血管重建术后再狭窄与血管重塑(文献综述)

血管重建术后再狭窄是影响血管通畅率的重要因素 ,因此明确其发生发展的过程有利于血管重建术后再狭窄的防治。本文将血管平滑肌细胞、细胞外基质和纤溶系统三方面与血管重塑机制之间的相互关系作一综述。     

血管重建术后再狭窄与血管重塑（文献综述）

血管重建术后再狭窄是影响血管通畅的重要因素，因此明确其发生发展的过程有利于血管重建术后再狭窄的防治。本文将血管平滑肌细胞、细胞外基质和纤溶系统三方面与血管重塑机制之间的相互关系作一综述。     

颈动脉血管重建术后超声监测及血管再狭窄超声评估研究进展

粥样硬化性颈动脉狭窄的治疗对于预防脑卒中具有重要意义。目前最常使用方法是血管内膜剥脱术及动脉支架植入术,而监测手术疗效、评估血管再狭窄等并发症是目前面临的最大难题。超声以其廉价、实时、动态、可重复性高等优势而被广泛应用于血管重建术后监测。本文对血管重建术后超声监测及血管再狭窄的超声评估的研究现状进行综述。     

纤溶系统和血管再狭窄

血管重建术后再狭窄的发生率较高 ,至今仍是一个临床难题。在血管损伤后再狭窄的过程中 ,纤溶酶原激活物 /纤溶酶系统尤其是尿激酶型纤溶酶原激活物及其受体起着非常重要的作用。本文就血管再狭窄过程中的作用机制加以综述     

纤溶系统和血管再狭窄

血管重建术后再狭窄的发生率较高，至今仍是一个临床难题。在血管损伤后再狭窄的过程中，纤溶酶原激活物／纤溶酶系统尤其是尿激酶型纤溶酶原激活物及其受体起着非常重要的作用。本文就血管再狭窄过程中的作用机制加以综述。     

血管重建术后再狭窄的防治现状

目的 了解血管重建术后再狭窄的各种防治手段。方法 对有关国内、外血管重建术后再狭窄防治方法的文献进行综述。结果 血管再狭窄的防治手段包括基因治疗、药物治疗、血管外支架和物理治疗等。基因治疗的方法包括转染能抑制血管平滑肌细胞增殖的基因和利用反义核酸技术或RNA干扰技术使能促进血管平滑肌细胞增殖的基因失活。结论 各种防治方法各有优、缺点，有些还存在争议。随着分子生物学技术的发展，基因治疗将会成为防治血管再狭窄的最有效手段。     

下肢动脉硬化闭塞症介入术后血管再狭窄的影响因素及防治进展

下肢动脉硬化闭塞症(LEASO)是动脉粥样硬化在下肢的临床表现。目前主要治疗方法包括支架置入术、球囊扩张成形术等, 但介入术后血管再狭窄有较高的发生率, 严重影响手术疗效和患者的预后。本文就LEASO介入术后血管再狭窄的发生机制、影响因素及最新防治进展进行综述, 对介入术后血管再狭窄的早期预防和提高临床治疗效果具有重要意义。     

动脉重建术后再狭窄相关miRNA表达谱分析及靶基因鉴定

目的 筛查动脉粥样硬化闭塞症( ASO)血管重建术后再狭窄相关miRNA基因表达谱,分析并鉴定表达差异显著的miRNA及其潜在靶基因.方法 取下肢ASO患者股动脉标本6例,3例未行血管重建术(A组),3例动脉重建术后再狭窄(R组),另取正常股动脉3例为正常对照(N组).利用miRNA基因芯片检测miRNA差异表达谱,以实时逆转录-聚合酶链反应(real-time RT-PCR)验证其表达,并通过构建双荧光素酶报告基因系统鉴定预测靶基因.结果 与N组比较,病变组(A组+R组)miRNA-1和miRNA-335表达下调,没有miRNA表达上调;R组miRNA-623表达上调,17个miRNAs下调;A组miRNA-1和miRNA-335表达下调,没有miRNA表达上调.与A组比较,R组17个miRNAs上调,9个miRNAs下调.表达下调以miRNA-1最显著,并经real-time RT-PCR证实(P＜0.05).双荧光素酶实验证实miRNA-1靶向抑制Kruppel样因子4(KLF4)的表达(P＜0.05).结论 miRNA可能参与ASO及动脉重建术后再狭窄的发病机制,其中miRNA-1可能起重要作用.     

