Jin‑Yi Hsua, An‑Bang Liua,b*
aDepartment of Neurology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan, bSchool of Medicine, Tzu Chi University, Hualien, Taiwan
Abstract
Patients with cancer‑associated ischemic stroke pose similar clinical manifestations and image characteristics, mainly embolic infarction, as patients with atrial fibrillation do. D‑dimer, a degraded product of fibrin polymer, is a useful indicator of hypercoagulability, which frequently increases in cancer‑associated stroke, but not in stroke resulted from atrial fibrillation. The
level of serum D‑dimer is associated with mortality, prognosis, and recurrence of systemic thromboembolism in these patients. Theoretically, drugs block coagulation cascade, such as heparin and low‑molecular‑weight‑heparin (LMWH), oral direct anticoagulants, could attenuate the status of hypercoagulation and decrease the amount of D‑dimer. These drugs may be helpful to prevent thromboembolic events in patients with cancer‑associated hypercoagulability. Vitamin K antagonist, warfarin, decreases the production of coagulation factors, but not interrupts coagulation cascade may not be helpful to decrease hypercoagulability, but increase the risk of bleeding. However, the treatment of cancer‑associated embolic stroke is still controversial. This article reviews relevant clinical studies and proposes the applicability of direct oral anticoagulants from the pathophysiological mechanism.
Keywords: Cancer‑associated stroke, D‑dimer, Hypercoagulability, Oral direct anticoagulants
