**14. Permissiveness**

In such events promotional permissiveness would prove a determining series of further pro‐ gression that calls into operative persistence the effects of hypoxia and of disturbed blood flow that primarily target the endothelial cell bed.

Extension, both laterally and also deeply into the vascular wall, requires the activation of response elements such as the shear stress response element that augments the distribution‐ al disturbance of interaction of tonicity of the vascular wall with disturbed dynamics of blood flow.

This phenomenon appears to augment further susceptibility to pro-inflammatory reactivity in the wake of an enlarging plaque that increasingly constitutes the phenotypic switching of such cell types as smooth muscle cells. Also, remodelling of the intima is both accumulative of proteoglycans and also modulatory in adapting to new blood flow dynamics.

Substantial reconstitution of the vessel wall, hence, is attempted in the form of replacement dynamics in the vascular wall in a manner that attempts the normalization, to some extent, of dynamics of blood flow. The adhesive molecules that are increasingly expressed on acti‐ vated and dysfunctional endothelial cells allow for the ingress of leukocytes such as mono‐ cytes and memory T lymphocytes in the face of destruction of the vascular wall. Such parametric phenomena are paralleled by the procoagulant pathways that create and deposit thrombus on the surface of the complicated or ulcerated atherosclerotic plaque.

tributional series of phenomena come to model the individual lesion as hypoxic condition‐ ing of the micro-environment and of attempts at neovascularization at the base of the lesion.

Attributes of Hypoxic Preconditioning Determine the Complicating Atherogenesis of Plaques

http://dx.doi.org/10.5772/51127

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Developmental dynamics hence are paramount considerations in the evaluation of a specific plaque dimensionality. The overall conformations of lesions are centrally operative but dy‐ namically progressive in the face of both accumulative and transforming pathways of ago‐ nist action and response adaptations. Hyperinsulinemia appears to promote macrophage foam

Hypoxia is generated as a primary abnormality of the endothelium and as further propagat‐

The parameters of further development of the injury to the endothelium allow for interface dynamics with abnormal blood flow that generate a secondary wave of proportional ampli‐ tude within the enlarging atherosclerotic plaque that evolves primarily as an end-stage com‐

Distributional forces are driven by a series of hypoxic preconditions that promotes the char‐ acterization of individual lesions within context of further lesion infliction in other regions of the endothelium. It is such premise that accounts for a multiplicity of events that create a multifocal representation of atherosclerosis within the arterial vascular system, as denoted by parameters of blood flow dynamics and as hypoxia-driven plastic effects on the endothelium.

It is in such manner that paramount representative pathways conform to a response to in‐ jury and also to primary agonistic action of a hypoxic conditioning of the microenvironment

Serial insult modulation of pathways include the re-establishment of multiple injuries to the endothelium that are essentially hypoxic in origin and which conform to the development of the plaque as primary emergent form of adaptation to endothelial involvement in particular.

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.

cell formation and may thus promote atherogenesis in type-2 diabetics [27].

ed via the vasa vasorum supplying the vascular wall.

of both endothelium and vascular intima.

**17. Concluding remarks**

**16. Hypoxia**

plicated plaque lesion.

In such manner of progression, primary systems of permissiveness implicate a plasticity that is morphologically mirrored in dynamics of involvement of the plaque by the neovascula‐ ture invading the base of the plaque. It is in terms of ongoing incremental dynamics that the essential morphological and dysfunctional attributes of a modelled plaque lesion come to re‐ constitute a focal lesion of dimensional origin within the vascular intima but that eventually progresses as luminal stenosis and plaque rupture.

The multiplicity of plaque creation in the vascular intima denotes an ongoing cooperative series of disturbances emanating from significant exposure of the endothelium to such le‐ sional promotional events as hypoxia and as further derived phenomena of a disturbed blood flow pattern. In such manner, the incremental mirroring of patterned progression in multiple plaques would correspond to representative further permissiveness in the face of increasing destruction of the vascular wall. High density lipoprotein reverses cholesterol transport and normalizes vascular function, in addition to antioxidative anti-inflammatory and anti-apoptotic actions [21].

Developmental aggregation of events hence is formulated as eventually complicated pla‐ ques that formulate thrombogenesis and deposition on the ulcerative but enlarging or com‐ plicated plaque.

Simple realization of events in plaque rupture comes to constitute a patterned progression that is transforming and which allows for the plasticity of reconstitutive pathways to emerge as complications of the atherosclerotic plaque.

It is perhaps in terms of significant interplay of multiple attempts at removal of oxidized lip‐ oprotein that the dimensions of attempted reconstitution of the vascular wall come to opera‐ tively include a pro-inflammatory component in further promoting normalization of blood flow dynamics.
