Visceral stent patency after fenestrated endovascular aneurysm repair using bare-metal stent extensions versus covered stents only.
- 作者列表："Khoury MK","Timaran DE","Knowles M","Timaran CH
OBJECTIVE:Fenestrated endovascular aneurysm repair (FEVAR) is an alternative to treat complex abdominal aortic aneurysms. Patency of visceral vessels remains high when covered stents are used. The use of distal uncovered stents to prevent kinking has been associated with loss of branch patency. The aim of this study was to evaluate branch-related outcomes of FEVAR using covered stents only vs the use of uncovered stents distal to covered stents. METHODS:During a 4-year period, 142 patients underwent FEVAR. Patients with suprarenal, juxtarenal, and type IV thoracoabdominal aneurysms were included. Patients treated with side branch devices were excluded. Covered iCAST (Maquet, Hudson, NH) stents were used as bridging stents in all cases. The primary end point was primary patency, defined as the absence of stenosis or occlusion that required intervention. Secondary end points included secondary patency, branch-related outcomes (kidney injury and gastrointestinal complications), branch instability, and mortality rates. RESULTS:A total of 442 target vessels were incorporated (49 scallops and 393 fenestrations). Uncovered stents were used in 38 (9.6%) visceral vessels. Median follow-up time was 11 (interquartile range, 6-13) months. Overall, visceral vessel primary patency was 91% at 12 and 24 months. The overall primary patency rate was 86% in the distal extension group vs 93% when only covered stents were used at 12 and 24 months (P = .8). Similarly, the rate of branch-related reinterventions at 12 months was 9% and 15% for each group, respectively, and 22% vs 32% at 24 months, respectively (P = .5). Overall, freedom from branch instability was 87% at 12 months and 81% at 24 months. Freedom from branch instability in the distal extension group was 82% at 12 and 24 months vs 89% at 12 months and 81% at 24 months when only covered stents were used (P =. 08). Mortality rate at 24 months was 15% for the bare-metal stent extension group vs 14% for the covered stent only group (P = .4). We found no statistical difference in acute kidney injury at any Kidney Disease: Improving Global Outcomes stage (P = 1.0) or gastrointestinal complications (P = 1.0) between the groups. CONCLUSIONS:The use of distal uncovered stents to prevent kinks was not associated with decreased early branch patency. The long-term outcomes of bare-metal stents remain to be determined. For now, the use of uncovered stents distal to covered stents may be considered to prevent kinks in complex anatomy.
目的: 开窗腔内修复术 (FEVAR) 是治疗复杂腹主动脉瘤的一种替代方法。使用覆膜支架时，内脏血管的通畅性仍然很高。使用远端未覆盖支架防止扭结与分支通畅性丧失有关。本研究的目的是评价仅使用覆膜支架的 FEVAR 与使用覆膜支架远端的未覆盖支架的分支相关结局。 方法: 在 4 年期间，142 例患者接受了 FEVAR。包括肾上、肾旁和 IV 型胸腹动脉瘤患者。排除使用侧支装置治疗的患者。所有病例均采用覆膜 iCAST (Maquet，Hudson，NH) 支架作为桥接支架。主要终点是原发性通畅性，定义为没有需要干预的狭窄或闭塞。次要终点包括二次通畅、分支相关结局 (肾损伤和胃肠道并发症) 、分支不稳定性和死亡率。 结果: 共纳入 442 条靶血管 (49 条扇贝和 393 条开窗)。未覆盖支架用于 38 例 (9.6%) 内脏血管。中位随访时间为 11 (四分位距，6-13) 个月。总体而言，12 个月和 24 个月时内脏血管原发性通畅率为 91%。远端伸展组的总一期通畅率为 86%，而在 12 个月和 24 个月时仅使用覆膜支架时为 93% (P =.8)。同样，每组 12 个月时的分支相关再干预率分别为 9% 和 15%，24 个月时分别为 22% 和 32% (P =.5)。总体而言，12 个月时无分支不稳定性为 87%，24 个月时为 81%。远端伸展组在 12 个月和 24 个月时无分支不稳定的发生率为 82%，在 12 个月和 24 个月时为 89%，仅使用覆膜支架时为 81% (P =。08)。24 个月时，裸金属支架延长组的死亡率为 15%，而仅覆膜支架组为 14% (P =.4)。我们发现在任何肾脏疾病的急性肾损伤方面没有统计学差异: 改善两组之间的总体结局分期 (P = 1.0) 或胃肠道并发症 (P = 1.0)。 结论: 使用远端未覆盖支架预防扭结与降低早期分支通畅率无关。裸金属支架的长期结局仍有待确定。目前，可以考虑在覆膜支架远端使用未覆盖支架，以防止复杂解剖结构中的扭结。
