BACKGROUND

That thrombosis might contribute significantly to plaque pathogenesis was originally proposed by the celebrated pathologist Carl von Rokitansky, 1 who postulated that the disease results from an abnormal intimal deposition of blood components, including fibrin. Thus, the" thrombogenic" or" encrustation" hypothesis of atherogenesis was born. This concept received tentative support from Mallory2 in 1913 and Clark et al3 in 1936, but became widely accepted only after the landmark observations of Duguid4 in 1946. There is now an extensive literature from pathologic observations in man that indicates that plaque growth is to a significant extent dependent on the organization and incorporation of mural thrombi. 5-13 Although studies on the morphology of advanced atherosclerotic plaques provide little insight into the initial events implicated in lesion pathogenesis, there are some structural footprints analogous to geologic sedimentary rock formations, which reflect the legacy of earlier episodic thrombotic events in plaque progression. These are reflected in the distinct laminar patterns frequently observed, and the layers of fibrin seen at many levels within the plaque itself. There is little definitive evidence that the incorporation of mural thrombi is a factor in plaque initiation. However, it is now clear that this mechanism plays a major role in the subsequent growth and progression of atherosclerotic lesions. 14 For these reasons, an appropriate alternative title for this presentation is" Rokitansky revisited"(Fig. 1).