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Use of Contrast-Enhanced Ultrasound in Carotid Atherosclerotic Disease: Limits and Perspectives.

Varetto G, Gibello L, Castagno C, Quaglino S, Ripepi M, Benintende E, Gattuso A, Garneri P, Zan S, Capaldi G, Bertoldo U, Rispoli P - Biomed Res Int (2015)

Bottom Line: The purpose of this review is to collect all the original studies available in literature (24 studies with 1356 patients enrolled) and to discuss the state of the art, limits, and future perspectives of CEUS analysis.The results of this work confirm the reliability of this imaging study for the detection of plaques with high risk of embolization; however, a shared, user-friendly protocol of imaging analysis is not available yet.The definition of this operative protocol becomes mandatory in order to compare results from different centers and to validate a cerebrovascular risk stratification of the carotid atherosclerotic lesions evaluated with CEUS.

View Article: PubMed Central - PubMed

Affiliation: Division of Vascular Surgery, Department of Surgical Sciences, University of Turin, Azienda Ospedaliera Universitaria Città della Salute e della Scienza, Molinette Corso Bramante 88, 10126 Torino, Italy.

ABSTRACT
Contrast-enhanced ultrasound (CEUS) has recently become one of the most versatile and powerful diagnostic tools in vascular surgery. One of the most interesting fields of application of this technique is the study of the carotid atherosclerotic plaque vascularization and its correlation with neurological symptoms (transient ischemic attack, minor stroke, and major stroke) and with the characteristics of the "vulnerable plaque" (surface ulceration, hypoechoic plaques, intraplaque hemorrhage, thinner fibrous cap, and carotid plaque neovascularization at histopathological analysis of the sample after surgical removal). The purpose of this review is to collect all the original studies available in literature (24 studies with 1356 patients enrolled) and to discuss the state of the art, limits, and future perspectives of CEUS analysis. The results of this work confirm the reliability of this imaging study for the detection of plaques with high risk of embolization; however, a shared, user-friendly protocol of imaging analysis is not available yet. The definition of this operative protocol becomes mandatory in order to compare results from different centers and to validate a cerebrovascular risk stratification of the carotid atherosclerotic lesions evaluated with CEUS.

No MeSH data available.


Related in: MedlinePlus

(a) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing the close correlation between plaque vascularization and the inflammatory response. (b) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing larger microvessels (red arrows) and areas of plaque hemorrhage.
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fig1: (a) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing the close correlation between plaque vascularization and the inflammatory response. (b) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing larger microvessels (red arrows) and areas of plaque hemorrhage.

Mentions: The inflammatory etiopathogenesis of atherosclerosis has been widely demonstrated in several animal models and later confirmed in human models [7]. In particular at the level of flow turbulence along the vascular tree (vessel bifurcation), the subintimal deposition of cholesterol and oxidized lipoproteins generates an inflammatory response with the recruitment of white blood cells, primarily macrophages, and the production of cytokines and enzymes. Among different cellular responses to the inflammatory stimulus there is the liberation from the smooth muscles cells of vascular endothelial growth factor (VEGF) with the consequent activation of neoangiogenesis of the vessel wall (Figure 1). The newly formed vessels inside the atherosclerotic plaque however are immature and leaky due to reduced gap junctions, thus serving as a port of entry for other inflammatory cells, lipids, and even red blood cells, which contribute to plaque growth. In the same contest macrophages produce metalloproteinases, like MMP-9 and other collagenases that destroy the connective fibrous tissue, thus stimulating the neovessels growth [8]. All these plaque changes lead to a vulnerable atherosclerotic plaque [7]. It is common experience in clinical practice that irregular, ulcerated plaque surfaces, lipid necrotic core, thin fibrous cap, anechoic-hypoechoic appearance, and intraplaque neovessels characterize potentially unstable atherosclerotic lesions with high risk of embolization and thrombosis. However, it is common experience that not all the atherosclerotic lesions behave in the same way. In fact some of them react to the inflammation stimulus with the precipitation of calcium salts (calcific plaques) and others with the simple transformation of muscular cells into connective cells (fibrous plaques). The exact mechanism of differentiation of the plaque is still partially unknown but some factors, such as genetic predisposition, uncontrolled risk factors like smoke, diabetes mellitus, hypertension, and dyslipidemia, may influence the process.


