DES植入后双联抗血小板治疗的现状与未来精要.pptVIP

总结 随着介入治疗的增加, 肝素诱导的血小板减少并不少见 及时发现，正确诊断，准确处理是减少并发症及灾难性事件的关键 国产和进口氯吡咯雷（帅泰）的解密 只要同等剂量,就有同等作用 ACS负荷剂量均为300-600mg 维持剂量均为75mg/d 持续时间均为至少一年 但减量时更为方便，每月每月减25mg/d 费用减少42% 小 结 晚期血栓形成引发DES安全争议 再内皮化延迟持续激活血小板是DES支架内血栓形成的病生理基础 过早终止抗血小板治疗是引发DES支架内血栓形成的重要原因 DES双联抗血小板治疗的最佳疗程仍存在争议 双抗时间需个体化；阿司匹林是双抗治疗基础 Thanks * * PCI的发展历经了3个过程：经皮冠状动脉成形术 （PTCA）、裸金属支架 （BMS）、药物洗脱支架（DES）。 上述多项随机研究和前瞻性注册研究表明支架术较球囊扩张术的血管再狭窄率低（32% vs.42%；17% vs.31%），而DES术后（无论是雷帕霉素支架或是紫杉醇支架）通过广泛的临床研究和血管造影证实通过定时释放聚合物可使血管再狭窄率降低至10%以下，较裸支架相比血管再狭窄率降低了近3-4倍。 Data from multiple randomized clinical trials and prospective registries suggest that DES incorporating either rapamycin or paclitaxel with a timed-release polymer are associated with a reduction in restenosis rates to less than 10% across a wide spectrum of clinical and angiographic subsets. * * * * Figure 2. DES reduce neointima formation but may increase stent thrombogenicity. Effect of sirolimus-eluting/paclitaxel-eluting stent strut on the local vessel wall after implantation. Sirolimus/paclitaxel reduces neointima formation by inhibiting vascular smooth muscle migration and proliferation (green arrows). However, the drugs also inhibit reendothelialization, induce tissue factor (TF), and may prevent homing and proliferation of endothelial progenitor cells (EPCs; red arrows/bars). DES减少新生内皮的形成，但可能增加支架血栓形成的能力，植入后，西罗莫司洗脱支架/紫杉醇洗脱支架支撑在局部血管壁上的作用。西罗莫司/紫杉醇通过抑制血管平滑肌啊细胞迁移和增生从而减少内皮增生。然而药物可抑制再内皮化，诱导组织因子，可预防内皮祖细胞（EPC）归巢和增生 * Figure 1. Rapamycin and paclitaxel increase tissue factor (TF) expression. Paclitaxel enhances c-Jun NH2-terminal kinase (JNK) phosphorylation, which in turn leads to an increase in TF protein expression and TF surface activity. The PI3-kinase and its downstream target, the mammalian target of rapamycin (mTOR), inhibit endothelial TF expression; rapamycin inhibits the mammalian target of rapamycin, which leads to a disinhibition of (and thus an increase in) TF expression and surface activity. MKKs indicates map kinase kinases (upstream regulators of JNK); PI