A Nonthrombogenic, Nonanticoagulant-Dependent Mitral Valve Prosthesis
1967
Thromboembolism stems from incompletely covered foreign body which is in physical continuity with tissue. Cardiac valve prostheses which remain partially exposed show, at the tissue-to-prosthesis junction, incomplete healing which is characterized by continuing granulation and proliferating immature unstable scar tissue, from which thrombosis originates and propagates. The principle of complete encapsulation with healthy granulation tissue, maturation into stable fibrous tissue without inflammation, covered by a normal antithrombogenic endothelial surface, is a more logical approach than [see Figure in the PDF file] methods which attempt to prevent thrombosis by altering the character of the surface of the exposed foreign body or the blood coagulation mechanism. A valve is described which functions eminently satisfactorily as a replacement for the calf mitral valve.
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