THROMBOPHILIA IN CRYPTOGENIC STROKE (THICK) STUDY

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。本研究的目的是：(1)确定静脉血栓形成是否是隐源性卒中的独立危险因素；(2)探讨在卵圆孔未闭的情况下静脉血栓形成是否是隐源性卒中的危险因素；(3)评价动脉性血栓在隐源性脑卒中发病中的独立作用；(4)评估CD39/ ntpase -1和血小板反应性在隐源性卒中发病机制中的作用。研究人员假设，静脉性血栓形成仅在卵圆孔未闭时是危险因素，而动脉性血栓形成是与卵圆孔未闭无关的危险因素。同样，研究人员假设，在卵圆孔未闭的情况下，ntpase -1活性降低和血小板活化增加是隐源性卒中的危险因素。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The aims of this study are to: (1) determine whether venous thrombophilias are independent risk factors for cryptogenic stroke; (2) examine whether venous thrombophilias are a risk factor for cryptogenic stroke in the presence of patent foramen ovale; (3) evaluate the independent role of arterial thrombophilias in the pathogenesis of cryptogenic stroke; and (4) assess the role of CD39/NTPDase-1 and platelet reactivity in the pathogenesis of cryptogenic strkoe. The investigators hypothesize that venous thrombophilias are risk factors only in the presence of a patent foramen ovale, whereas arterial thrombophilias are risk factors independent of a patent foramen ovale. Similarly, the investigators hypothesize that reduced NTPDase-1 activity and increased platelet activation are risk factors for cryptogenic stroke in the absence of patent foramen ovale.