103Pd同位素支架预防支架内再狭窄的实验研究

目的 探讨103Pd同位素支架对支架植入术后再狭窄的预防作用,方法 对雄性新西兰白兔50只进行腹主动脉球囊拉伤后,分别置入103pd同位素支架（同位素支架组）和普通支架（普通支架组）各25只。两组分别于术后3d和1,2,4,8周分批进行血管病理形态学,免疫组织化学测定和血管造影检查。结果 血管拉伤后8周,血管造影显示,同位素支架组血管最小内径显大于普通支架组（P＜0．05）,血管狭窄程度明显减低（P＜0．05）,病理形态学和免疫化学染色分析表明,两组血管损伤程度相同,受同位素辐射作用后,血管内膜增生到显抑制,管腔狭窄程度减轻,结论 103Pd同位素支架在动物实验中具有明显预防支架内血管再狭窄的作用。     

化学镀法制备32P放射性支架预防再狭窄的实验研究

目的 :评价3 2 P放射性支架对兔髂动脉狭窄的预防作用。方法 :以化学镀法制备3 2 P放射支架 ,与非放射支架配对后 ,随机置入兔双侧髂动脉 ,术前、术后即刻及术后 30d造影观察动脉狭窄程度 ,并进行病理组织学观察内膜面积及管腔内径的变化。结果 :术后 30d ,两种支架置入后的动脉最小腔径 (MLD)均比术后即刻显著减小 ;放射支架侧的MLD显著大于对照侧 (P <0 .0 1) ,而其后期丢失、丢失指数、狭窄程度等 3项指标则显著小于对照侧 (P <0 .0 1)。两种支架置入均使血管内膜增生 ;放射支架侧血管管腔面积显著大于对照侧 (P <0 .0 5 ) ,而其新生内膜面积显著小于对照侧 (P <0 .0 1)。未发现两种支架置入后对支架边缘部位的影响。结论 :化学镀法制备的放射性3 2 P支架安全有效 ,较低的放射活度即可有效防止支架内狭窄 ;以短球囊扩张支架可能会避免边缘部位狭窄的发生     

卡托普利对血管成形术后血管壁血小板源性生长因子基因表达的影响

球囊拉伤血管加高脂饲养建立兔髂动脉粥样硬化模型进行球囊血管成形术，随机分为治疗组（ｎ＝８）和对照组（ｎ＝８）。治疗组于术前７天至术后第２８天每天接受卡托普利（１２．５ｍｇ／ｋｇ）治疗。术后４用处死动物．分离血管，应用斑点印迹杂交技术检测成形段血管血小板源。术后４周处死动物，分离血管，应用斑点印迹杂交技术检测成形段血管血小板源性生长因子基因及其受体基因表达。结果表明，卡托普利能抑制血管成形术后成形段血管血小板源性生长因子基因及其受体基因表达。     

血小板源生长因子β受体反义寡核苷酸对血小板源生长因子诱导大鼠血管平滑肌细胞迁移的影响

为研究血小板源生长因子β受体反义寡核苷酸对血小板源生长因子诱导的大鼠血管平滑肌细胞迁移的影响和作用机制,利用激光共聚集显微镜观察平滑肌细胞对异硫氰酸荧光素标记的反义寡核苷酸的摄取和细胞内定位,改良Boden's小室法观察平滑肌细胞迁移。结果发现,加入反义寡核苷酸培养24h及48h后荧光分别位于细胞浆内和细胞核内,5umol/L以上浓度反义寡核苷酸作用36h后,被血小板源生长因子诱导迁移通过Boyden's小室碳纤维素膜的细胞数量小于空白对照组;正义,错义寡核苷酸和5umol/L以下浓度反义寡核苷酸迁移抑制不明显,提示血小板源生长因子β受体反义寡核苷酸在细胞核内呈时间和浓度依赖性抑制血小板源生长因子诱导的血管平滑肌细胞迁移。     

