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.