Carotid Plaque Inflammation Assessed with <sup>18</sup>F-FDG PET/CT is Higher in Symptomatic Compared with Asymptomatic Patients

Skagen, Karolina; Johnsrud, Kjersti; Evensen, Kristin; Scott, Helge; Krohg‐Sørensen, Kirsten; Reier-Nilsen, Frode; Revheim, Mona-Elisabeth; Fjeld, Jan Gunnar; Skjelland, Mona; Russell, David

doi:10.1111/ijs.12430

Cited by 45 publications

(66 citation statements)

References 33 publications

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“…We know that excised plaques both shrink 17 and may be partly damaged. 17,25 The strength of our study was the close timing between the PET examinations and the endarterectomies. Our study patients had plaques not only presumed highly inflammatory giving recent symptoms, but also plaques removed prophylactically from asymptomatic patients.…”

Section: Discussionmentioning

confidence: 99%

“…assessment on selected sections from this study cohort and found that the amount of inflammatory cells was in the same 5% category at both assessments for 73% of the sections (Kappa = 0.73). 25 The amount of inflammation per plaque was 6.8% (SD 4.0; range 0.4-17.9).…”

Section: Endarterectomy and Histological Analysismentioning

confidence: 94%

“…The histological analysis has been described previously. 25 In brief, plaques were removed en bloc at carotid endarterectomy, fixed in 4% formaldehyde, decalcified in ethylenediaminetetraacetic acid, and cut into 2-to 3-mm slices. After dehydration, the slices were embedded in paraffin and a 5-lm histological section from each slice was cut and stained with hematoxylin and eosin (H&E).…”

Section: Endarterectomy and Histological Analysismentioning

confidence: 99%

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18F-FDG PET/CT for the quantification of inflammation in large carotid artery plaques

Johnsrud

Skagen

Seierstad

et al. 2019

Journal of Nuclear Cardiology

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Background. There is currently no consensus on the methodology for quantification of 18 F-FDG uptake in inflammation in atherosclerosis. In this study, we explore different methods for quantification of 18 F-FDG uptake in carotid atherosclerotic plaques and correlate the uptake values to histological assessments of inflammation.Methods and Results. Forty-four patients with atherosclerotic stenosis ‡70% of the internal carotid artery underwent 18 F-FDG PET/CT. Maximum standardized uptake values (SUV max ) from all plaque-containing slices were collected. SUV max for the single highest and the mean of multiple slices with and without blood background correction (by subtraction (cSUV) or by division (target-to-background ratio (TBR)) were calculated. Following endarterectomy 30 plaques were assessed histologically. The length of the plaques at CT was 6-32 mm. The 18 F-FDG uptake in the plaques was 1.15-2.66 for uncorrected SUVs, 1.16-3.19 for TBRs, and 0.20-1.79 for cSUVs. There were significant correlations between the different uptake values (r 5 0.57-0.99, P < 0.001). Methods with and without blood background correction showed similar, moderate correlations to the amount of inflammation assessed at histology (r 5 0.44-0.59, P < 0.02).Conclusions. In large stenotic carotid plaques, 18 F-FDG uptake reflects the inflammatory status as assessed at histology. Increasing number of PET slices or background correction did not change the correlation. (J Nucl Cardiol 2017)

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Section: Discussionmentioning

confidence: 99%

Section: Endarterectomy and Histological Analysismentioning

confidence: 94%

Section: Endarterectomy and Histological Analysismentioning

confidence: 99%

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18F-FDG PET/CT for the quantification of inflammation in large carotid artery plaques

Johnsrud

Skagen

Seierstad

et al. 2019

Journal of Nuclear Cardiology

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“…One study assessed 18-FDG uptake vs. histology (r = 0.521, p = 0.003) [32] and showed that the SUV was signifi cantly higher in symptomatic (1.75) vs. asymptomatic (1.43) patients. Oxidized (ox) LDL has been shown to increase F-18-FDG uptake and glycolytic metabolism by more than an order of magnitude via the upregulation of GLUT1 expression and hexokinase activity [33,34].…”

Section: F-18-fdg Uptake At the Cellular Levelmentioning

confidence: 99%

Molecular imaging of atherosclerotic lesions by positron emission tomography - can it meet the expectations?

