Cardiovascular Materials
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cardiovascular materials is thrombosis, a combination of the coagulation of the blood proteins (which traps red cells, thus obstructing vessel channels) and the activation and déposition of blood platelets, cells that rapidly aggregate with other platelets to obstruct the channel. Coagulation and platelet aggregation are interdependent, highly volatile processes, acting like two positive feedback cascade amplification processes. Thrombosis is prevented in clinical practice by administering heparin,
Table I: Blood-Material Interactions. Coagulation Platelet Activation & Aggregation Complément Protein Activation Leukocyte Activation Macrophage & Giant Cell Invasion inflammatory response Thickened Intimai Layer hyperplastic response Calcification Toxic Dégradation (selected materials)
dustrial use for many years and whose synthesis and properties are well known. But new, sometimes exotic materials and coatings are under development. Thèse new materials frequently rely on knowledge of spécifie steps in the complex interaction between blood and foreign materials, and methods to blunt those steps. So detailed knowledge about blood-materials interactions is imperative to obtaining biocompatibiHty. A truly biocompatible cardiovascular material must avoid ail the biological responses listed in Table I. Current materials partially meet some, but not ail thèse criteria. The most important early response to
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a naturally occuring agent that complexes with another circulating substance, antithrombin III, to block the coagulation cascade (Figure 1). Results, while permitting perfusion of cardiovascular devices in many clinical situations, do not absolutely prevent thrombosis. Many cases of récurrent thrombus formation are known. The endothelial cell, the natural lining to ail vessels in the circulatpry System, is the only truly nonthrombogenic surface. Blood has a complex relationship with the endothelial cell, but éléments of that interaction serve as models for means to improve biocompatibility. Three functions of the endothelial cell illustrate this complex -
ity. The endothelial cell releases heparin and heparan sulfate, natural anticoagulants, in response to various external stimuli. Endothelial cells produce prostacyclin, which prevents platelet activation by surface contact and is also a powerful, shortacting vasodilator. Prostacyclin release is modulated by fluid shear stresses on the endothelial membrane, among other stimuli. Endothelial cells bind the coagulation enzyme thrombin to thrombomodulin, one of the endothelial membrane proteins, removing it from circulation but also enhancing the activation of protein C, another circulating protein which inhibits blood coagulation. Création of a material that would precisely mimic ail functions of the endothelial cell is a daunting task. Fortunately, more prosaic materials exist that may be purified or modified to elicit minimal biological responses. Progress in developing thèse materials wil[ be di
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