@article {KirmaniS119作者= {Jawad f•基尔马尼和Ammar Alkawi Spozhmy Panezai和马丁Gizzi}, title ={溶栓治疗急性缺血性中风的进步},体积={79},数量={13补充1},页面= {S119——S125} = {2012}, doi = {10.1212 / WNL。出版商0 b013e3182695882} = {Wolters Kluwer健康,公司代表美国神经病学学会},文摘={在过去50年里,溶栓药物设计,目的是recanalizing闭塞冠状血管,首页和后来,应用于急性缺血性中风的设置。药物一般都瞄准了纤溶酶原{\ textendash}物血纤维蛋白溶酶转换,促进纤维蛋白溶解的自然过程。新代理与不同程度的纤维蛋白选择性和药物半衰期影响血管再通率和出血性并发症,内部和外部的中枢神经系统。动脉内的纤维蛋白溶解剂(IA)管理增加的血栓的药物在更高浓度较小的数量,因此降低系统性风险。机械血栓中断或萃取允许药血栓的表面积更大。延迟与IA疗法可能恶化的风险/效益比溶栓;因此,组合IA-IV治疗研究。到目前为止,没有直接的比较试验表明,血管内管理更有效或有出血性并发症的风险低于静脉组织纤溶酶原激活物。GLOSSARYAIS =急性缺血性中风; DIAS=Desmoteplase in Acute Ischemic Stroke Trial; ECASS=European Cooperative Acute Stroke Studies; FDA=US Food and Drug Administration; IA=intra-arterial; ICH=intracerebral hemorrhage; MCA=middle cerebral artery; MMPs=matrix metalloproteinases; MRA=magnetic resonance angiography; NIHSS=NIH Stroke Scale; NINDS=National Institute of Neurological Disorders and Stroke; PROACT=Prolyse in Acute Cerebral Thromboembolism; rtPA=recombinant tissue plasminogen activator; TIMI=thrombolysis in myocardial ischemia; tPA=tissue plasminogen activator}, issn = {0028-3878}, URL = {//www.ez-admanager.com/content/79/13_Supplement_1/S119}, eprint = {//www.ez-admanager.com/content/79/13_Supplement_1/S119.full.pdf}, journal = {Neurology} }