γ干扰素对兔血管内膜损伤后平滑肌细胞表达血小板源性生长因子B-mRNA和增殖的影响

目的探讨γ干扰素抑制血管内膜增生和防治血管再狭窄的体内机制。方法建立兔血管狭窄模型,动态观察肌内给予重组γ干扰素对损伤后不同时期血管内膜平滑肌细胞(vSMCs)原位表达血小板源性生长因子B链mRNA(PDGF-BmRNA)和增殖细胞核抗原的影响。结果γ干扰素显著抑制1周和4周时内膜vSMCs表达增殖细胞核抗原,抑制率分别为88.5％和58.9％;显著抑制各观察时期新生内膜表达PDGF-BmRNA。结论γ干扰素通过下调vSMCs原位表达PDGF-BmRNA抑制血管vSMCs的增殖和内膜增生,可能用于临床再狭窄的防治。     

脑心通胶囊对血管支架成型术后再狭窄预防作用的研究

目的 评价脑心通胶囊预防支架内再狭窄的效果.方法 以48例血管内支架成形术术后患者作为研究对象.术后随机分为两组,治疗组23例服用脑心通胶囊;对照组25例应用噻氯匹定(抵克力得)治疗.术后6个月复查脑血管造影,计算机定量测定血管病变的直径狭窄程度(QCA ).结果 治疗组参照血管直径与西药对照组比较无统计学意义,支架段血管直径差异不明显(2.22 mm±0.21 mm与2.18 mm±0.25 mm,P＞0.05).血管直径减少指数治疗组与对照组分别为0.50 mm±0.16 mm、0.51 mm±0.11 mm(P＞0.05).治疗组再狭窄率(17.4%) 及再介入率(13.1%)与对照组(20%、12%)比较,差异无统计学意义( P＞0.05),但治疗组并发症明显低于对照组.结论 脑心通胶囊干预可降低血管内支架成型治疗术后再狭窄的发生率,且有较少的并发症.     

生物可降解血管内支架：希望和挑战

生物可降解血管内支架(BDS)具有较好的生物相容性和可吸收性,能在短期内支撑血管,达到血运重建的目的.由于完成使命后可在体内降解,生物可降解支架可以避免金属永久支架引起的并发症.目前的研制主要包括可降解聚合物材料、金属镁和铁.上世纪80年代BDS已经进入临床且取得了一定的效果,它使血管成形术向前跨进了一步.目前的生物可降解血管内支架存在着一些缺陷,需要进一步改进和验证.     

生物可降解血管内支架：希望和挑战

生物可降解血管内支架（BDS）具有较好的生物相容性和可吸收性，能在短期内支撑血管，达到血运重建的目的。由于完成使命后可在体内降解，生物可降解支架可以避免金属永久支架引起的并发症。目前的研制主要包括可降解聚合物材料、金属镁和铁。上世纪80年代BDS已经进入临床且取得了一定的效果，它使血管成形术向前跨进了一步。目前的生物可降解血管内支架存在着一些缺陷，需要进一步改进和验证。     

冠状动脉支架置入对分支血管的影响

目的 比较观察不同药物洗脱支架及普通支架置入术后分支血管的自然发展情况,探讨分支血管闭塞及再通的影响因素。方法回顾性分析在解放军总医院心内科接受支架置入术并进行造影随访的183例患的病例资料及术前、术中、术后的造影光盘资料,分析支架覆盖的所有分支血管。结果支架术后分支血管的闭塞率是8．9％,其中Cypher药物支架组为10．5％,Taxus药物支架组为11．1％,普通支架为7．8％,72．0％的闭塞分支在随访时再通,其中Cypher组是90．9％,Taxus组为66．7％,普通支架组为66．7％;三组间差异无统计学意义;分支开口狭窄和起始部位有病变是分支血管闭塞的独立危险因素;支架内再狭窄、病变类型及分支情况等都不会影响闭塞分支的再通。结论不同类型的药物支架和普通支架在对分支血管的影响方面基本一致;分支开口狭窄和分支起始部位病变是分支血管闭塞的独立危险因素;闭塞的分支血管自然预后良好,大部分会自行再通。     

