晚期支架贴壁不良研究进展

与裸金属支架相比,药物洗脱支架植入后更易发生支架贴壁不良。血管内超声研究证实,引起晚期支架贴壁不良的主要机制是正性重构。发生支架内血栓的部位有的存在支架贴壁不良现象,由此推测,晚期支架贴壁不良可能会引起支架内血栓形成。支架贴壁不良与临床不良事件的关系尚需进一步研究。     

晚期支架贴壁不良研究进展

与裸金属支架相比,药物洗脱支架植入后更易发生支架贴壁不良。血管内超声研究证实,引起晚期支架贴壁不良的主要机制是正性重构。发生支架内血栓的部位有的存在支架贴壁不良现象,由此推测,晚期支架贴壁不良可能会引起支架内血栓形成。支架贴壁不良与临床不良事件的关系尚需进一步研究。     

晚期获得性支架贴壁不良研究进展

药物洗脱支架可大大降低支架置入术后再狭窄的发生,因而被誉为介入心脏病学史上"第三个里程碑".但随其广泛使用,相关问题随之浮现.支架贴壁不良[1](stent malapposition,SM)是指在支架置入术后,至少有1处或以上的支架梁与动脉管壁内膜未能完全贴合(非覆盖于边支的支架),而且在支架梁后存在血流.     

冠状动脉支架断裂致极晚期支架内血栓形成1例

<正>1病例患者男性,69岁,主因“冠脉支架置入术后6年,再发胸痛9 d”。患者于2018年因“不稳定型心绞痛”于武汉亚心总医院心脏中心行冠状动脉（冠脉）造影显示：前降支近中远段弥漫、迂曲狭窄80%～95%;回旋支近段狭窄90%;右冠脉近段及中段轻度斑块浸润。介入手术步骤：右侧桡动脉路径,置入6Fr动脉血管鞘。送入6Fr指引导管EBU3.5,操控Runthrough指引导丝至左前降支（LAD）远段,送2.0 mm×20 mm Sprinter Legend预扩球囊至LAD病变处预扩张,送支架2.5 mm×36 mm Partner至LAD中远段病变处扩张植入支架,送支架3.0 mm×33 mm Firebird至LAD近中段病变处,扩张植入支架,再送入3.0 mm×15 mm Quantum后扩球囊至LAD支架内充分扩张使支架贴壁,重复造影LAD支架植入处,未见残余狭窄。术后坚持服用“拜阿司匹林、倍林达（18个月后停用）、辛伐他汀、美托洛尔”等药物,一直无胸闷、胸痛症状。     

光学相干断层成像评价药物洗脱支架置入术后晚期支架贴壁不良

目的 探讨药物洗脱支架(DES)置入术后晚期支架贴壁不良的特点.方法 分析32例(包括51支血管、共置入71个支架)置入DES 1年后[(14.8±5.2)个月]行光学相干断层成像(OCT)检查的患者资料,对支架节段的OCT图像每间隔0.5 mm取1帧图像进行分析,找出贴壁不良的支架金属结构,测量支架到参照血管内壁的距离及支架表面内膜厚度,分析晚期支架贴壁不良的特点.结果 OCT检查在7例(21.9%)患者中检出支架贴壁不良,其中4例合并支架段血管的正性重构,1例重叠置入支架,2例发现由血栓覆盖支架金属结构,7例患者随访期间无心脏不良事件发生.97.6%的支架金属结构完全贴壁并不同程度的内膜覆盖,2.4%的支架金属结构贴壁不良,包括1.2%的支架金属结构位于血管分支开口.位于血管分支开口的支架金属结构与其他贴壁不良支架表面的内膜覆盖厚度差异无统计学意义[(0.06±0.05)mm比(0.05±0.03)mm,P>0.05].绪论晚期支架贴壁不良见于DES置入最初的贴壁不良、血管壁正性重构、重叠置入支架以及支架金属结构位于分支血管开口;贴壁不良的支架金属结构表面亦有不同程度的内膜覆盖.     

冠状动脉支架术后三年支架内膜增生和贴壁不良一例

患者男性,55岁.因活动后胸痛5年,再次发作1 d于2008年8月29日入院.患者2005年在上楼过程中出现胸痛,并向肩背部放射,持续约2 min,休息后即可缓解,饱餐或行走50 m后即可诱发胸痛,连续发作数日,以"冠心病"收入我院.行冠状动脉造影,显示前降支近段闭塞,钝缘支近段70%狭窄.于前降支放入2枚雷帕霉素洗脱支架,钝缘支放入1枚雷帕霉素洗脱支架,术后恢复良好.2008年8月28日再次发作上述症状,再次入院治疗.既往无糖尿病史,无高血压病史,无烟酒嗜好.入院查体:体温36℃,脉搏68次/min,呼吸17次/min,血压111/76 mm Hg(1 mm Hg=0.133 kPa).     

