冠状动脉球囊成形术及支架术后再狭窄

绝大部分冠心病患者的临床表现是由冠状动脉严重狭窄所致 ,很少一部分冠状动脉狭窄虽不严重 ,但合并痉挛仍可引起心绞痛或心肌梗塞。冠心病的治疗除了药物治疗及危险因素的控制方面近年来发展较快外 ,冠状动脉的血运重建治疗近二十年来也有了长足的进步。目前经皮冠状动脉球囊成形术(ＰＴＣＡ)已成为与药物、外科搭桥手术并驾齐驱的主要治疗手段。虽然ＰＴＣＡ治疗冠心病即刻临床效果满意 ,但术后血管再狭窄在一定程度上影响了治疗的最终效果 ,并限制了ＰＴＣＡ的发展。近十年冠状动脉内支架的应用 ,显著降低了治疗时的急性缺血并发症 ,同时…     

Development of a platform to evaluate and limit in-stent restenosis

The objective of this work was to develop a platform to evaluate and deliver putative therapeutic agents for in-stent restenosis. Arterial stenting is applied in more than 60% of balloon angioplasties for treating cardiovascular disease. However, stented arteries encounter accelerated rates of restenosis. No prior platform has allowed evaluation or local management of in-stent restenosis without perturbing the very system being examined. A stainless steel, balloon-expandable stent was modified to serve as an ablumenal drug delivery platform. Several combinations of bioerodible polymer microspheres and gels were evaluated for channel retention under in vitro flow and in vivo conditions. A stent-anchored hybrid system prevented material embolization under all conditions. Unlike prior platforms, these stents do not alter local inflammation or in-stent plaque formation relative to conventional Palmaz-Schatz stents after in vivo deployment. The system also proved sensitive enough to detect plaque reduction with an antirestenotic agent. We conclude that a platform to evaluate and deliver therapeutic agents for in-stent restenosis has been achieved.     

Association of leukocyte activation, but not the common cold, with restenosis after percutaneous coronary intervention in patients with angina pectoris

We investigated the relationship between the common cold and restenosis after percutaneous coronary intervention (PCI) in Japanese patients with angina pectoris, because suffering from a common cold during the follow-up period after PCI may be involved in the development of restenosis. In addition, we measured the soluble (s) L-selectin level early after PCI in patients with and without restenosis. The study group included 104 effort angina pectoris patients. We examined whether or not they had had a common cold in the 6 months following angioplasty. Finally, 88 patients, whose common cold status was known, were selected as the study subjects. Twelve patients caught a common cold after PCI. All of these patients were given antibiotics and/or anti-inflammatory agents and recovered within 2 weeks. None had clinically detectable influenza infection. Thirty-three patients suffered from restenosis and 55 did not. There was no significant difference in the restenosis frequency between effort angina pectoris patients with and without a common cold. The sL-selectin level was significantly increased in patients with restenosis early after PCI, whereas in patients without restenosis, sL-selectin remained unchanged. These findings suggest that restenosis development after PCI in patients with effort angina pectoris may involve leukocyte activation early after PCI, while suffering from a common cold during the follow-up period after PCI has no effect.     

骨髓间充质干细胞联合益气养阴化瘀中药干预糖尿病下肢动脉再狭窄模型犬

背景：目前大量研究已经证实了中药制剂、骨髓间充质干细胞在防治血管再狭窄中的有效性,但二者联合应用防治糖尿病下肢动脉介入成形后血管再狭窄的相关研究较少。 目的：观察骨髓间充质干细胞联合益气养阴化瘀中药对犬糖尿病股动脉介入成形后血管再狭窄的影响。 方法：采用四氧嘧啶静脉注射结合球囊损伤建立糖尿病下肢血管再狭窄犬模型,造模成功后将22只犬随机分为3组,即糖尿病模型组(模型组,n=6)、益气养阴化瘀方治疗组(中药组,n=8)及益气养阴化瘀方联合骨髓间充质干细胞治疗组(联合治疗组,n=8)。分别在经皮腔内血管成形前、治疗后1,2,4,8周采用ELISA法检测血清中血管内皮生长因子水平。治疗后8周取股动脉血管标本进行病理血管形态学观察及增生程度的定量分析,并取心肝肾胰腺组织标本行病理切片苏木精-伊红染色评价干细胞静脉移植安全性。 结果与结论：治疗后1周,中药组和联合治疗组血清血管内皮细胞生长因子均开始升高,模型组治疗后4周开始升高(与治疗前比较,P < 0.05)。同期各阶段,血清血管内皮细胞生长因子水平联合治疗组最高,模型组最低(P < 0.05)。血管增生程度定量分析结果显示,治疗后8周新生内膜面积、新生内膜/中膜面积及狭窄率,模型组最高,联合治疗组最低(P < 0.05)。干细胞移植安全性评价结果显示,治疗后8周心肝肾胰腺组织内部结构形态正常,未见组织坏死现象。综上,骨髓间充质干细胞联合益气养阴化瘀方比单纯中药治疗在防治糖尿病下肢动脉介入成形后再狭窄中作用更显著,是一种安全、有效的防治糖尿病下肢动脉介入成形后血管再狭窄发生的手段。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

