**6. Complicated plaque**

The complicated atherosclerotic plaque is thus a series of overlying pathways of influence that concurrently participate in identifying the different component systems in pathogene‐ sis. Regulating T cells and serum interleukin-10 may exert a protective role against plaque rupture in patients with coronary atherosclerosis [11]. It is with contextual reference to oxi‐ dized lipoprotein deposits within the intima that phenomena of adherence to dysfunctional endothelium induce leukocytes as systemic agonists in atherogenesis. The role of platelets in atherothrombosis is well established [9].

The sharp distinction in identification of progression of an individual plaque from the rup‐ tured plaque permits the emergence of multiple profiles in developmental history of lesions that individually evolve but that are systemically compounding and overlapping in profile determination. NF-E2 related factor 2 pathway restores redox homeostasis and Nrf2 cross talks with the proteasome [4].

The realization of injury to endothelial cells is therefore only an initial event in the once-real‐ ized reactivity to injury to multiple components of the vascular wall.

The dynamics of orchestration of various injurious agonists thus emerge as an essential component system in atherogenesis in a manner that calls into operative participation multi‐ ple heterogeneous pathways ranging from procoagulant effect of disturbed blood flow, hy‐ poxia, dysfunctional reduction in nitric oxide production and action, and especially the chemotactic influences as induced by oxidized lipoproteins deposited in the intima. Arachi‐ donic acid increases inflammation and enhances the ability of endothelial cells to bind mon‐ ocytes in vivo [12]. The further participation of remodelling of the intima as a result of migration and proliferation of smooth muscle cells is evidence for a series of phenotypic switches that allow permissive injury to multiple cell components and to matrix production of proteoglycans.

It is within a systemically integrative series of active realizations that atherogenesis proves an integrative expression of component pathways; this paradoxically determines a com‐ pound pathobiologic profile that is individually determined by constituent components of the vascular wall affected. Macrophages are exquisitely sensitive to their microenvironment, influencing plaque rupture and thrombosis [40].

It is therefore in terms of quantitative realization that atherogenesis is both initiating and progressive influence in the determination of profile progression of the individual athero‐ sclerotic plaque.