药物洗脱支架极晚期血栓形成并自溶一例

患者男,49岁.无高血压病、糖尿病、血脂异常、吸烟史及冠心病家族史.2004年9月因"急性前壁心肌梗死"于当地医院行急诊冠状动脉造影,术中显示前降支(LAD)起始部闭塞,回旋支起始部轻度狭窄,于LAD置入Cypher支架(美国Cordis公司西罗莫司洗脱支架,具体型号不详)1枚,过程顺利.     

药物洗脱支架与晚期、极晚期支架血栓

第一代药物洗脱支架在显著降低再狭窄率的同时,也带来了支架血栓尤其是晚期、极晚期支架血栓这一棘手问题.晚期、极晚期支架血栓虽然发生率较低,但一旦发生往往带来灾难性后果.晚期、极晚期支架血栓的发生机制包括血管再内皮化延迟、多聚物过敏反应、支架晚期贴壁不良及新生动脉粥样硬化斑块破裂等.第二代和第三代药物洗脱支架在安全性上可能优于第一代.生物全降解支架代表了药物洗脱支架的发展方向,有望从根本上解决药物洗脱支架的晚期和极晚期支架血栓问题.现对近年来药物洗脱支架晚期及极晚期支架血栓的发生机制及新一代药物洗脱支架的研究进展做一综述.     

未充分覆盖与贴壁不良易致支架内血栓形成

正虽然冠脉支架的发展大大地改善了冠心病的死亡率,但支架内血栓仍然影响着PCI术后的患者,甚至心梗和死亡率可达80%。早期支架内血栓形成主要是支架类型或边缘夹层和支架膨胀不全,但药物涂层支架(DES)植入1年后发生的极晚期支架内血栓形成(VLST)的具体机制仍未明确。为此,来自瑞士的Masanori博士及其同事借助光学相干     

急性冠状动脉综合征患者雷帕霉素洗脱支架晚期贴壁不良及其对临床预后的影响

目的 观察急性冠状动脉综合征(ACS)患者雷帕霉素洗脱支架晚期贴壁不良发生率及其对临床预后的影响.方法 观察2005年2月至2007年3月因ACS(ACS组,54例)和稳定性心绞痛(对照组,83例)行雷帕霉素洗脱支架治疗并于1年后行血管内超声检查患者,检测支架晚期贴壁不良发生率,并观察血管内超声检查后1年内主要不良心血管事件及支架内血栓发生率.结果 所有137例患者219处病变中,16例患者25处病变检测到晚期支架贴壁不良.25处晚期支架贴壁不良中ACS组和对照组分别为20处(22.2%)和5处(3.9%)(P＜0.001).两组患者参照血管外弹力膜面积、参照血管和支架段血管管腔面积和新生内膜面积均相似,但ACS组患者支架段血管外弹力膜面积[(15.34±5.44)mm2比(13.83±4.51)mm2,P=0.026]、支架段血管外弹力膜面积与参照血管外弹力膜面积比值(1.13±0.22比1.02±0.18,P＜0.001)、斑块和中膜面积[(8.43±3.93)mm2比(7.01±2.93)mm2,P:0.002]较对照组明显增大.Logistic多元回归分析显示,ACS(OR=6.477,P＜0.001)和支架长度≥23 mm(OR=3.680,P=0.025)为晚期支架贴壁不良的独立危险因素.血管内超声检查后临床随访1年,两组主要不良心血管事件发生率差异无统计学意义.结论 雷帕霉素洗脱支架置入后,ACS患者较稳定性心绞痛患者更多发生晚期支架贴壁不良,然而随访1年的主要不良心血管事件发生率差异无统计学意义.     

