**1. Introduction**

Atherogenesis constitutes a prominent mechanism in inducing stenosis of the vascular lu‐ men by multiple mechanisms within contextual reference of heterogeneity of pathways and phenotype determinants. Reduction of low-density lipoprotein-C has well-established value and constitutes a major guideline for cardiovascular disease prevention [38]. Redox state im‐ balance plays a role in preclinical atherosclerosis [7]. The realization of events constituting the acute coronary syndromes is particularly critical in the evolution of lesions that further compromise blood supply to target tissues. It is highly significant to consider the distribu‐ tion of individual lesions with reference to disturbed blood flow patterns within the vascu‐ lar arterial tree, as further evidenced by selectivity to vascular branch points. Disturbed flow may hinder transport of nitric oxide particularly distal to a stenosis [17].

Evidential parameters confirm a primarily quantitative series of dimensional effects that participates in the development of lesions and that ranges from constitutional progression to environmental gene promotion particularly in the activation and dysfunction of endothe‐ lial cells.

High density lipoprotein has a wide range of functions including antiatherogenic, anti-in‐ flammatory and anti-oxidant action [30].

In such manner, also a highly heterogeneous series of conditioning influences participate in inducing not only the creation of individual atherosclerotic plaques but also the evolution of such plaques to unstable lesions inducing acute coronary events. Molecular mediators in‐ clude members of the chemokine family of leukocyte chemoattractants and their G proteincoupled receptors [37].

© 2013 Agius; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Distributional patterns of lesion infliction correlate also with procoagulant effects that system‐ ically compromise recoverability from injury to various components of the vascular wall.

may necessitate new UPS-based therapeutic modalities [29]. Indeed, the very identity of the dysfunctional state of overlying endothelial cells may prove a derived parameter of conse‐ quence within systems of active remodelling of the intima as induced by such phenotypic

Attributes of Hypoxic Preconditioning Determine the Complicating Atherogenesis of Plaques

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

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Aldose reductase in the polyol pathway promotes excessive accumulation of intracellular re‐

The systems of promotional realization of injury as induced by atherosclerotic plaques are a significant compound system that incriminates adhesion of monocytes to dysfunctional or

The participation of injury to the arterial wall is complex and acts as a series of overlapping influences that further contributes to injury as evidenced by the action of evolving hypoxic influence and by procoagulant activity. Almost all coagulant proteins including tissue factor are found in atherosclerotic plaques [19]. Low matrix metalloproteinase-2 levels correlate

The overlapping series of dynamic events in atherogenesis is permissive in promoting a pathway realization that is central to hypoxia inducing further progression of the lesions. High glycemic load glycemic index are related to significantly increased risk for atherogene‐

In such manner, the promotional distributional significance of concurrent foci of injury is paramount parameter in inducing the characterization of lesions that essentially progress. Toll-like receptor signalling may link chronic inflammation with cardiovascular disease pro‐

It is significant to view the parameters of quantitative nature in the development of individ‐ ual lesions that hemodynamically are closely related often to disturbed blood flow at vascu‐

It is with referential background components of various identifiable elements of the vascular wall that atherogenesis proves an integrative phenomenon of progression in its own right. High density lipoprotein particle functionality is at least as important as HDL-C levels due

The individual participating roles played by such processes as monocyte rolling and subse‐ quent firm adhesion to endothelial cells helps characterize specific attributes of the activated or dysfunctional endothelium. The decreased production of nitric oxide by dysfunctional

shifts in activity of smooth muscle cells in particular.

with intra-cranial location of atherosclerosis [15].

**4. Injury**

activated endothelium.

sis in women in particular [20].

gression and immune activation [31].

to effects on inflammation, hemostasis and apoptosis [22].

**5. Progression**

lar branch points.

active oxygen species in various tissues of diabetic patients [34].