316L不锈钢冠状动脉支架再狭窄研究进展

支架植入术是解决经皮冠状动脉血管形成术(PTCA)后再狭窄的有效途径,但支架植入后 仍存在一定程度的再狭窄。本文详细阐述了临床上常用的316L不锈钢冠状动脉支架植入后再狭窄的机 理及其改性研究进展。     

经皮冠状动脉介入治疗术后支架内再狭窄的遗传学与表观遗传学研究进展

冠状动脉粥样硬化性心脏病(简称冠心病)是人类最主要的死亡原因之一,也是消耗巨大医疗资源的疾病.经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)是冠心病治疗的重大进展之一.然而,PCI治疗面临支架内再狭窄(in-stent restenosis,ISR)的重大挑战.尽管药物支架减少了ISR的发生,再狭窄发生率仍达5％～10％.支架后血管内皮细胞过度增生和平滑肌细胞移行是支架术后再狭窄的主要原因.再狭窄个体差异的确切机制还不完全明确,可能存在多种原因.除了高年龄、吸烟、糖尿病等可能增加再狭窄率外,越来越多的研究发现遗传因素和表观遗传学因素对疾病的进展有着重要影响.本文主要对冠心病患者PCI术后发生支架内再狭窄的遗传学和表观遗传学研究进行综述,以期初步确定冠心病患者PCI术后再狭窄发生的遗传危险因素.     

反义凝血酶受体基因表达抑制大鼠动脉内膜损伤后内膜增生

目的 了解凝血酶及其受体在血管损伤后动脉内膜增生中的作用,以进一步阐明经皮冠状动脉血管腔内成形术（PTCA）后再狭窄的发生机制,为寻找再狭窄的防治途径提供线索。方法 采用球囊导管损伤动脉内膜的方法建立大鼠颈动脉球囊损伤模型。用纳米粒子包装凝血酶受体重组反义基因质凿pLXSN/ATR,用保护灌注的方法局部定位转染损伤后的大鼠颈动脉。结果 PCR检测发现重组基因整合,RNA斑点杂交观察到实验组大鼠颈动脉壁内有重组反义凝血酶受体基因表达,正义凝血酶受体基因的表达受到明显抑制,反义基因转染组新生内膜,中膜比例降低了40．9％。结论 反义凝因酶受体重组基因转基因表达对大鼠颈动脉球囊损伤后动脉内膜的增生具有抑制作用,提示凝血酶及其受体在PTCA后再狭窄过程中有重要作用,为再狭窄的防治提供了新的线索。     

血管内支架材料特点与缺血性脑卒中的治疗效果

背景：新型血管内支架材料是目前脑血管疾病介入治疗的研究热点。 目的：分析血管内支架材料学特征及缺血性脑卒中治疗效果。 方法：第一作者于2012年12月应用计算机检索数据库的相关文章,中文检索词为“缺血性脑卒中;血管内支架;支架材料;介入治疗”,检索时间范围在2003至2012年,共检索到相关文献120篇,符合纳入标准并用于分析的文献24篇。 结果与结论：①金属裸支架在血液中长期存放有腐蚀、金属离子溶出和凝血性等现象,为解决金属材料存在的问题,可以通过金属支架表面改性来处理,提高金属材料的血液相溶性。②药物支架是将治疗药物涂于支架表面,使药物能够持续并高浓度的释放,防止支架置入后再狭窄。③覆膜血管内支架是在金属支架外表覆以可降解或不可降解的聚合物薄膜,抑制血管内皮增生,对血管平滑肌细胞具有良好的生物相容性,可以预防血管支架置入后再狭窄。血管内支架治疗可以降低缺血性脑卒中的风险,是一种安全有效的治疗手段,同时还可以改善缺血性脑病患者的认知功能障碍。基因及细胞种植支架材料在防治脑血管介入后再狭窄方面也具有一定优势,是血管内支架材料研究的新方向。     

Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty

To examine the role of antiplatelet therapy in the prevention of arterial restenosis after percutaneous transluminal coronary angioplasty (PTCA), we conducted a randomized, double-blind, placebo-controlled study in 376 patients. The active treatment consisted of an oral aspirin-dipyridamole combination (330 mg-75 mg) given three times daily, beginning 24 hours before PTCA. Eight hours before PTCA, the oral dipyridamole was replaced with intravenous dipyridamole at a dosage of 10 mg per hour for 24 hours, and oral aspirin was continued. Sixteen hours after PTCA, the initial combination was reinstituted. Treatment was continued in patients with a successfully dilated vessel until follow-up angiography four to seven months after PTCA--or earlier, if symptoms dictated. Of 249 patients who underwent follow-up angiography, 37.7 percent of patients receiving the active drug had restenosis in at least one segment, as compared with 38.6 percent of patients taking placebo (P not significant). The number of stenotic segments was virtually the same in the two groups. Among the 376 randomized patients, there were 16 periprocedural Q-wave myocardial infarctions--13 in the placebo group and 3 in the active-drug group (6.9 percent vs. 1.6 percent, P = 0.0113). Although the use of this antiplatelet regimen before and after PTCA did not reduce the six-month rate of restenosis after successful coronary angioplasty, it markedly reduced the incidence of transmural myocardial infarction during or soon after PTCA. Thus, the short-term use of antiplatelet agents in relation to PTCA can be recommended.     

Localized intracoronary gamma-radiation therapy to inhibit the recurrence of restenosis after stenting

BACKGROUND: Although the frequency of restenosis after coronary angioplasty is reduced by stenting, when restenosis develops within a stent, the risk of subsequent restenosis is greater than 50 percent. We report on a multicenter, double-blind, randomized trial of intracoronary radiation therapy for the treatment of in-stent restenosis. METHODS: Of 252 eligible patients in whom in-stent restenosis had developed, 131 were randomly assigned to receive an indwelling intracoronary ribbon containing a sealed source of iridium-192, and 121 were assigned to receive a similar-appearing nonradioactive ribbon (placebo). RESULTS: The primary end point, a composite of death, myocardial infarction, and the need for repeated revascularization of the target lesion during nine months of follow-up, occurred in 53 patients assigned to placebo (43.8 percent) and 37 patients assigned to iridium-192 (28.2 percent, P=0.02). However, the reduction in the incidence of major adverse cardiac events was determined solely by a diminished need for revascularization of the target lesion, not by reductions in the incidence of death or myocardial infarction. Late thrombosis occurred in 5.3 percent of the iridium-192 group, as compared with 0.8 percent of the placebo group (P=0.07), resulting in more late myocardial infarctions in the iridium-192 group (9.9 percent vs. 4.1 percent, P=0.09). Late thrombosis occurred in irradiated patients only after the discontinuation of oral antiplatelet therapy (with ticlopidine or clopidogrel) and only in patients who had received new stents at the time of radiation treatment. CONCLUSIONS: Intracoronary irradiation with iridium-192 resulted in lower rates of clinical and angiographic restenosis, although it was also associated with a higher rate of late thrombosis, resulting in an increased risk of myocardial infarction. If the problem of late thrombosis within the stent can be overcome, intracoronary irradiation with iridium-192 may become a useful approach to the treatment of in-stent restenosis.     

