Kalamara TV, Dodos K, Georgakopoulou VE. Antiplatelet therapy in pulmonary embolism: Mechanisms and evidence. World J Transl Med 2026; 12(3): 121879 [DOI: 10.5528/wjtm.121879]
Corresponding Author of This Article
Vasiliki E Georgakopoulou, MD, Department of Pathophysiology, Laiko General Hospital, Medical School of National and Kapodistrian University of Athens, 17 Agiou Toma Street, Athens 11527, Greece. vaso_georgakopoulou@hotmail.com
Research Domain of This Article
Respiratory System
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review-article
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World J Transl Med. Sep 28, 2026; 12(3): 121879 Published online Sep 28, 2026. doi: 10.5528/wjtm.121879
Antiplatelet therapy in pulmonary embolism: Mechanisms and evidence
Tsampika-Vasileia Kalamara, Konstantinos Dodos, Vasiliki E Georgakopoulou
Tsampika-Vasileia Kalamara, Konstantinos Dodos, Laboratory of Physiology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki 54124, Kentrikí Makedonía, Greece
Vasiliki E Georgakopoulou, Department of Pathophysiology, Laiko General Hospital, Medical School of National and Kapodistrian University of Athens, Athens 11527, Greece
Author contributions: Kalamara TV conceived the study and performed the majority of the writing; Dodos K performed data accusation and writing; Georgakopoulou VE coordinated and supervised the writing and critically revised the manuscript; and all authors approved the final version of the manuscript and agree to be accountable for all aspects of the work.
AI contribution statement: The manuscript was not generated by artificial intelligence. The scientific content, data interpretation, and conclusions are entirely the original work of the authors. ChatGPT was used only to assist with minor language editing, such as grammar, syntax, and clarity improvements. This tool was used strictly for linguistic refinement and did not contribute to the scientific content, data analysis, interpretation, or conclusions of the manuscript. No images included in the manuscript were generated by artificial intelligence. All figures are original and comply with the journal’s requirements. All references were selected, verified, and curated by the authors. No references were generated by AI tools without manual verification and approval by the authors.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
Corresponding author: Vasiliki E Georgakopoulou, MD, Department of Pathophysiology, Laiko General Hospital, Medical School of National and Kapodistrian University of Athens, 17 Agiou Toma Street, Athens 11527, Greece. vaso_georgakopoulou@hotmail.com
Received: April 3, 2026 Revised: July 14, 2026 Accepted: August 31, 2026 Published online: September 28, 2026 Processing time: 153 Days and 6.8 Hours
Abstract
Pulmonary embolism (PE) is a common and potentially fatal manifestation of venous thromboembolism, typically resulting from thrombus formation in the venous circulation and subsequent embolization to the pulmonary arterial tree. Its pathobiology reflects the convergence of venous stasis, hypercoagulability, and endothelial dysfunction, which together initiate a thrombo-inflammatory cascade involving coagulation factors, vascular cells, and innate immune pathways. Although PE thrombi have classically been characterized as fibrin- and erythrocyte-rich structures, accumulating evidence supports an active and regulatory role for platelets across key stages relevant to PE, including thrombus formation, embolization potential, clot stabilization, resolution, and recurrence. Anticoagulation remains the foundation of PE prevention and treatment, with low-molecular-weight heparins, vitamin K antagonists, and direct oral anticoagulants representing the main therapeutic options in contemporary practice. In contrast, the role of antiplatelet therapy in PE remains to be further investigated. While antiplatelet agents may provide modest benefit in selected clinical settings—such as specific prophylactic scenarios and secondary prevention after discontinuation of anticoagulation—their efficacy is generally inferior to anticoagulants, and they are not recommended as first-line therapy for acute PE management. Mechanistically, platelets can contribute to PE-related thrombogenesis by providing procoagulant surfaces, amplifying thrombin generation, and mediating crosstalk with endothelial and innate immune cells, particularly neutrophils and monocytes. These interactions promote immunothrombosis, neutrophil extracellular trap formation, and thrombus stabilization, reinforcing the link between inflammation and coagulation within the venous-to-pulmonary thromboembolic continuum. The primary objective of this review is to critically interpret the role of antiplatelet therapy specifically in PE by integrating recent preclinical insights with contemporary clinical evidence. By synthesizing advances in platelet biology, experimental models, and clinical studies, this article evaluates the therapeutic potential, limitations, and future directions of platelet-targeted strategies in PE. A deeper understanding of platelet-driven mechanisms may inform the development of safer, more precise antithrombotic approaches that complement established anticoagulant therapies and improve outcomes in patients with PE.
Core Tip: Although pulmonary embolism (PE) is classically considered a fibrin-rich, anticoagulation-responsive disorder, platelets are increasingly recognized as active participants in venous thrombogenesis and thrombo-inflammatory signaling. This mini-review examines the mechanistic and clinical evidence linking platelets to PE and critically evaluates the current and potential role of antiplatelet therapy in its prevention and management.