血管内皮生长因子、支架直径和支架长度对支架内再狭窄的联合预测价值

目的 探讨血管内皮生长因子（vascular endothelial growth factor,VEGF）、支架直径和支架长度对冠状动脉药物洗脱支架(drug-eluting stent, DES)置入术后支架内再狭窄（in-stent restenosis,ISR）患者的联合预测价值。 方法 收集2014年6月至2016年8月在承德市中心医院心内科行DES置入的不稳定型心绞痛患者332（男178,女154）例。根据术后1年复查冠脉造影结果将其分为ISR组（n=41）和非ISR组（n=291）,比较两组的一般临床资料及冠脉支架手术资料。采用酶联免疫吸附试验（ELISA）测定冠脉支架置入术前、术后6个月、术后12个月患者血清VEGF的水平,比较两组间VEGF的表达差异。 结果 ISR组及非ISR组患者术前VEGF水平无明显差异[（499±39）ng/L vs（503±35）ng/L];术后两个时间点ISR组VEGF水平显著低于非ISR组[（377±33）ng/L vs（462±56）ng/L;（184±34）ng/L vs（361±45）ng/L],差异均有统计学意义（均P<0.01）。Logistic回归分析表明:术后VEGF水平（OR=0.95,95%CI:0.92-0.97;P<0.01）是ISR的保护性因素;2型糖尿病（OR=14.81,95%CI:1.96-111.81;P<0.01）、术后吸烟（OR=32.74,95%CI:4.74-226.03;P<0.01）与ISR密切相关,是ISR的独立危险因素;支架长度（OR=1.26,95%CI:1.09-1.46;P<0.01）与ISR成正相关;支架直径（OR=0.03,95%CI:0.00-0.23;P<0.01）与ISR呈反相关。经绘制ROC曲线及支架直径、支架长度的联合指标的ROC曲线显示VEGF对ISR的预测价值较好,而VEGF联合支架长度及直径指标优于单独指标。 结论 术后VEGF水平与ISR密切相关,是ISR的一项独立预测因素,可作为临床评估ISR的一项指标,而VEGF联合支架直径和支架长度指标对预测ISR效能最优。     

Stenting the stent: Alternative strategy for treating in-stent restenosis

Several approaches have been taken to relieve restenosis inside a vascular stent. In a patient with a complicated history of coronary artery disease, a restenotic lesion inside a Glanturco-Roubin flex stent was relieved by angioplasty and deployment of three 10 mm Palmaz P-104 “billary” stents, with urokinase and verapamil used to prevent thromboembolism and the no-reflow phenomenon. An angiographic study 6 months later showed a patent graft with no residual stenosis. © 1996 Wiley-Liss, Inc.     

在小型猪模型由蛋白涂层金属支架局部转染尿激酶前体基因对冠状动脉再狭窄的影响

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Late restenosis following placement of a sirolimus eluting stent for in-stent restenosis

Drug eluting stents (DES) are rapidly replacing intravascular brachytherapy for the treatment of bare metal in-stent restenosis (ISR). To date, there are no long-term follow up data supporting this practise. We report symptomatic repeat in-stent restenosis occurring 27 months after sirolimus eluting stent deployment for de novo in-stent restenosis. This case suggests that in a subgroup of patients with ISR, as with brachytherapy, the drug eluting stent may be simply delaying rather than inhibiting the restenotic process.     