冠状动脉支架置入后相关炎症因子的变化及其干预

背景：冠状动脉粥样硬化性心脏病支架置入治疗后的炎症反应以及其严重程度与再狭窄明显存在相关性,医学工作者试图从中寻找新思路预防支架置入后再狭窄,提高治疗质量。 目的：评价各种干预措施以及监测手段在冠状动脉置入术后炎症治疗中的应用价值和临床前景。 方法：电子检索EMbase(1980-01/2011-05),MEDLINE(1966-01/2011-05),中国生物医学文献数据库(CBM,1978/2011-05)和中国期刊全文数据库(CNKI),筛查相关文章的参考文献。中文检索词“冠状动脉支架,炎症因子,炎症,CRP,再狭窄”,英文检索词为“Coronary stent,inflammatory cytokines,inflammation,CRP,restenosis”。 结果与结论：临床试验结果显示支架置入后炎症反应明显加重,使用雷帕霉素药物洗脱支架,添加地塞米松、塞来昔布、瑞舒伐他汀等可更大程度上降低支架置入后炎症反应。动物试验发现使用雷帕霉素洗脱支架可减少支架置入段新生内膜的形成和缩小炎症面积。提示各种干预措施可降低支架置入后炎症反应从而降低远期再狭窄的发生,可进一步改良加以应用于临床观察其疗效。     

冠状动脉内放射治疗防止血管成形术后再狭窄的研究进展

再狭窄已经成为经皮冠状动脉腔内成形术(ＰＴＣＡ)广泛应用的最大障碍 ,约 4 0 %～ 60 %的患者在成功的完成ＰＴＣＡ术之后数月内发生再狭窄[1] 。再狭窄的机制非常复杂 ,目前多认为包括以下几方面 :术后血管弹性回缩 ;血管的重塑、平滑肌细胞迁移、增殖、细胞外基质形成新生内膜 ;局部血栓的形成与机化 ;许多细胞因子和生长因子的分泌参与再狭窄的过程[2 ,3] 。针对再狭窄的发生机制 ,许多研究试图通过各种药物进行预防 ,包括肝素和血小板ＧＰＩＩｂ -ＩＩＩａ受体拮抗剂在内的所有药物在临床实践中并未明显降低再狭窄率。支架置入术能够减…     

Decreased rate of coronary restenosis after lowering of plasma homocysteine levels.

BACKGROUND: We have previously demonstrated an association between elevated total plasma homocysteine levels and restenosis after percutaneous coronary angioplasty. We designed this study to evaluate the effect of lowering plasma homocysteine levels on restenosis after coronary angioplasty. METHODS: A combination of folic acid (1 mg), vitamin B12 (400 microg), and pyridoxine (10 mg)--referred to as folate treatment--or placebo was administered to 205 patients (mean [+/-SD] age, 61+/-11 years) for six months after successful coronary angioplasty in a prospective, double-blind, randomized trial. The primary end point was restenosis within six months as assessed by quantitative coronary angiography. The secondary end point was a composite of major adverse cardiac events. RESULTS: Base-tine characteristics and initial angiographic results after coronary angioplasty were similar in the two study groups. Folate treatment significantly lowered plasma homocysteine levels from 11.1+/-4.3 to 7.2+/-2.4 micromol per liter (P<0.001). At follow-up, the minimal luminal diameter was significantly larger in the group assigned to folate treatment (1.72+/-0.76 vs. 1.45+/-0.88 mm, P=0.02), and the degree of stenosis was less severe (39.9+/-20.3 vs. 48.2+/-28.3 percent, P=0.01). The rate of restenosis was significantly lower in patients assigned to folate treatment (19.6 vs. 37.6 percent, P=0.01), as was the need for revascularization of the target lesion (10.8 vs. 22.3 percent, P=0.047). CONCLUSIONS: Treatment with a combination of folic acid, vitamin B12, and pyridoxine significantly reduces homocysteine levels and decreases the rate of restenosis and the need for revascularization of the target lesion after coronary angioplasty. This inexpensive treatment, which has minimal side effects, should be considered as adjunctive therapy for patients undergoing coronary angioplasty.     

Is inflammation a contributor for coronary stent restenosis?

The development of coronary stent has revolutionized the field of interventional cardiology by reducing the incidence of restenosis after balloon angioplasty. Despite significant progress in its prevention and treatment, however, in-stent restenosis (ISR) is still common, and remains a challenge for the interventional cardiologist. Restenosis after stent implantation is mainly caused by neointimal proliferation through the stent struts. Currently, there are three major factors has been demonstrated to be contributors for ISR, namely patients-, lesion- and genetic-related factors in large number of clinical trials. However, the triggers and pathophysiological mechanisms for ISR are not fully elucidated. Experimental as well as clinical studies indicate a marked activation of inflammatory cells at the site of stent structs, which are likely to play a key role in the process of neointimal proliferation and stent restenosis. Those data suggest that inflammation may be a major contributor for ISR. In fact, coronary stenting is a strong inflammatory stimulus and the acute systemic response to local inflammation produced by coronary stenting is highly individual and predicts restenosis and event-free survival. Thus, the attention should be paid on anti-inflammatory therapeutic approaches for ISR, and the benefit of anti-inflammatory therapy during the periprocedural period and long-term follow-up is dependent on the inflammatory status. Measurement of cytokine and acute phase proteins, such as C-reactive protein, therefore, may be important to identify high-risk subjects and develop specific treatment tailored to the individual patients.     

