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.
- Anticoagulation treatment. Drug
Intervention Desc: Details of anticoagulation treatment information will be gathered including low molecular-weight heparin (enoxaparin 1 mg/kg) vs. NOAC (rivaroxaban 15 or 20 mg), vs. warfarin (target INR2.0-3.0) or no use of anticoagulation per physicians' decision and patients' conditions.
- Observation: Cohort
- Perspective: Prospective
- Sampling: Non-Probability Sample
Acute ischemic stroke patients with active cancer
|Type||Measure||Time Frame||Safety Issue|
|Primary||Recurrent stroke or systemic embolism||up to 6 months||No|
|Secondary||90-days modified Rankin Scale score||examined at 90 days after stroke symptom onset in each patients||No|
|Secondary||Effect of anticoagulation treatment||up to 14 days||No|
|Secondary||Symptomatic hemorrhagic transformation||up to 6 months||Yes|