Recurrent episodes of very late stent thrombosis in a patient with aspirin hypersensitivity, stent fracture and malapposition

Late stent thrombosis represents a life-threatening event, usually triggered by inadequate antiplatelet therapy and promoted by multiple risk factors, such as stenting of a chronic total occlusion, overlapping stenting, an abnormal vascular response to the eluted drug, stent malapposition and stent fracture. A 57-year-old man with aspirin hypersensitivity underwent successful percutaneous revascularization of a chronic total occlusion of the left anterior descending artery (LAD). He received two sirolimus-eluting stents overlapping for 2 mm and was discharged on clopidogrel and picotamide. Two years later, 15 days after clopidogrel discontinuation, he experienced an anterior ST-segment elevation myocardial infarction and underwent rescue percutaneous LAD thrombectomy after unsuccessful fibrinolysis. Coronary angiography showed fracture of the distal stent, with a 5 mm gap between the two portions, as well as severe late stent malapposition, confirmed by optical coherence tomography. Despite treatment with clopidogrel and picotamide, in the following days the patient experienced two new episodes of stent thrombosis, treated with thrombectomy and deployment of bioengineered stents. The patient underwent successful oral aspirin desensitization, with a complete in vitro inhibition of platelet function, and was discharged on aspirin, clopidogrel and warfarin, without experiencing other events at 6-month follow-up.     

Stent malapposition,as a potential mechanism of very late stent thrombosis after bare-metal stent implantation: A case report

A 90-year-old man was admitted to our hospital with acute ST-segment elevation myocardial infarction. He had a history of post-infarction angina pectoris 79 months ago and had a bare-metal stent (BMS) implanted in the proximal left anterior descending artery at our hospital. Emergent coronary angiography demonstrated thrombotic occlusion in the previously stented segment. After catheter thrombectomy, antegrade flow was restored, but 90% stenosis with haziness persisted in the proximal and distal portions of the previously stented segment. Intravascular ultrasound imaging showed interstrut cavities or stent malapposition at the proximal and distal sites of stented segment. In close proximity to the sites, residual thrombi were also observed. Optical coherence tomography (OCT) demonstrated neither lipid-laden neointimal tissue nor rupture but clearly demonstrated residual thrombus adjacent to the malapposed region in addition to the stent malapposition. PCI with balloon was successfully performed and stent apposition was confirmed by OCT. Stent malapposition is an unusual mechanism of very late stent thrombosis after BMS implantation. OCT can clearly reveal the etiology of stent thrombosis.     

Very late stent thrombosis in late stent malapposition after sirolimus-eluting stent implantation

Late stent malapposition (LSM) has been demonstrated to be more common after drug-eluting stent (DES) implantation than after bare-metal stent (BMS) implantation. To date, this unusual intravascular ultrasonic finding after DES implantation, however, has not received enough attention, because previous studies suggested few adverse clinical sequelae from LSM. We present a case of angiographically-confirmed very late stent thrombosis (ST) in LSM after elective implantation of sirolimus-eluting stents. In this 32-year-old male patient, very late ST occurred at 29 months after DES implantation and at 20 months after the identification of LSM. Although this patient had received sufficient dual antiplatelet therapy with aspirin and clopidogrel for more than 1 year, he suffered from ST shortly after the discontinuation of clopidogrel. Thus, patients with LSM may pose a significant risk for very late ST after discontinuation of dual antiplatelet therapy. The findings suggest that dual antiplatelet therapy should be further prolonged in patients with LSM.     

Thrombosis and acute myocardial infarction as consequences of very late stent malapposition after implantation of a drug-eluting stent

The use of drug-eluting stents (DES) provides early and late benefits demonstrated by angiographic and clinical outcomes. Here we report a case of late stent thrombosis and acute myocardial infarction caused by late stent malapposition (LSM) of a DES at 16 months after the procedure. We successfully treated the patient with balloon angioplasty after intravenous thrombolytic therapy. This case illustrates that a LSM can develop at any time after DES implantation and can result in acute coronary syndrome. Therefore, clinicians should be aware of the possibility of late cardiac events after implantation of DES.     

Incidence and mechanism of late stent malapposition after phosphorus-32 radioactive stent implantation

Late stent malapposition is a potential complication of intracoronary brachytherapy. The aim of our study was to determine the incidence and mechanism of late stent malapposition after implantation of phosphorus-32 radioactive stents. We analyzed 159 patients for de novo lesions after the implantation of phosphorus-32 radioactive stents. There were 15 late stent malappositions. The incidence of malapposition was higher in patients who received Hot-Ends Isostents. External elastic membrane expansion greater than plaque increase in malapposed segments was observed. Late stent malapposition is caused by a localized increase in external elastic membrane that is greater than the increase in plaque area; this is believed to be a dose-dependent phenomenon because it was more common with Hot-Ends Isostents.