There have been in excess of 90 implantations of several different types of artificial heart (TAH) into patients. The bulk of these implantations have been using the Jarvik TAH as a bridge to provide interim circulatory support for the failed heart while a donor heart is being located and transported. Attempt to use the Jarvik TAH as a permanent, long-term heart substitute were complicated by hemorrhaging, sepsis, peripheral-organ failure and strokes [1]. These latter sequelae are thought to be due to thromboembolism and this concept is supported by the examination of explanted TAH from Barney Clark, the first recipient of the Jarvik TAH, which revealed large thrombus formation around the valve seats and microthrombi on the diaphragm that may have been the sites of thromboemboli [2]. In the case of bridges, the implantation periods are shorter, averaging 10 to 14 days but still a significant number of these patients have had thromboembolic events and explanted TAH have had microscopic aggregations of platelets and thrombi [3,4]. The response of blood to the constituent biomaterials of all cardiovascular devices is highly variable [5]. The documentation of thrombus on a biomaterial surface does not prove it will detach nor does the lack of thrombus on a surface indicate that the surface is benign, as thrombus could have formed and embolized. We have used two approaches to study the dynamic process of thrombogenesis and thromboembolism, in vivo and in vitro. Whole arterial blood samples were analyzed for thromboemboli as an in vivo assessment and epifluorescent videomicroscopy was used to monitor the mechanism of thrombosis, in vitro. Microparticles were found in the arterial circulation of patients with a Jarvik TAB and platelet thrombi were observed to form and embolize from Biomer-coated surfaces during perfusion.