血管外科研究进展

血管再狭窄及闭塞的成因及防治 血管重建后的再狭窄是至今未解决的临床难题,随着对细胞周期、信号转导、细胞凋亡的深入研究,对再狭窄的机制有了进一步的认识,其实验性治疗方法也应运而生.     

血管外科实验研究与应用技术的进展与热点

随着实验研究的深入和新技术的应用,血管外科在基础研究和临床相关研究方面都取得了明显进步.现就近年来在血管重建后再狭窄、人工血管和支架材料、腹主动脉瘤的发生机制等几方面进行的实验研究及发展方向,以及转化医学和糖组学在血管外科研究中的发展前景作简要述评. 一、血管重塑与动脉再狭窄 动脉血管重建后约30%～60%的患者出现血管再狭窄,迄今为止这依然是悬而未决的一个临床难题.     

自体移植静脉再狭窄基因水平的研究进展

为防治移植静脉再狭窄,基因水平的研究显然具有重要意义.笔者就近年来国内外针对移植静脉再狭窄的基因水平的探索进行综述,主要内容包括应用促血管再内皮化基因、抗血栓形成基因、抑制血管平滑肌细胞增殖和胞外基质沉积基因以及联合多基因共同治疗移植静脉再狭窄的研究,并指出未来基因水平研究发展方向.     

Serum Indoxyl Sulfate Associates with Postangioplasty Thrombosis of Dialysis Grafts

Hemodialysis vascular accesses are prone to recurrent stenosis and thrombosis after endovascular interventions. In vitro data suggest that indoxyl sulfate, a protein-bound uremic toxin, may induce vascular dysfunction and thrombosis. However, there is no clinical evidence regarding the role of indoxyl sulfate in hemodialysis vascular access. From January 2010 to June 2013, we prospectively enrolled patients undergoing angioplasty for dialysis access dysfunction. Patients were stratified into tertiles by baseline serum indoxyl sulfate levels. Study participants received clinical follow-up at 6-month intervals until June 2014. Primary end points were restenosis, thrombosis, and failure of vascular access. Median follow-up duration was 32 months. Of the 306 patients enrolled, 262 (86%) had symptomatic restenosis, 153 (50%) had access thrombosis, and 25 (8%) had access failure. In patients with graft access, free indoxyl sulfate tertiles showed a negative association with thrombosis-free patency (thrombosis-free patency rates of 54%, 38%, and 26% for low, middle, and high tertiles, respectively; P=0.001). Patients with graft thrombosis had higher free and total indoxyl sulfate levels. Using multivariate Cox regression analysis, graft thrombosis was independently predicted by absolute levels of free indoxyl sulfate (hazard ratio=1.14; P=0.01) and free indoxyl sulfate tertiles (high versus low, hazard ratio=2.41; P=0.001). Results of this study provide translational evidence that serum indoxyl sulfate is a novel risk factor for dialysis graft thrombosis after endovascular interventions.     

Regulation of vascular smooth muscle cell growth by survivin

The inhibitor of apoptosis protein survivin has long been of interest in the cancer literature for its role in both the regulation of cell proliferation and the inhibition of apoptosis. A growing body of literature has implicated survivin in the maladaptive pathways following vascular injury and, in particular, in the growth of vascular smooth muscle cells that comprise the hyperplastic neointimal lesions that characterize midterm vein bypass graft failure and restenosis following angioplasty and stenting. This review focuses on the emerging role of survivin in the regulation of smooth muscle cell growth and its implications for the prevention of restenosis following revascularization procedures. The expression, regulation, and function of survivin are addressed, as well as the current state of understanding regarding the effects of survivin inhibition in vitro and in vivo.     

