**16. Hypoxia**

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

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

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

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

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

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

The thrombus that is deposited on the surface of plaques is also an attempt at streamlining the luminal contours of the vessel wall in an attempt to accommodate new flow dynamics.

The response to injury hypothesis only partly accounts for the pathogenesis of an athero‐ sclerotic plaque that is centered on a core of involvement of the vascular intima. It is the ad‐ ditional formulation of a hypoxic micro-environment that further proves a driving initiative in the development of serial plastic events that conformationally confirm the dimensions of a plaque reconstitution at the interface of abnormal blood flow dynamics. Hence, the redis‐

thrombus on the surface of the complicated or ulcerated atherosclerotic plaque.

progresses as luminal stenosis and plaque rupture.

emerge as complications of the atherosclerotic plaque.

and anti-apoptotic actions [21].

plicated plaque.

246 Current Trends in Atherogenesis

flow dynamics.

**15. Thrombosis**

Hypoxia is generated as a primary abnormality of the endothelium and as further propagat‐ ed via the vasa vasorum supplying the vascular wall.

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‐ plicated plaque lesion.

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 of both endothelium and vascular intima.

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.
