2013

DOI: 10.1148/radiol.12120499

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Dynamic Contrast-enhanced MR Imaging of Carotid Atherosclerotic Plaque: Model Selection, Reproducibility, and Validation

Michaela Gaens¹,

Walter H. Backes²,

et al.

Abstract: The Patlak model is most suited for describing carotid plaque enhancement. Correlation with histologic findings validated K(trans) as an indicator of plaque microvasculature, and the reproducibility of K(trans) was good.

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The Plaque Neovascularization1

Additional Effects Of Inflammation1

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Cited by 81 publications

(117 citation statements)

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“…49 This technique has been shown to be highly reproducible and reliable. 33 Millon et al demonstrated that neovascularity is seen in up to 97% of areas with Gd enhancement on postcontrast images, whereas macrophage infiltration is seen in 87% of regions of Gd enhancement.…”

Section: 123mentioning

confidence: 99%

Contemporary carotid imaging: from degree of stenosis to plaque vulnerability

³

et al. 2016

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abbreviatioNs AHA = American Heart Association; CAS = carotid artery stenting; CEA = carotid endarterectomy; CEUS = contrast-enhanced ultrasonography; CTA = CT angiography; DCE = dynamic contrast-enhanced; DSCT = dual-source CT; FDG = fluorodeoxyglucose; FSE = fast spin echo; Gd = gadolinium; HU = Hounsfield units; IPH = intraplaque hemorrhage; LRNC = lipid-rich necrotic core; MDCT = multidetector-row CT; MDCTA = MDCT angiography; MES = microembolic signal; MMP-9 = matrix metalloproteinase-9; MRA = MR angiography; PDW = proton density-weighted; SUV = standardized uptake value; SUVmax = maximal SUV; TBR = target-to-background ratio; TCD = transcranial Doppler ultrasonography; TIA = transient ischemic attack; TOF = time of flight; USPIO = ultrasmall superparamagnetic iron oxide. Carotid artery stenosis is a well-established risk factor of ischemic stroke, contributing to up to 10%-20% of strokes or transient ischemic attacks. Many clinical trials over the last 20 years have used measurements of carotid artery stenosis as a means to risk stratify patients. However, with improvements in vascular imaging techniques such as CT angiography and MR angiography, ultrasonography, and PET/CT, it is now possible to risk stratify patients, not just on the degree of carotid artery stenosis but also on how vulnerable the plaque is to rupture, resulting in ischemic stroke. These imaging techniques are ushering in an emerging paradigm shift that allows for risk stratifications based on the presence of imaging features such as intraplaque hemorrhage (IPH), plaque ulceration, plaque neovascularity, fibrous cap thickness, and presence of a lipid-rich necrotic core (LRNC). It is important for the neurosurgeon to be aware of these new imaging techniques that allow for improved patient risk stratification and outcomes. For example, a patient with a low-grade stenosis but an ulcerated plaque may benefit more from a revascularization procedure than a patient with a stable 70% asymptomatic stenosis with a thick fibrous cap. This review summarizes the current state-of-the-art advances in carotid plaque imaging. Currently, MRI is the gold standard in carotid plaque imaging, with its high resolution and high sensitivity for identifying IPH, ulceration, LRNC, and inflammation. However, MRI is limited due to time constraints. CT also allows for high-resolution imaging and can accurately detect ulceration and calcification, but cannot reliably differentiate LRNC from IPH. PET/CT is an effective technique to identify active inflammation within the plaque, but it does not allow for assessment of anatomy, ulceration, IPH, or LRNC. Ultrasonography, with the aid of contrast enhancement, is a cost-effective technique to assess plaque morphology and characteristics, but it is limited in sensitivity and specificity for detecting LRNC, plaque hemorrhage, and ulceration compared with MRI. Also summarized is how these advanced imaging techniques are being used in clinical practice to risk stratify patients with low- and high-grade carotid artery stenosis....

“…49 This technique has been shown to be highly reproducible and reliable. 33 Millon et al demonstrated that neovascularity is seen in up to 97% of areas with Gd enhancement on postcontrast images, whereas macrophage infiltration is seen in 87% of regions of Gd enhancement.…”