慢性下肢缺血搭桥术后再狭窄分析

目的 探讨慢性下肢缺血患者行人工血管搭桥术后再狭窄的病因及治疗方法.方法 回顾性分析2002年1月至2007年4月收治的慢性下肢缺血患者的临床资料,其中股腘动脉搭桥术后再狭窄行二次手术的52例患者作为实验组,同时随访资料完整的32例搭桥术后人工血管通畅者作为对照组.分析两组问伴随疾病及高危因素,检测血脂、纤维蛋白原及C反应蛋白水平.结果 实验组纤维蛋白原(4.48±1.68)g/L、CRP(9.5±2.6)mg/L、低密度脂蛋白(4.5±1.7)mmol/L高于对照组(3.50±0.72)g/L、(4.0±3.2)mg/L、(2.8±0.9)mmol/L,差异有统计学意义(P＜0.01).实验组高密度脂蛋白为(1.02±0.32)mmol/L略低于对照组(1.12±0.28)mmol/L,差异无统计学意义(P＞0.05).实验组再次手术中见吻合口处重度内膜增生并继发血栓形成42例,人工血管内原发血栓形成10例.二次术后人工血管保持通畅28例,截肢10例,人工血管感染取出3例,死亡5例.结论 人工血管搭桥术后再狭窄主要原因是吻合口内膜增生.CRP、纤维蛋白原、低密度脂蛋白增高可能是导致吻合口内膜增生、人工血管闭塞的重要高危因素.     

Therapeutisches Potenzial der Stickstoffmonoxid-Synthase-Isoformen in Restenose, Transplantat- und Bypassarteriosklerose

The diverse biological effects of nitric oxide (NO) have led to intense research into its roles in vascular physiology and pathophysiology. Using recombinant DNA and gene transfer the effects of endogenous NO production by the family of NO synthase (NOS) enzymes can be elegantly studied in a variety of tissues. In addition, the feasibility of vascular NOS gene therapy has been demonstrated in animal models. However, technical and safety limitations have to be addressed before NOS gene therapy for cardiovascular disease is available for humans. Since NO exerts critical functions in vascular pathology, including atherosclerosis, post-angioplasty restenosis, vein graft atherosclerosis, transplant atherosclerosis and cardiac allograft vasculopathy, this article reviews recent progress in the field with a focus on potential future applications of NOS-modulating therapies.     

Endovascular repair of chronic mesenteric occlusive disease: the role of duplex surveillance

BACKGROUND: Chronic occlusive mesenteric ischaemia can be treated surgically or endovascularly. Endovascular techniques as elsewhere in the vascular tree are limited by restenosis. The aim of this study was to determine if duplex ultrasound proven restenosis correlates with recurrence of symptoms. METHODS: Our study looks at successful percutaneous revascularization of the mesenteric circulation associated proven restenosis using colour Doppler ultrasound and the relation to recrudescence of symptoms or weight loss. A retrospective review of five patients treated endovascularly at our institution for mesenteric angina secondary to visceral artery stenosis was carried out. RESULTS: Technical success was achieved in four out of the five patients in our study. One patient had a procedure complicated by thrombus in the coeliac axis and superior mesenteric artery (SMA) stents, subsequently showed SMA occlusion and 90% stenosis of the CA and inferior mesenteric artery and required an aorto-mesenteric graft. Three of the four patients with a technically successful procedure had significant (>70%) restenosis of the SMA. All three, including one patient with both SMA restenosis and chronic inferior mesenteric artery occlusion, remain asymptomatic and have maintained their postprocedural weight gain. CONCLUSION: Although ultrasound is a convenient, non-invasive tool for follow up of endovascular treatment of mesenteric stenosis, its use is unclear as in our study restenosis did not correlate with recrudescence of symptoms.     