Reduction in the rate of early restenosis after coronary angioplasty by a diet supplemented with n-3 fatty acids

To determine the safety and benefit of n-3 fatty acid therapy in the prevention of early restenosis after coronary angioplasty, we conducted a randomized, unblinded study comparing a conventional antiplatelet regimen (325 mg of aspirin and 225 mg of dipyridamole per day; control group) with a similar regimen supplemented with 3.2 g of eicosapentaenoic acid per day (treatment group). Treatment began seven days before angioplasty and continued for six months afterward. All angiographic analyses were blinded and performed by a method that was validated by comparison with quantitative coronary angiography. In 82 male patients, 103 coronary lesions were dilated. Both groups had similar base-line clinical and angiographic characteristics. The incidence of early vessel restenosis, as determined on a second angiogram three to four months after angioplasty, was 36 percent in the control group and 16 percent in the treatment group (P = 0.026). The incidence of restenosis per patient was also significantly lower in the treatment group (46 vs. 19 percent). Both multiple logistic regression and Mantel-Haenszel statistical analyses demonstrated a significant independent benefit of treatment with n-3 fatty acids. No important bleeding complications developed in the treated patients. These results, in a male population at relatively high risk for restenosis, suggest that a dietary supplement of n-3 fatty acids, administered for one week before and for six months after coronary angioplasty, is safe and reduces the occurrence of early restenosis after that procedure. Whether this beneficial effect also applies to other populations is unknown.     

Coronary atherosclerosis and interventions: Pathological sequences and restenosis

The primary cause of cardiac morbidity and mortality in developed countries is ischemic (coronary) heart disease. The incidence of this disease is virtually all due to atherosclerosis, and ischemic heart disease is also the most prevalent disease in the industrialized world, causing over 40% of all deaths in the United States and Western Europe. In Japan, the incidence of ischemic heart disease due to coronary atherosclerosis is gradually increasing as well. Compared with the classical nomenclature of atherosclerosis; that is, fatty streak, fibrous plaque and complicated lesions, the term Stary's classification has been universally accepted because it reflects the more recently acquired knowledge about the morphological and biochemical details of the processes in coronary atherosclerosis, which have been obtained by new strategies such as angioscopy, intravascular ultrasound and molecular biological methods. The term Stary's classification has been applied for the coronary atherosclerosis of patients with acute coronary syndrome at the National Cardiovascular Center, for the analysis of predisposing atherosclerosis of these patients. The recent findings regarding acute coronary syndrome resulting from a rupture of coronary atherosclerotic plaques indicate that this syndrome is probably the most important mechanism underlying the sudden onset. It has been found that the risk of plaque rupture may depend more on plaque composition than on plaque size. Plaques rich in soft extracellular lipids and macrophages are possibly more vulnerable to plaque rupture. Two of the goals of the present review are to clarify how plaque disruption occurs and to elucidate the relationship between plaque disruption and coronary risk factors in elderly Japanese patients with acute coronary syndrome. Coronary stents have been shown to be efficacious in the treatment of acute and threatened closure complicating percutaneous transluminal coronary angioplasty (PTCA) and have produced encouraging initial results in the prevention of restenosis. In the autopsy study of restenosis after PTCA, it was observed that dense caps of collagen fibers in the adventitia in the vicinity of the disrupted internal elastic laminae were present in all of the remodeling lesions. It is suggested that remodeling, which resulted in adventitial scarring, is one of the major causative factors of restenosis after PTCA. The long-term success of stenting, however, remains limited by the occurrence of late in-stent restenosis, with an incidence of 20-42% depending on the stent design and the patient population studied. Another aim of the present review is to describe the pathological mechanism of restenosis after PTCA and/or stent replacement and, consequently, the vascular remodeling that occurs around adventitial tissue after PTCA and intimal hyperplasia that is chronically irritated by a foreign body granulomatous reaction after stenting. Finally, the results of the investigation of the effect of a tissue factor pathway inhibitor on the prevention of interventional restenosis is described.     

