Purpose: Cancer associated intravascular coagulopathy is the primary mechanism of cancer-related stroke, particularly in those without conventional stroke etiologies. Randomized clinical trials have investigated efficacy of vitamin K-dependent oral anticoagulant (warfarin), low-molecular-weight heparin (LMWH) and non-vitamin K-dependent oral anticoagulant (NOAC) for the prevention of systematic venous thromboembolism. However, relatively little is known about the biological changes underlying intravascular coagulopathy and mechanisms of anticoagulation therapy in patients with cancer-related stroke. The aim of this study is to evaluate to determine the biological markers for intravascular coagulopathy causing stroke and for monitoring the effects of anticoagulation therapy, in patients with active cancer and stroke.

Inclusion Criteria:

• Age 20 years and older
• Acute ischemic stroke presented within 7 days of symptom onset
• Cancer related stroke: active cancer (diagnosis of cancer within 6 months of stroke onset, any treatment for cancer within the previous 6 months, or recurrent or metastatic cancer) and ischemic stroke which could not be explained by conventional stroke mechanisms including large artery atherosclerosis, cardioembolism, lacunar infarction, or other etiologies (e.g., dissection)
• Signed informed consent or appropriate signed deferral of consent where approved

Exclusion Criteria:

• Primary intracranial malignancy
• Incomplete workup for stroke etiology (either vascular or cardiologic studies)
• Any signs of infectious or immunological diseases which may influence plasma D-dimer levels
• Patients with stroke suspected to be caused by the tumor itself (i.e., tumor emboli) or cancer treatment (i.e., chemotherapy-induced stroke)

Acute ischemic stroke patients with active cancer