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In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
Published on: May 24, 2020
[Haemostatic mechanisms in the process of atherotrombosis]
1Tromboické Centrum, Vedoucí Lékar doc. MUDr. Tomás Kvasnička, CSc., Ústav Lékarské Biochemie a Laboratorní Diagnostiky 1. Lékarské Fakulty UK a VFN Praha. tomas.kvasnicka@vfn.cz
Hemostasis play an essentials role in protecting of vascular integrity and maintaining normal blood flow, and anatomically and functionally is entwined with the vasculature. The classic concept of atherosclerosis assigns a pivotal role to inflammation in the onset and progression of this disease. Accumulating data suggest an intimate cross-talk between hemostasis and inflammation, underscoring the role of both systems in many complex diseases, including atherothrombosis. An experimental data indicate that platelets and the coagulation system are important determinants of both atherogenesis and atherothrombosis. The hemostatic system is well known for its capacity to exert a multitude of actions on the vasculature. The current concept of a vulnerable plaque suggests that repeated plaque microruptures, followed by subclinical thrombosis, are critical for plaque growth and vulnerability.
Hemostasis play an essentials role in protecting of vascular integrity and maintaining normal blood flow, and anatomically and functionally is entwined with the vasculature. The classic concept of atherosclerosis assigns a pivotal role to inflammation in the onset and progression of this disease. Accumulating data suggest an intimate cross-talk between hemostasis and inflammation, underscoring the role of both systems in many complex diseases, including atherothrombosis. An experimental data indicate that platelets and the coagulation system are important determinants of both atherogenesis and atherothrombosis. The hemostatic system is well known for its capacity to exert a multitude of actions on the vasculature. The current concept of a vulnerable plaque suggests that repeated plaque microruptures, followed by subclinical thrombosis, are critical for plaque growth and vulnerability.
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