The variable spectrum of possible complicatons affecting the established atheromatous plaque constitutes an integrally composite system in the active process of atherogenesis. Indeed, superimposed thrombosis and endothelial ulceration would directly promote the depositionof atheroma in a manner conducive to subsequent injury to subintima and tunica media. The prominent implication of smooth muscle cell proliferation in the genesis of atheroma would contrast with the centrla role played by damaged and permeable endothelium in the propagation of atherogenesis. One might view onset dynamcis and integral constitution of atherogenic pathways in terms particularly of participation of endothelial ulceration, fissureing, thrombosis and intraplque hemorrhage. Neonangiogenesis appears to evolve in terms relatie to centrality of involvement by hypoxia in the subintima.
- complicated plaque
- smooth muscle cells