Open AccessAnticoagulants for cancer-associated ischemic stroke
Author(s) -
JinYi Hsu,
An-Bang Liu
Publication year - 2019
Publication title -
tzu-chi medical journal/cí-jì yīxué
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.343
H-Index - 15
eISSN - 2223-8956
pISSN - 1016-3190
DOI - 10.4103/tcmj.tcmj_55_19
Subject(s) - medicine , atrial fibrillation , stroke (engine) , cancer , vitamin k antagonist , warfarin , coagulation , heparin , low molecular weight heparin , d dimer , thrombosis , cerebral infarction , cardiology , ischemia , mechanical engineering , engineering
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.