Stroke is the third most common cause of death in developed countries. Various mechanisms of ischemic stroke exist. However, in young population, in a third of cases, the cause of a stroke cannot be determined despite an extensive evaluation. Many studies have highlighted the link between stroke and fibrinolysis. Genetic variants of tPA and PAI-1 genes have been suggested to be the risk factors for stroke.

ANXA2 plays a pivotal role in plasmin generation and fibrinolysis. Several studies showed the role of ANXA2 and S100A10 subunits in regulation of fibrinolysis in vivo. Recently, the efficacy of recombinant ANXA2 for fibrinolytic therapy in a rat embolic stroke has been demonstrated. Some single nucleotide polymorphisms in ANXA2 gene could be associated with increased risk of stroke in sickle cell disease.

Therefore, these data invite us to test hypothesis that genetic variants of ANXA2 gene could be associated with ischemic stroke.

Inclusion Criteria:

• Completed ischemic stroke defined as a rapidly developing focal neurologic deficit with no apparent cause other than a vascular origin that persisted beyond 24 hours in surviving patients
• Age from 18 years old

Exclusion Criteria:

• Transient ischemic attack
• Pregnancy