Pigs with von Willebrand disease may be resistant to experimental infective endocarditis.

Indirect evidence suggests that the blood platelet is important in the pathogenesis of experimental infective endocarditis. Mechanical injury to the endocardial surface causes deposition of fibrin and platelets; injected microorganisms quickly localize to this lesion. Endocarditis pathogens also bind to and activate platelets. We used our previously described animal model for inducing infective endocarditis in normal pigs and applied it to animals with severe von Willebrand disease. The model uses catheter-induced trauma to the aortic valve and endocardium, followed by intravenous injection of group C streptococci. Control animals all showed typical clinical and laboratory evidence of endocarditis. In contrast, in pigs with von Willebrand disease (n = 4) endocarditis failed to develop. Studies in vitro of platelet-bacteria interactions showed that platelets derived from both normal and diseased pigs were equal in their ability to bind to and be activated by group C streptococci. These data suggest that normal platelet function is important in the pathogenesis of experimental infective endocarditis.