**17. Concluding remarks**

The distributional anatomy of the individual atheromatous plaque is consistently repro‐ duced in multiple regions of the arterial vascular tree and in a manner of conformational re-establishment of lesions as hypoxia of the endothelium and as dynamics of abnormal blood flow. In such manner, the constituent representations of micro-environment pre-con‐ ditioning is paramount driving force in the creation of an essential plaque that conforma‐ tionally further propagates as multiple other plaques. The individuality of the plastic events in atherogenesis relate to vascular wall injury and to destruction within the contextual further evolution of lipoprotein core formation and as a series of potential complications. The neovascularization events are responsive elements to a hypoxia generated within the intima and affecting in particular the endothelial cells. Such endothelium is both activat‐ ed to express adhesion molecules and also dysfunctional with particular reduction in ni‐ tric oxide production.

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The further amplification of vascular wall injury is indicative of parameters of parallel but overlapping proportions in the creation of a highly plastic series of preconditioned microenvironments. It is in terms not only of a response to injury but also of a series of reactivities to hypoxia to the endothelium and intima that atherosclerosis proves a self-progressive lesion.

The dynamics of abnormal blood flow are constituent parameters to which the emergent plaque conforms to in partial manner. The neovascularization of the lesion core adopts the contextual conformation that responds to hypoxia and evolving enlargement of the individ‐ ual atherosclerotic plaque.
