Device-Induced Thrombosis in Blood-Contacting Medical Devices: Mechanisms and Emerging Prevention Strategies

Medical devices such as catheters, vascular grafts, and extracorporeal circuits play a vital role in modern clinical care but remain limited by the persistent risk of device-related thrombosis. This review explores the multifaceted mechanisms driving device-induced thrombosis, emphasizing the pivotal role of the contact activation pathway (factors XII and XI), leukocyte adhesion, complement system activation, and red blood cell hemolysis. This paper details how protein adsorption, especially fibrinogen and contact factors, initiates a cascade of platelet activation and coagulation, leading to thrombus formation on artificial surfaces. In response, diverse prevention strategies have emerged, including passive surface modifications (e.g., PEG, PEO, pyrolytic carbon), bioactive coatings (e.g., heparin, thrombomodulin, nitric oxide-releasing polymers), and novel approaches like endothelialization and stimuli-responsive materials. Additionally, pharmacologic innovations targeting the contact system via antisense oligonucleotides, monoclonal antibodies, aptamers, and natural protease inhibitors show promise for reducing thrombosis risk while preserving hemostasis. Integrating these strategies with advanced in vitro evaluation platforms and AI-assisted data integration and analysis marks a new era in the development of hemocompatible biomaterials. This review underscores the need for multidisciplinary efforts to design the next generation of blood-contacting medical devices with enhanced safety, efficacy, and patient outcomes.