The utility of ultrasound and computed tomography in the assessment of carotid artery plaque vulnerability–A mini review

Singh, Aniruddha; Nasir, Usama; Segal, J.; Waheed, Tayyab Ali; Ameen, Muhammad; Hafeez, Hamza

doi:10.3389/fcvm.2022.1023562

Cited by 6 publications

(4 citation statements)

References 53 publications

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“…Several scores have been proposed. In the Gray Weale-Nicolaides (GWN) classification lipid-rich plaques appear echolucent, while those with fibrous and calcific content appear echogenic [ 74 , 75 ]. The Gray Scale Median (GSM) score constitutes the quantified measurement of plaque echogenicity and an important, objective, valid, marker of carotid plaque vulnerability [ 76 ] associated with increased cardiovascular mortality [ 77 ].…”

Section: Detection Of Arterial and Atherosclerotic Calcificationmentioning

confidence: 99%

The Complex Mechanisms and the Potential Effects of Statins on Vascular Calcification: A Narrative Review

Kadoglou,

Stasinopoulou,

Velidakis

et al. 2024

Rev. Cardiovasc. Med.

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Vascular calcification (VC) is a complex process of calcium deposition on the arterial wall and atherosclerotic plaques and involves interaction between vascular smooth muscle cells, inflammatory and VC mediators. The latter are independent predictors of cardiovascular morbidity and mortality and potential targets of pharmaceutical therapy. This paper is a narrative review of the complex mechanisms of VC development and in this context the potential anti-atherosclerotic effects of statins. At the initial stages of atherosclerosis VC correlates with atherosclerosis burden and in the long-term with cardiovascular morbidity and mortality. A plethora of animal and clinical studies have proposed statins as the cornerstone of primary and secondary prevention of atherosclerotic cardiovascular disease. Based on coronary computed tomography data, high doses of statins may have negligible or even positive effects on the progression of coronary artery calcification. Growing data support an increase in atherosclerotic plaque calcification in peripheral arteries (e.g., carotids), after long-term, statin-therapy. Despite the paradox of increasing VC, those effects of statins have been associated with higher plaque stability, reducing the risk of consequent adverse events. Statins seem to promote a “favorable” atherosclerotic calcification, suppressing atherosclerotic lesion expansion and their vulnerability. More studies are required to clarify the underlying mechanisms.

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Section: Detection Of Arterial and Atherosclerotic Calcificationmentioning

confidence: 99%

The Complex Mechanisms and the Potential Effects of Statins on Vascular Calcification: A Narrative Review

Kadoglou,

Stasinopoulou,

Velidakis

et al. 2024

Rev. Cardiovasc. Med.

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“…The development of new pathological capillaries promotes macrophage infiltration, inflammation, and lipid deposition as well as intraplaque hemorrhages that contribute to a progressive increase in the instability of plaques [37]. A rupture is commonly found in the plaques where the fibrous cap thickness is less than 0.065 mm and the lipid core volume constitutes 40% of the total plaque volume [38]. Also, an intraplaque hemorrhage is considered to be a risk factor for plaque rupture [39,40].…”

Section: Vulnerable Plaquesmentioning

confidence: 99%

“…It uses a grading system based on echogenicity that classifies atherosclerotic plaques into five types. Type 1 is uniformly echolucent and mostly composed of lipid and necrotic components; type 2 is predominantly echolucent, with small areas of echogenicity caused by calcifications of up to 25% of the plaque volume; type 3 is predominantly echogenic, with small areas of echolucency and calcifications that consist of up to 50% of the plaque volume; type 4 is uniformly echogenic due to calcification of over 50% of the volume; and type 5 consists of plaques that cannot be classified owing to heavy calcification and acoustic shadows [38]. Hypoechoic plaques (types 1 and 2) (Figure 1) are associated with intraplaque hemorrhages and lipid accumulation, whereas hyperechoic homogeneous plaques are predominantly fibrous or calcified in nature [64].…”

Section: Gray-weale-nicolaides Scalementioning

confidence: 99%

Contrast-Enhanced Ultrasound Feasibility in Assessing Carotid Plaque Vulnerability—Narrative Review

Kopyto,

Czeczelewski,

Mikos

et al. 2023

JCM

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The risk assessment for carotid atherosclerotic lesions involves not only determining the degree of stenosis but also plaque morphology and its composition. Recently, carotid contrast-enhanced ultrasound (CEUS) has gained importance for evaluating vulnerable plaques. This review explores CEUS’s utility in detecting carotid plaque surface irregularities and ulcerations as well as intraplaque neovascularization and its alignment with histology. Initial indications suggest that CEUS might have the potential to anticipate cerebrovascular incidents. Nevertheless, there is a need for extensive, multicenter prospective studies that explore the relationships between CEUS observations and patient clinical outcomes in cases of carotid atherosclerotic disease.

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“…In fact, CT is considered to be the most effective imaging technique for identifying calcification in carotid plaques [ 133 ]. On CT, a soft plaque is generally defined as a low-attenuation plaque with approximately <60 HU, whereas fibrous tissue is considered to be between 60–130 HU and >130 HU is considered to be a calcified plaque [ 134 ]. However, there is significant overlap in HU values among LRNC, connective tissue, and IPH, and the presence of calcification artifact limits its usefulness in plaque analysis [ 131 , 135 ].…”

Section: Biomarkers Of Non-invasive Imagingmentioning

confidence: 99%

Novel Imaging-Based Biomarkers for Identifying Carotid Plaque Vulnerability

et al. 2023

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Carotid artery disease has traditionally been assessed based on the degree of luminal narrowing. However, this approach, which solely relies on carotid stenosis, is currently being questioned with regard to modern risk stratification approaches. Recent guidelines have introduced the concept of the “vulnerable plaque,” emphasizing specific features such as thin fibrous caps, large lipid cores, intraplaque hemorrhage, plaque rupture, macrophage infiltration, and neovascularization. In this context, imaging-based biomarkers have emerged as valuable tools for identifying higher-risk patients. Non-invasive imaging modalities and intravascular techniques, including ultrasound, computed tomography, magnetic resonance imaging, intravascular ultrasound, optical coherence tomography, and near-infrared spectroscopy, have played pivotal roles in characterizing and detecting unstable carotid plaques. The aim of this review is to provide an overview of the evolving understanding of carotid artery disease and highlight the significance of imaging techniques in assessing plaque vulnerability and informing clinical decision-making.

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The utility of ultrasound and computed tomography in the assessment of carotid artery plaque vulnerability–A mini review

Cited by 6 publications

References 53 publications

The Complex Mechanisms and the Potential Effects of Statins on Vascular Calcification: A Narrative Review

The Complex Mechanisms and the Potential Effects of Statins on Vascular Calcification: A Narrative Review

Contrast-Enhanced Ultrasound Feasibility in Assessing Carotid Plaque Vulnerability—Narrative Review

Novel Imaging-Based Biomarkers for Identifying Carotid Plaque Vulnerability

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