Use of Contrast-Enhanced Ultrasound in Carotid Atherosclerotic Disease: Limits and Perspectives.

Varetto G, Gibello L, Castagno C, Quaglino S, Ripepi M, Benintende E, Gattuso A, Garneri P, Zan S, Capaldi G, Bertoldo U, Rispoli P - Biomed Res Int (2015)

(a) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing the close correlation between plaque vascularization and the inflammatory response. (b) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing larger microvessels (red arrows) and areas of plaque hemorrhage.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4491377&req=5

fig1: (a) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing the close correlation between plaque vascularization and the inflammatory response. (b) Histopathological preparation of a carotid atherosclerotic plaque colored with CD31 endothelial-specific stain (brown) showing larger microvessels (red arrows) and areas of plaque hemorrhage.
Mentions: The inflammatory etiopathogenesis of atherosclerosis has been widely demonstrated in several animal models and later confirmed in human models [7]. In particular at the level of flow turbulence along the vascular tree (vessel bifurcation), the subintimal deposition of cholesterol and oxidized lipoproteins generates an inflammatory response with the recruitment of white blood cells, primarily macrophages, and the production of cytokines and enzymes. Among different cellular responses to the inflammatory stimulus there is the liberation from the smooth muscles cells of vascular endothelial growth factor (VEGF) with the consequent activation of neoangiogenesis of the vessel wall (Figure 1). The newly formed vessels inside the atherosclerotic plaque however are immature and leaky due to reduced gap junctions, thus serving as a port of entry for other inflammatory cells, lipids, and even red blood cells, which contribute to plaque growth. In the same contest macrophages produce metalloproteinases, like MMP-9 and other collagenases that destroy the connective fibrous tissue, thus stimulating the neovessels growth [8]. All these plaque changes lead to a vulnerable atherosclerotic plaque [7]. It is common experience in clinical practice that irregular, ulcerated plaque surfaces, lipid necrotic core, thin fibrous cap, anechoic-hypoechoic appearance, and intraplaque neovessels characterize potentially unstable atherosclerotic lesions with high risk of embolization and thrombosis. However, it is common experience that not all the atherosclerotic lesions behave in the same way. In fact some of them react to the inflammation stimulus with the precipitation of calcium salts (calcific plaques) and others with the simple transformation of muscular cells into connective cells (fibrous plaques). The exact mechanism of differentiation of the plaque is still partially unknown but some factors, such as genetic predisposition, uncontrolled risk factors like smoke, diabetes mellitus, hypertension, and dyslipidemia, may influence the process.

Bottom Line: The purpose of this review is to collect all the original studies available in literature (24 studies with 1356 patients enrolled) and to discuss the state of the art, limits, and future perspectives of CEUS analysis.The results of this work confirm the reliability of this imaging study for the detection of plaques with high risk of embolization; however, a shared, user-friendly protocol of imaging analysis is not available yet.The definition of this operative protocol becomes mandatory in order to compare results from different centers and to validate a cerebrovascular risk stratification of the carotid atherosclerotic lesions evaluated with CEUS.

View Article: PubMed Central - PubMed

Affiliation: Division of Vascular Surgery, Department of Surgical Sciences, University of Turin, Azienda Ospedaliera Universitaria Città della Salute e della Scienza, Molinette Corso Bramante 88, 10126 Torino, Italy.

ABSTRACT
Contrast-enhanced ultrasound (CEUS) has recently become one of the most versatile and powerful diagnostic tools in vascular surgery. One of the most interesting fields of application of this technique is the study of the carotid atherosclerotic plaque vascularization and its correlation with neurological symptoms (transient ischemic attack, minor stroke, and major stroke) and with the characteristics of the "vulnerable plaque" (surface ulceration, hypoechoic plaques, intraplaque hemorrhage, thinner fibrous cap, and carotid plaque neovascularization at histopathological analysis of the sample after surgical removal). The purpose of this review is to collect all the original studies available in literature (24 studies with 1356 patients enrolled) and to discuss the state of the art, limits, and future perspectives of CEUS analysis. The results of this work confirm the reliability of this imaging study for the detection of plaques with high risk of embolization; however, a shared, user-friendly protocol of imaging analysis is not available yet. The definition of this operative protocol becomes mandatory in order to compare results from different centers and to validate a cerebrovascular risk stratification of the carotid atherosclerotic lesions evaluated with CEUS.

No MeSH data available.


Related in: MedlinePlus