Section: 123mentioning

confidence: 99%

Contemporary carotid imaging: from degree of stenosis to plaque vulnerability

³

et al. 2016

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abbreviatioNs AHA = American Heart Association; CAS = carotid artery stenting; CEA = carotid endarterectomy; CEUS = contrast-enhanced ultrasonography; CTA = CT angiography; DCE = dynamic contrast-enhanced; DSCT = dual-source CT; FDG = fluorodeoxyglucose; FSE = fast spin echo; Gd = gadolinium; HU = Hounsfield units; IPH = intraplaque hemorrhage; LRNC = lipid-rich necrotic core; MDCT = multidetector-row CT; MDCTA = MDCT angiography; MES = microembolic signal; MMP-9 = matrix metalloproteinase-9; MRA = MR angiography; PDW = proton density-weighted; SUV = standardized uptake value; SUVmax = maximal SUV; TBR = target-to-background ratio; TCD = transcranial Doppler ultrasonography; TIA = transient ischemic attack; TOF = time of flight; USPIO = ultrasmall superparamagnetic iron oxide. Carotid artery stenosis is a well-established risk factor of ischemic stroke, contributing to up to 10%-20% of strokes or transient ischemic attacks. Many clinical trials over the last 20 years have used measurements of carotid artery stenosis as a means to risk stratify patients. However, with improvements in vascular imaging techniques such as CT angiography and MR angiography, ultrasonography, and PET/CT, it is now possible to risk stratify patients, not just on the degree of carotid artery stenosis but also on how vulnerable the plaque is to rupture, resulting in ischemic stroke. These imaging techniques are ushering in an emerging paradigm shift that allows for risk stratifications based on the presence of imaging features such as intraplaque hemorrhage (IPH), plaque ulceration, plaque neovascularity, fibrous cap thickness, and presence of a lipid-rich necrotic core (LRNC). It is important for the neurosurgeon to be aware of these new imaging techniques that allow for improved patient risk stratification and outcomes. For example, a patient with a low-grade stenosis but an ulcerated plaque may benefit more from a revascularization procedure than a patient with a stable 70% asymptomatic stenosis with a thick fibrous cap. This review summarizes the current state-of-the-art advances in carotid plaque imaging. Currently, MRI is the gold standard in carotid plaque imaging, with its high resolution and high sensitivity for identifying IPH, ulceration, LRNC, and inflammation. However, MRI is limited due to time constraints. CT also allows for high-resolution imaging and can accurately detect ulceration and calcification, but cannot reliably differentiate LRNC from IPH. PET/CT is an effective technique to identify active inflammation within the plaque, but it does not allow for assessment of anatomy, ulceration, IPH, or LRNC. Ultrasonography, with the aid of contrast enhancement, is a cost-effective technique to assess plaque morphology and characteristics, but it is limited in sensitivity and specificity for detecting LRNC, plaque hemorrhage, and ulceration compared with MRI. Also summarized is how these advanced imaging techniques are being used in clinical practice to risk stratify patients with low- and high-grade carotid artery stenosis....

“…MRI also can assess the presence of neovasculature in carotid artery plaques [82][83][84][85]. A recent study by Gaens et al [85] showed that dynamic contrast-enhanced MR of carotid atherosclerotic plaques can assess plaque neovasculature and that the Patlak model is well-suited for describing carotid plaque enhancement; the authors found that the K(trans) is an indicator of plaque microvasculature (validated by histology) and that the reproducibility of K(trans) was good.…”

Section: The Plaque Neovascularizationmentioning

confidence: 99%

Imaging of the Carotid Artery Vulnerable Plaque

Saba¹,

²

,

³

et al. 2013

Cardiovasc Intervent Radiol

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Atherosclerosis involving the carotid arteries has a high prevalence in the population worldwide. This condition is significant because accidents of the carotid artery plaque are associated with the development of cerebrovascular events. For this reason, carotid atherosclerotic disease needs to be diagnosed and those determinants that are associated to an increased risk of stroke need to be identified. The degree of stenosis typically has been considered the parameter of choice to determine the therapeutical approach, but several recently published investigations have demonstrated that the degree of luminal stenosis is only an indirect indicator of the atherosclerotic process and that direct assessment of the plaque structure and composition may be key to predict the development of future cerebrovascular ischemic events. The concept of ''vulnerable plaque'' was born, referring to those plaque's parameters that concur to the instability of the plaque making it more prone to the rupture and distal embolization. The purpose of this review is to describe the imaging characteristics of ''vulnerable carotid plaques.''

“…Among many biological targets implicated in plaque inflammation, macrophages and neovessels have gained broad interest because they are abundant and detectable by clinical imaging modalities such as 18 F-fluorodeoxyglucose (FDG) positron emission tomography (PET) and dynamic contrast-enhanced (DCE) MRI. [3][4][5][6] Increased metabolic activity measured as target-to-background ratio (TBR) is thought to indicate enhanced macrophage recruitment and activation. 3,7 In contrast, the transfer constant (K trans ) in DCE-MRI is considered to reflect microvessel density and permeability.…”

mentioning

confidence: 99%

“…3,7 In contrast, the transfer constant (K trans ) in DCE-MRI is considered to reflect microvessel density and permeability. 5,6 As 2 integral components of the inflammatory process, previous studies have suggested that cellular events, including macrophage recruitment and activation, and vascular adaptation, including angiogenesis and increased permeability, could affect each other during atherogenesis.…”

mentioning

confidence: 99%

Varying Correlation Between ¹⁸ F-Fluorodeoxyglucose Positron Emission Tomography and Dynamic Contrast-Enhanced MRI in Carotid Atherosclerosis

¹

,

²

,

³

et al. 2014

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Background and Purpose— 18 F-fluorodeoxyglucose positron emission tomography and dynamic contrast-enhanced MRI have been proposed to quantitatively assess plaque inflammation by probing macrophages and neovessels, respectively. We examined their correlation to study the in vivo relationship between macrophage and neovessel activities in atherogenesis. Methods— Forty-one patients (34 men; aged 65±12 years) with a total of 68 carotid plaques (thickness ≥2 mm on ultrasound; 20 symptomatic) were assessed by both 18 F-fluorodeoxyglucose positron emission tomography/computed tomography and dynamic contrast-enhanced MRI within 2 weeks, measured as target-to-background ratio and transfer constant ( K trans ), respectively. Results— Overall, the correlation between target-to-background ratio and K trans was weak and marginal ( r =0.22; P =0.068). They were correlated in the symptomatic plaques ( r =0.59; P =0.006) but not in the asymptomatic plaques ( r =0.07; P =0.625; P =0.033 for difference in r ). Neither target-to-background ratio nor K trans was significantly higher in the symptomatic plaques, but both showed an inverse relationship with time since last neurological event ( r =−0.94 and −0.69 for target-to-background ratio and K trans , respectively). Conclusions— The correlation between 18 F-fluorodeoxyglucose positron emission tomography and dynamic contrast-enhanced MRI measurements varied with clinical conditions, pointing to a complex interplay between macrophages and neovessels under different pathophysiological conditions. The moderate correlation shown only in symptomatic plaques indicates the presence of acute plaque inflammation with increased metabolic activity and cytokine production by inflammatory cells.

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