Abstract
Blood-contacting medical devices of different biomaterials are often used to treat various cardiovascular diseases. Thrombus formation is a common cause of failure of cardiovascular devices. Currently, there are no clinically available biomaterials that can totally inhibit thrombosis under the more challenging environments (e.g., low flow in the venous system). Although some biomaterials reduce protein adsorption or cell adhesion, the issue of biomaterial associated with thrombosis and inflammation still exists. To better understand how to develop more thrombosis-resistant medical devices, it is essential to understand the biology and mechano-transduction of thrombus nucleation and progression. In this review, we will compare the mechanisms of thrombus development and progression in the arterial and venous systems. We will address various aspects of thrombosis, starting with biology of thrombosis, mathematical modeling to integrate the mechanism of thrombosis, and thrombus formation on medical devices. Prevention of these problems requires a multifaceted approach that involves more effective and safer thrombolytic agents but more importantly the development of novel thrombosis-resistant biomaterials mimicking the biological characteristics of the endothelium and extracellular matrix tissues that also ameliorate the development and the progression of chronic inflammation as part of the processes associated with the detrimental generation of late thrombosis and neo-atherosclerosis. Until such developments occur, engineers and clinicians must work together to develop devices that require minimal anticoagulants and thrombolytics to mitigate thrombosis and inflammation without causing serious bleeding side effects.
Highlights
Venous and arterial thromboses are set in motion by biological processes that activate both coagulation and inflammation
Blood-contacting medical devices need to reduce/avoid thrombosis initiated by platelet activation, tissue factor, and contact coagulation factors, thereby limiting generation of proinflammatory components like microparticles released from activated cells, platelets, and/or apoptotic cells
Atherothrombosis is a complex and abnormal chronic inflammatory/immune arterial wall remodeling initiated by the deposition of lipids and oxidative stress followed by recruitment of circulating leukocytes, proliferative responses with atheromatous plaque growth, proteolysis, neo-angiogenesis, apoptosis, calcification, fibrosis, plaque rupture, and thrombosis (Martin-Ventura et al, 2017)
Summary
Specialty section: This article was submitted to Biomaterials, a section of the journal Frontiers in Bioengineering and Biotechnology. We will address various aspects of thrombosis, starting with biology of thrombosis, mathematical modeling to integrate the mechanism of thrombosis, and thrombus formation on medical devices Prevention of these problems requires a multifaceted approach that involves more effective and safer thrombolytic agents but more importantly the development of novel thrombosis-resistant biomaterials mimicking the biological characteristics of the endothelium and extracellular matrix tissues that ameliorate the development and the progression of chronic inflammation as part of the processes associated with the detrimental generation of late thrombosis and neo-atherosclerosis.
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