Endovascular treatment of a symptomatic suture aneurysm caused by an aortic isthmus restenosis

After operative treatment of aortic isthmus stenoses, late complications, such as aneurysm formation or aortic restenosis, might occur, with relevant morbidity and mortality rates during open surgical reintervention. We report on the endovascular repair of a symptomatic suture aneurysm caused by an aortic isthmus restenosis by thoracic aortic stent graft implantation and additional intraoperative balloon dilatation. Based on our experience, endovascular repair of thoracic aortic aneuryms caused by native aortic isthmus stenosis or postcoarctation restenosis is a valuable treatment option, especially in symptomatic patients with an imminent risk of rupture or a difficult immediate transthoracic surgical approach. Long-term follow-up is required to assess the durability of the stent graft treatment.     

Cell biology of human vascular smooth muscle.

Vascular smooth muscle is the cellular substrate of most significant arterial diseases. Restenosis after angioplasty and surgery mainly represents vascular smooth muscle reaction to trauma, a process which is also significant in the early stages of atherogenesis. Empirical approaches, based on findings in animal models of vascular injury, have notably failed to make any impact on human restenosis. We have developed and validated growth of the human VSMC in culture as a model of restenosis. Intimal hyperplastic lesions producing vascular restenosis contain cells that have reduced sensitivity to physiological growth inhibition by heparin in cell culture conditions, compared with cells from normal vascular tissue. Undiseased saphenous vein obtained from patients with intimal hyperplastic restenoses also contain cells that are relatively resistant to heparin inhibition. Arterial healing that progresses to restenosis may have distinct and fundamental differences at the cellular level from the normal process of arterial healing after injury.     

Endothelial cell seeding on prosthetic surfaces

Once thought to be a monolayer of passive cells lining the vasculature, endothelial cells are now known to be important regulators of normal vascular physiology. Unfortunately, these critically important cells are destroyed or removed by interventional and surgical procedures performed to recanalize or bypass vascular obstructions. The loss of these cells contributes to thrombosis and restenosis, the major complications observed after angioplasty, stent deployment, and prosthetic graft implantation. One approach to preventing these complications is the placement of endothelial cells on stents or prosthetic grafts prior to their placement in vivo in the hope that these cells will, after growth and maturation, release the factors necessary to inhibit thrombosis and intimal thickening. The purpose of this review paper is to provide an overview of the physiologic functions of normal and dysfunctional endothelial cells, and to discuss experiments in which endothelial cells have been placed on metallic stents and prosthetic grafts.     

Polytetrafluoroethylene interposition grafts for carotid reconstruction.

Polytetrafluoroethylene interposition grafts were used for carotid reconstruction in 26 operations performed in 23 patients during a 7-year period. There were 10 men and 13 women with a mean age of 66 years. The indication for interposition graft placement was recurrent stenosis with inability to perform endarterectomy in nine operations, a severe kink or technical problem during endarterectomy in nine, aneurysmal changes of the artery in six, and thrombosis of the endarterectomy site segment with stroke in two. There were no perioperative deaths and no further perioperative neurologic complications. Follow-up with performance of yearly duplex scans was obtained in all patients, and the mean duration of follow-up was 36 months. One patient (4%) died of end-stage pulmonary disease during the study interval. Occlusion of the polytetrafluoroethylene graft occurred at 12 months in one patient (4%). Hemodynamically significant restenosis developed in two patients (8%), and two patients (8%) had mild restenosis. Evidence of a second restenosis developed in three of the nine patients who underwent polytetrafluoroethylene interposition graft placement for carotid restenosis. On the basis of our study results, we conclude that polytetrafluoroethylene can be used effectively for carotid reconstruction when an interposition graft is required. However, recurrent stenosis occurs. Patients who undergo polytetrafluoroethylene interposition graft placement for carotid restenosis appear to be at high risk for a second restenosis.