Morphology of Atherosclerotic Plaque: Its Feature by Imaging Study

Abstract

Atherosclerotic plaque plays a crucial role for the development of ischaemic diseases and, therefore, its early diagnosis and feature can help to reduce the incidence of cardiovascular events. Detection of early atherogenesis and characterization of plaque feature are the major end-points of research in cardiovascular imaging. Different techniques have been proposed as instrument for morphological and functional study of vascular walls. The purpose of this review is to underline the possibility of in vivo detecting the different stages of atherogenesis by using imaging techniques as well as their relationship with other risk factors in an attempt to assess the meaning of vascular lesions. Very promising results seem to emerge by the analysis of the literature on the subject, although different patterns are yet to be clarified.

Understanding Atherosclerosis Pathophysiology: Can Additive Manufacturing Be Helpful?

“…Atherosclerosis is a chronic systemic inflammatory disease [ 23 ] associated with plaque accumulation within the vessel wall and characterized by intramural lipid retention coupled with inflammation and dyslipidemia [ 20 ]. Inflammation is, indeed, a critical event involved in the pathological process of atherosclerosis [ 24 ].…”

“…Just as with every vascular disease, the initial stage of atherosclerosis is triggered by a disturbance in blood flow, caused mainly by the exposition to different cardiovascular risk factors, external stimuli, or damage, that leads to a drastic change in the expression of regulatory molecules and a subsequent unbalanced release of pro- and anti-inflammatory factors, which in turn activates the endothelium [ 23 , 24 ].…”

“…Endothelial activation is nothing more than a loss of normal homeostatic properties of the endothelium, and it is a phenomenon associated with several activities: (1) the recruitment of immune cells, like monocytes and leukocytes; (2) the secretion of inflammatory cytokines and growth factors; and (3) the release of prothrombotic mediators and platelet activation that confers a procoagulant status instead of a normal anticoagulant response [ 3 ]. Parallelly, the permeability of the endothelial monolayer is altered, favoring the transmigration of leucocytes within the subendothelial space [ 23 ]. The persistence of the inflammatory response within the subendothelial space instigates the migration and proliferation of SMCs that become intermixed with the inflammation area, progressively thickening the vessel wall [ 3 , 23 ].…”

“…Parallelly, the permeability of the endothelial monolayer is altered, favoring the transmigration of leucocytes within the subendothelial space [ 23 ]. The persistence of the inflammatory response within the subendothelial space instigates the migration and proliferation of SMCs that become intermixed with the inflammation area, progressively thickening the vessel wall [ 3 , 23 ]. This pro-inflammatory environment also promotes the oxidation of low-density lipoproteins (LDLs) previously accumulated in the vessel wall (specifically in the tunica intima) due to endothelial activation.…”

“…This pro-inflammatory environment also promotes the oxidation of low-density lipoproteins (LDLs) previously accumulated in the vessel wall (specifically in the tunica intima) due to endothelial activation. Oxidized LDL (oxLDL) are engulfed by monocyte-derived macrophages through phagocytosis, and the retention of oxLDL in the cytoplasm transforms macrophages into lipid-filled foam cells [ 26 ], constituting the core of atheroma [ 23 ]. The necrotic lipid core comprises foam cells, cellular debris, and extracellular lipids and is surrounded by a fibrous cap.…”