THROMBOPHILIA IN CRYPTOGENIC STROKE (THICK) STUDY

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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.