A focal lesion of the intimal layer structured with a lipid core encased in a fibrous cap and surrounded by endothelium is named atherosclerotic plaque.
On the basis of its morphology such a lesion is called "stable" when it presents a small amount of lipids and a large quantity of smooth muscle cells and collagen.
This type of plaque is protected from disruption by its own structure, fibrous and homogeneous.
When a plaque is defined "unstable", it shows a thin, fibrous cap and a large, soft core of extra-cellular lipids with a small amount of smooth muscle cells.
This type of plaque has a natural tendency to expand or to develop thrombotic complications.
The inflammatory reaction of the plaque is provoked and kept under control by a lot of macrophages, T lymphocytes, dendritic cells and mast cells.
The consequent production of pro-inflammatory cytokines and proteases leads to the fibrous cap degradation.
In a "vulnerable" plaque neovessels formation may often and easily occur with subsequent plaque bleeding and final acute breakup.
As these microvessels are usually accompanied by a large amount of adhesion molecules and infiltrates of inflammatory cells, they are suspected of recruiting leukocytes inside the lesion.
Even a slight flaw in the fibrous cap makes the lipid core be exposed to the blood stream with a consequent massive activation of the clotting system usually resulting in the complete thrombotic occlusion of the vessel. Plaque vulnerability is generally linked to some inflammatory factors (such as Matrix Metalloproteinases, High Sensitivity C reactive protein) while plaque instability is often correlated to shear stress.
Bearing in mind that "shear" is the friction exerted by the blood flow across an area, the risk of arterial damage and of plaque instability increases in patients with low wall shear as a consequence of higher fluid resonance time, of major platelet and macrophages adhesion to the arterial wall and modulation of platelet-derived growth factor.
Neovascularization seems to be another factor linked to plaque instability and vasavasorum is involved as the cause of atherosclerotic plaque growth.
Plaque morphology can be studied in vivo thanks to B-mode ultrasound (US), high resolution magnetic resonance (MRI), spiral computer tomography (CT) and positron emission tomography (PET).
A connection between echogenicity and histopathologic features has been studied and reported in literature: intraplaque haemorrhage and lipids make a plaque hypoechoic and heterogeneous while a fibrous plaque appears to be hyperechoic and homogeneous.
Plaque echodensity can be evaluated quantitatively using standardized US imaging and digital post-processing by means of the Gray Scale Median (GSM). GSM value higher than 25 is associated with stable plaque morphology. GSM value lower than 25 is associated with low echogenicity (echolucency), with complex plaque composition and with a serious risk for neurological problems.
The plaque components (necrotic core and fibrous cap) can be easily identified and assessed qualitatively through High Resolution MRI that is of great help to provide detailed images of the plaque composition.
To obtain image contrast, targeted (super paramagnetic iron oxide nanoparticles and gadolinium chelates) and "activatable" MRI agents are essential for exploiting molecular target or cellular processes: these agents allow to enhance the inflammation areas inside the plaque and to pick out microthrombus or neovascularization.
CT scan with or without contrast media injection allows to spot plaque liquid content. The presence of calcium inside the plaque can arise a technical problem referred to as "shadowing" because it makes more difficult to evaluate the stenosis and the plaque components.
PET scanning is a highly sensitive imaging modality good for detecting inflammation in an atherosclerotic plaque because captation increases remarkably (hypercaptation).
The emerging field of molecular imaging that aims at the study of pathologic molecular and cellular mechanisms present in the plaque has proven really useful for discovering the atherosclerotic disease at an early stage, for stratifying the different disease subsets and for monitoring the efficacy of medical therapy.

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