Brammen

Steiner

Berent³

et al. 2016

Vasa

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Summary:Early non-invasive imaging of atherosclerosis and in particular the detection of lesions at risk with high specifi city could significantly affect cardiovascular morbidity and mortality. Conventional nuclear medicine approaches, in particular using autologous radiolabeled lipoproteins, can be related to histopathological fi ndings; however, they fail to identify lesions at risk. Positron emission tomography (PET) tracers with much better physical properties have been examined, the most detailed information being available for F-18-deoxyglucose (FDG) and F-18-sodium fl uoride (NaF). These two approaches are sensitive to different biochemical mechanisms, i.e. infl ammation and microcalcifi cation. Initial enthusiasm, in particular for F-18-FDG, has disappeared, although for F-18-NaF there is some hope, but this is not a breakthrough. No tracer is available so far that is able to identify a specifi c characteristic of a lesion prone to rupture. Other PET tracers in the pipeline have been examined, mainly in experimental models and only a few in patients, but they failed to contribute signifi cantly to early lesion discovery and do not support great expectations. The key question is: Do we understand what we see? Moreover, methodological problems, a lack of standardization of imaging protocols and aspects of quantifi cation provide a wide range for potential future improvements. While monitoring a therapeutic intervention seems to be possible for both F-18-FDG and F-18-NaF, highly specifi c early identifi cation of lesions at risk by PET imaging is still far away. As of today, PET is not ready for routine clinical judgment of atherosclerotic lesions at risk to rupture. Even if all these problems can be solved, radiation exposure will still remain a concern, in particular for repeated studies.

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“…In this line, Figueroa et al followed 513 patients without symptomatic cardiovascular disease for a mean of 4.2 years, and found that 18 F-FDG uptake within the wall of the ascending aorta was an independent predictor of future cardiovascular events [9]. The carotid plaque inflammation, as measured by 18 F-FDG PET and correlated with the degree of macrophage infiltration and plaque erosion [10], has been also associated with a high risk of early stroke recurrence, independently of the degree of stenosis [11], and may, thus, be a useful imaging biomarker for high-risk carotid plaque [10,12], especially in case of imminent vascular event [11,13], and for yet symptomatic plaques [14].…”

mentioning

confidence: 99%

Predictive medicine: towards a multi-parametric imaging for a personal risk stratification

Guedj

Cammilleri

Verger

2016

Eur J Nucl Med Mol Imaging

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Carotid Plaque Inflammation Assessed with ¹⁸F-FDG PET/CT is Higher in Symptomatic Compared with Asymptomatic Patients

Cited by 45 publications

References 33 publications

18F-FDG PET/CT for the quantification of inflammation in large carotid artery plaques

18F-FDG PET/CT for the quantification of inflammation in large carotid artery plaques

Molecular imaging of atherosclerotic lesions by positron emission tomography - can it meet the expectations?

Predictive medicine: towards a multi-parametric imaging for a personal risk stratification

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Carotid Plaque Inflammation Assessed with 18F-FDG PET/CT is Higher in Symptomatic Compared with Asymptomatic Patients

Cited by 45 publications

References 33 publications

18F-FDG PET/CT for the quantification of inflammation in large carotid artery plaques

18F-FDG PET/CT for the quantification of inflammation in large carotid artery plaques

Molecular imaging of atherosclerotic lesions by positron emission tomography - can it meet the expectations?

Predictive medicine: towards a multi-parametric imaging for a personal risk stratification

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Carotid Plaque Inflammation Assessed with ¹⁸F-FDG PET/CT is Higher in Symptomatic Compared with Asymptomatic Patients