Abstract

Ancrod (Arvin) on slow intravenous administration converts fibrinogen into fibrin at a rate which does not cause intravascular thrombosis. The fibrin is eliminated from the circulation and the blood is thus rendered incoagulable. To test the efficacy of ancrod in the prevention of thrombosis after prosthetic replacement of the heart valves, the tricuspid valve was replaced with a polypropylene mitral valve in 17 calves, using cardiopulmonary bypass. Five calves were eliminated from the study. Eleven calves were treated with ancrod, and one untreated calf was used as a control. Four out of five prosthetic valves in calves treated with ancrod for up to 72 hours were free of thrombus formation, and one out of three at one week. In the long-term study, fibrinogen titres rose after varying intervals, in spite of continual treatment with ancrod. This `escape' of fibrinogen titres from the control of ancrod may be due to species resistance or to the development of immunity. Further study is in progress to elucidate this point and to gain further knowledge for the clinical application of ancrod.