がん関連脳卒中に対する急性期血管内再開通療法の考え方

抄録

Mechanical thrombectomy has become the standard of care for acute ischemic stroke caused by large vessel occlusion, with indications expanding based on evidence from randomized controlled trials. Patients with active or advanced cancer are at increased risk of ischemic stroke ; however, they are excluded from randomized controlled trials because of limited life expectancy, and the benefit of endovascular reperfusion therapy in this population remains unclear. This review summarizes the pathophysiology of cancer–associated stroke, indications for endovascular therapy, and considerations for procedural strategy.

Cancer–associated stroke includes heterogeneous mechanisms, among which arterial thrombosis caused by cancer–related hypercoagulability―referred to here as “cancer-related stroke”―is characterized by platelet–rich, erythrocyte–poor thrombi. Histopathological studies of retrieved thrombi have demonstrated a predominance of platelet and fibrin components, particularly in nonbacterial thrombotic endocarditis and cancer–related cryptogenic stroke. Imaging findings such as the absence of hyperdense vessel sign or susceptibility vessel sign, the presence of a three–territory sign, and elevated D–dimer levels may suggest this thrombus phenotype.

Observational studies indicate that although patients with active cancer have poorer functional outcomes and higher mortality after thrombectomy, successful recanalization rates are comparable to those in patients without cancer ; thus, active cancer alone should not preclude endovascular therapy. Considering thrombus characteristics, contact aspiration with large–bore catheters may be an appropriate first–line strategy. Treatment decisions should be individualized through shared decision–making based on prognosis, risks, and patient preferences. Ongoing registry studies, including the ESPOIR registry, are expected to provide further evidence to optimize patient selection and therapeutic strategies for cancer–associated stroke.