Related Experiment Video
Updated: Feb 4, 2026

A Porcine Model of Acute Autologous Pulmonary Embolism
Published on: September 6, 2024
Successful treatment of a massive pulmonary embolism using rivaroxaban in a patient with antithrombin III deficiency
Junji Yamaguchi1, Nobuhiro Hara1, Tetsuo Yamaguchi1
1Department of Cardiology, Japanese Red Cross Musashino Hospital, Tokyo, Japan.
Abstract:
We report a case of acute massive pulmonary embolism in a patient with antithrombin III deficiency. The patient was treated with rivaroxaban. The patient responded well to the therapy, and contrast-enhanced computed tomography showed nearly complete disappearance of the pulmonary embolism. Patients with low antithrombin III activity may have resistance to heparin therapy, leading to insufficient anticoagulation during the acute phase of thromboembolism. This case suggests that direct oral anticoagulants, such as rivaroxaban, may be effective first-line agents for treating venous thromboembolism in patients with antithrombin III deficiency. <Learning objective: Recently, direct oral anticoagulants represent a novel treatment option for venous thromboembolism with several practical advantages over conventional therapy. Antithrombin-III deficiency may lead to insufficient anticoagulation during the acute phase of thromboembolism. The present case suggests that rivaroxaban is a direct Factor Xa inhibitor and does not require cofactors such as antithrombin-III, thus it is suitable for anticoagulation therapy in patients with low antithrombin-III activity.>.
More Related Videos
Related Concept Videos
Pulmonary Embolism III: Nursing Management
Pulmonary Embolism I: Introduction
Pulmonary Tuberculosis III
The first classification is based on the development of the disease, and it includes the following categories:
Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care
Ecological Succession
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...