Influence of lesion length on restenosis after coronary stent placement

The length of a coronary lesion is a significant predictor of restenosis after balloon angioplasty. The influence of lesion length has not comprehensively been assessed after coronary stent placement. This study includes 2,736 consecutive patients with coronary stent placement. Only patients with recent or chronic occlusions before the intervention were excluded. Patients were divided in 2 groups: 573 patients with long lesions (≥15 mm) and 2,163 patients with short lesions (<15 mm). There were no significant differences between the groups with respect to the procedural success rate and incidence of subacute thrombosis. One-year event-free survival was lower in patients with long lesions (73.3% vs 80.0%, p = 0.001). Six-month angiography was performed in 82.5% of the eligible patients. The incidence of binary restenosis (≥50% diameter stenosis) was higher in patients with long lesions (36.9% vs 27.9%, p <0.001). Similarly, patients with long lesions presented more late lumen loss than those with short lesions (1.29 ± 0.89 vs 1.07 ± 0.77 mm, p <0.001). Multivariate models for both binary restenosis and late lumen loss demonstrated that lesion length was an independent risk factor for restenosis. The risk was further increased by multiple stent placement and overlapping stents that were also independent risk factors of restenosis. Stented segment length did not show any independent effect. Therefore, long lesions represent an independent risk factor for restenosis after coronary stent placement. The results of this study suggest that a possible way to reduce the risk is to cover the lesion with a minimal number of nonoverlapping stents.     

Local drug-delivery balloon for proliferative occlusive in-stent restenosis after drug-eluting stent

Drug-coated balloon has been developed as an alternative to drug-eluting stents for in-stent restenosis but the performance of drug infusion balloon in such setting has not been previously described. We present a case of particularly aggressive in-stent restenosis after drug eluting stent implantation treated with a new kind of drug infusion balloon developed in order to overcome the impossibility to inflate regular drug-coated balloon for several dilatation.     

In-stent restenosis in the drug-eluting stent era

The introduction of the drug-eluting stent (DES) proved to be an important step forward in reducing rates of restenosis and target lesion revascularization after percutaneous coronary intervention. However, the rapid implementation of DES in standard practice and expansion of the indications for percutaneous coronary intervention to high-risk patients and complex lesions also introduced a new problem: DES in-stent restenosis (ISR), which occurs in 3% to 20% of patients, depending on patient and lesion characteristics and DES type. The clinical presentation of DES ISR is usually recurrent angina, but some patients present with acute coronary syndrome. Mechanisms of DES ISR can be biological, mechanical, and technical, and its pattern is predominantly focal. Intravascular imaging can assist in defining the mechanism and selecting treatment modalities. Based upon the current available evidence, an algorithm for the treatment approaches to DES restenosis is proposed.     

Gene transfer of human vascular endothelial growth factor 165 for prevention of stent restenosis after transjugular intrahepatic portosystemic shunt

OBJECTIVE: To test the hypothesis that locally directed gene transfer of human vascular endothelial growth factor 165 (hVEGF₁₆₅) is able to passivate hepatic venous metallic stents by accelerating endo­thelialization and augmenting the biocompatibility of endovascular stents. METHODS: Complexes of pAdtrackCMV‐hVEGF₁₆₅ and lipofectamine were smeared homogeneously on the surface of the stents coated with poly‐L ‐lysine. Bare stents were used as controls. All stents were implanted into the right hepatic vein by transjugular intrahepatic venous stent deployment. RESULTS: At the end of the first week after implantation, green fluorescence and the expression of the hVEGF₁₆₅ gene were detected in the transferred stent vessels of the treated group, but were not detected in the control group. Scanning electron microscopy revealed that the endothelialization of stents was more pronounced in the treated group than that in the control group. At the end of the eighth week after implantation, quantitative angiography analysis showed the internal diameter of the stent was significantly greater in the treated group than in the control group. The de novo intima, their mean areas and percentage cross‐sectional area narrowing in the treated group were significantly less than those in the control group. Immunohistochemical analysis indicated that the proliferation of vascular smooth muscle cells was more active in the control group than that in the treated group. CONCLUSION: Local gene transfer of hVEGF₁₆₅ can passivate endovascular stents by accelerating stent endothelialization and enhancing their biocompatibility in the hepatic vein, resulting in a reduction of thrombus formation and attenuation of intimal hyperplasia.     

Early coronary artery stent restenosis: Utility of percutaneous coronary angioscopy

Restenosis of an endovascular stent may be caused by thrombus, intimal hyperplasia, or extrinsic compression. Angiography may not adequately define the etiology of restenosis. We describe a patient in whom angioscopy proved important in diagnosing intimal hyperplasia obviating the need for thrombolytic therapy and prolonged anti-coagulation.