Blood coagulation cascade consists of intrinsic, extrinsic and final common pathways forming fibrin network. Thrombus is divided into fibrin thrombus and platelet thrombus. The former is formed by low shear condition and treated by anticoagulants. The latter is formed by platelets activated by high shear stress in the stenotic arteries. The concept of Virchow's triad such as blood stasis, hypercoagulability and vascular injury is still available in considering clinical thrombogenesis. Atrial fibrillation becomes prevalent in older generation, and its major complication is cardioembolic stroke. This type of stroke is caused mainly by left atrial thrombus. Therefore, this stroke should be prevented by oral anticoagulants including vitamin K-dependent anticoagulant (warfarin) or direct oral anticoagulant (DOAC). Warfarin suppresses several steps of coagulation cascade, whereas DOAC inhibits thrombin (dabigatran) or factor Xa (ribaroxaban, apixaban, and edoxaban) directly and specifically. These agents of DOAC are characterized by short half-lives, more predictable pharmacodynamics and pharmacokinetics, less interaction with other drugs, and less frequent adverse effects of intracranial bleeding in comparison with conventional warfarin. Since critical step of final common pathway in coagulation cascade is inhibited directly by DOAC, these agents may impair the fibrin polymerization and mechanical clot stabilization. Although efficacy and safety of DOAC are recognized clinically, hemorheological effects of DOAC on thrombus formation, structure and property under the hydrodynamic blood flowing warrant future study.