METHODS:Aims : We sought to investigate the thrombogenicity of different DES and BMS in an in vitro system of stent perfusion. Material and Methods: The experimental model consisted of a peristaltic pump connected to 4 parallel silicone tubes in which different stents were deployed. Blood was drawn from healthy volunteers and the amount of stent surfaced -induced thrombus deposition was determined using 125 I -fibrinogen. Results: Compared to Resolute, Biomatrix and Vision, Xience was associated with the lowest amount of stent surface -induced thrombus formation, with a significant difference compared to Vision (125 I -fibrinogen median value deposition [IQ range]: 50 ng [25 -98] versus 560 ng [320 - 1,520], respectively, p<0.05), but not to other DES. In the second set of experiments Fluoropolymer -coated BMS not eluting drug was associated with a significant 3 -fold reduction in 125 I -fibrinogen deposition (245 ng [80 -300]) compared to Vision (625 ng [320 -760], p<0.05), but a 7 -fold increase compared to Xience (35 ng [20 -60], p<0.05). Finally Xience was associated with a significantly greater absorption of albumin compared to BMS. Conclusions: In an in vitro system of stent perfusion, Xience was associated with the lowest amount of stent surface -induced thrombus formation compared with Resolute, Biomatrix and Vision, with a noted synergistic effect between the fluoropolymer and the drug.
METHODS::Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with decreased Akt1/mTOR signaling. Targeting Fn-EDA in human aortic SMCs suppressed the synthetic phenotype and downregulated Akt1/mTOR signaling. These results reveal that SMC-derived Fn-EDA potentiates phenotypic switching in human and mouse aortic SMCs and neointimal hyperplasia in the mouse. We suggest that targeting Fn-EDA could be explored as a potential therapeutic strategy to reduce neointimal hyperplasia.
METHODS:OBJECTIVE:The goal of this study was to determine the impact of late-acquired stent malapposition (LASM) on long-term clinical outcomes in patients treated with coronary stent implantation. Approach and Results: We investigated major adverse cardiac event during 10 years after 6-month intravascular ultrasound examination using our previous studies database. A total of 732 patients treated with bare-metal stent (54 LASM versus 678 non-LASM) and 529 patients treated with first-generation drug-eluting stent (82 LASM versus 447 non-LASM), who did not have clinical event or censoring at the time of follow-up intravascular ultrasound, were included for the present analysis. major adverse cardiac event was defined as the composite of cardiac death, target vessel-related myocardial infarction, target lesion revascularization and stent thrombosis. Multivariable adjustment and inverse probability weight were performed to consider baseline differences. After multivariable adjustment, LASM was related to a greater risk of major adverse cardiac event (hazard ratio, 1.666 [95% CI, 1.041-2.665]; P=0.0333) and very-late stent thrombosis (hazard ratio, 3.529 [95% CI, 1.153-10.798]; P=0.0271) than non-LASM in patients treated with first-generation drug-eluting stent, but not in those treated with bare-metal stent. Results were consistent after inverse probability weight. Among patients with LASM of first-generation drug-eluting stent, no late stent thrombosis occurred in patients who continued to receive dual antiplatelet therapy. CONCLUSIONS:The relationship between LASM and major adverse cardiac event might depend on the type of implanted stents during the long-term follow-up, highlighting the clinical significance of polymers and drugs in drug-eluting stent system.