Gene therapy for restenosis--what now, what next?

Late luminal loss after coronary angioplasty has resisted pharmacological and physical attempts at prevention for over twenty years. As a consequence of the resistance of restenosis to traditional therapeutic approaches it has become a popular target for DNA-based treatment modalities. In this review we consider what is currently known of the basic pathophysiology of restenosis and briefly outline the previous attempts to influence the long-term outcome after coronary intervention. We then discuss the animal models of vascular injury that have been used for studies of gene therapy and the vectors that have been applied to the setting of vascular gene transfer before considering the many studies in which the effects of specific gene transfer have been studied in the setting of vascular injury. These transgenes are considered in four broad groupings: those that act by the suppression of cellular proliferation in the vessel wall; those that inhibit cell migration; anti-thrombotic transgenes; and transgenes that have multiple effects within the vessel. We finally consider why, although more than eight years have passed since publication of the first studies of gene transfer to inhibit the vascular responses to endoluminal injury, little progress has been made in translating gene therapy for restenosis into the human setting. Principle reasons for the disappointingly slow clinical implementation of gene therapy for restenosis are an incomplete understanding of the vascular biology of restenosis, the difficulty of translating findings in animal models into the human setting and the technical difficulties incumbent upon localised gene delivery into coronary arteries.     

他汀类药物联合抗血小板药物降低冠状动脉搭桥术后血管再狭窄的研究

冠状动脉旁路移植术（CABG）是治疗冠心病有效手段之一,但是其术后易发生桥静脉再狭窄甚至闭塞,发生复发性心绞痛、心肌梗死以及再次血运重建的风险增加。抗血小板药物和他汀类药物是临床提高桥血管通畅率的常用药物,抗血小板药物能减少早期的血栓形成,他汀类药物能够延缓中期的内膜增厚和晚期的粥样斑块的形成。本文就联合使用抗血小板药物和他汀类药物降低CABG术后血管再狭窄的研究作一综述,并对综合治疗CABG术后血管再狭窄的方法进行展望。     

Coronary ischemia and percutaneous intervention

The interventional treatment of ischemia is a complex issue grounded on an understanding of basic pathophysiology, but translated and implemented in practice by extensive clinical trial data representing patients with a spectrum of ischemia-causing clinical syndromes and anatomical variations of coronary artery disease (CAD). Percutaneous coronary intervention (PCI) has evolved to treat ischemia within this matrix of clinical and anatomical subsets using a wide array of techniques. Initial techniques using balloon angioplasty were promising, but demonstrated significant rates of restenosis due to negative arterial remodeling. The advent of stent technology prevented arterial recoil and provided a viable treatment for flow-limiting coronary dissections, thereby facilitating improved long-term patency of coronary vessels without the need for repeat revascularization. In-stent restenosis has been successfully addressed with drug elution, but late stent thrombosis has emerged as a complex issue involving dual antiplatelet therapy, patient compliance, and reexamination of the delicate balance between reducing restenosis and promoting endothelial proliferation. Finally, complex coronary lesions associated with heavy calcification or extensive plaque/thrombus burden that introduce unique challenges in obtaining ideal angiographic results have led to the development of new debulking devices aimed at optimizing procedural outcomes. This review will describe a variety of percutaneous coronary interventional techniques and technologies that are employed in the invasive treatment of ischemia under the guidance of clinical guidelines and evidence-based medicine.     

Molecular and cellular basis of restenosis after percutaneous coronary intervention: the intertwining roles of platelets, leukocytes, and the coagulation-fibrinolysis system

The major limitation of percutaneous coronary intervention (PCI) is restenosis. Restenosis is considered to be an overreaction of the natural healing process after traumatic balloon dilatation. An elaborate web of cellular and molecular responses, including the interaction of platelets, leukocytes, and the coagulation-fibrinolysis system, as well as the secretion of various growth factors and pro-inflammatory cytokines, contributes to neointimal hyperplasia and the development of restenosis. Moreover, platelet and neutrophil activation after stenting appears to be different from that after balloon angioplasty alone. Pharmacotherapy targeting the cell-to-cell interaction between platelets and neutrophils may potentially offer an effective treatment strategy against restenosis after PCI.