Cardiovascular Materials

Abstract

The search for biocompatible cardiovascular materials has gone on for more a century, beginning with the metallic and glass blood vessel substitutes of Alexis Carrel. The quest has become more involved as the need for flexible polymeric materials became apparent, and as knowledge has been gained about the reactions of blood with artificial surfaces. Current materials in clinical practice are, for the most part, standard polymers that have been in incardiovascular materials is thrombosis, a combination of the coagulation of the blood proteins (which traps red cells, thus obstructing vessel channels) and the activation and deposition 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, 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. Creation of a material that would precisely mimic all 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 these materials will be discussed in the context of typical cardiovascular devices.