlated with I+M area in both strains (P<.001;Fisher z transform, Bonferroni corrected, Spearman’s ρ -0.8 for both). Ongoing studies will further delineate the potential causative relationship between these microbes and neointimal hyperplasia.


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