Carotid plaque inflammation on <sup>18</sup>F‐fluorodeoxyglucose positron emission tomography predicts early stroke recurrence

Marnane, Michael; Merwick, Áine; Sheehan, Orla C.; Hannon, Niamh; Foran, Paul; Grant, Tim; Dolan, Eamon; Moroney, Joan T.; Murphy, Seán; O’Rourke, Killian; O’Malley, K; O’Donohoe, Martin K.; McDonnell, Ciarán; Noone, Imelda; Barry, Mary; Crowe, Morgan; Kavanagh, Eoin; O’Connell, Martin; Kelly, Peter

doi:10.1002/ana.23553

Cited by 213 publications

(170 citation statements)

References 32 publications

(97 reference statements)

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“…Our correlation coefficient for blood background of 0.75 inevitably increases the inter-observer variability of all background-corrected values. Other 18 F-FDG uptake reproducibility studies in localized carotid artery plaques have reported moderate (background corrected) 28 to excellent (with and without background correction) 22,29 inter-observer agreement. The slightly inferior inter-observer agreement for background-corrected values found in our study could be related to differences in the placement of the ROI in the jugular vein as the diameter of the jugular vein often was small, making the measurement susceptible to image noise.…”

Section: Discussionmentioning

confidence: 85%

“…Currently, the most used measure for assessment of plaque inflammation has been the mean SUV max . 17,21,22 No clinical studies have assessed the use of whole plaque max SUV max . Max SUV max is easily obtained, highly reproducible, and less influenced by partial-volume effects.…”

Section: Discussionmentioning

confidence: 99%

“…16 The uptake values are either normalized to the blood background activity, 15,17,19,20 corrected for the background activity with subtraction 11 or not corrected for background activity. 13,21,22 The rationale for background correction has been strongly criticized. 9,23 The aim of this study was to explore different methods for the quantification of 18 F-FDG uptake in large carotid artery plaques, and to correlate the uptake values to the amount of inflammation on histology.…”

Section: Introductionmentioning

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: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

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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“…In patients with symptomatic carotid atherosclerosis, 18 FDG uptake correlates with macrophage-rich areas of plaque, matrix metalloproteinase-9 (MMP-9) expression (Rudd et al 2010;Tawakol et al 2006;Graebe et al 2009), distal microembolic signals and early recurrence of cerebrovascular events (Moustafa et al 2010;Marnane et al 2012).…”

Section: The Immune System and Strokementioning

confidence: 99%

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Smith

Lawrence

Rodriguez‐Grande

et al. 2013

J Neuroimmune Pharmacol

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Stroke represents an unresolved challenge for both developed and developing countries and has a huge socio-economic impact. Although considerable effort has been made to limit stroke incidence and improve outcome, strategies aimed at protecting injured neurons in the brain have all failed. This failure is likely to be due to both the incompleteness of modelling the disease and its causes in experimental research, and also the lack of understanding of how systemic mechanisms lead to an acute cerebrovascular event or contribute to outcome.Inflammation has been implicated in all forms of brain injury and it is now clear that immune mechanisms profoundly influence (and are responsible for the development of) risk and causation of stroke, and the outcome following the onset of cerebral ischemia. Until very recently, systemic inflammatory mechanisms, with respect to common comorbidities in stroke, have largely been ignored in experimental studies. The main aim is therefore to understand interactions between the immune system and brain injury in order to develop novel therapeutic approaches. Recent data from clinical and experimental research clearly show that systemic inflammatory diseases -such as atherosclerosis, obesity, diabetes or infectionsimilar to stress and advanced age, are associated with dysregulated immune responses which can profoundly contribute to cerebrovascular inflammation and injury in the central nervous system. In this review, we summarize recent advances in the field of inflammation and stroke, focusing on the challenges of translation between pre-clinical and clinical studies, and potential anti-inflammatory/immunomodulatory therapeutic approaches.

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“…older age, smoking, hypertension, diabetes mellitus, and hyperlipidemia) and are elevated in patients with systemic inflammatory conditions conferring increased cardiovascular risk, such as rheumatoid arthritis and psoriasis [119][120][121]. Data from the prospective Dublin Carotid Atherosclerosis Stroke Study showed that increased carotid artery 18 F-FDG uptake can identify patients with increased risk of early stroke recurrence, independent of age and stenosis severity (Figure 4a,b) [122]. Moreover, a retrospective study of imaging from 513 cancer-free patients examined over a 4-year period found that aortic 18 F-FDG uptake strongly predicted risk of cardiovascular events independent of traditional risk factors (hazard ratio: 4.71, P < 0.001), with nearly 30% net reclassification improvement over Framingham risk score in the highest risk group [123].…”

Section: Positron Emission Tomographymentioning

confidence: 99%

Invasive or non-invasive imaging for detecting high-risk coronary lesions?

Patel

Tarkin

Serruys

et al. 2017

Expert Review of Cardiovascular Therapy

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Introduction: Advances in our understanding about atherosclerotic evolution have enabled us to identify specific plaque characteristics that are associated with coronary plaque vulnerability and cardiovascular events. With constant improvements in signal and image processing an arsenal of invasive and non-invasive imaging modalities have been developed that are capable of identifying these features allowing in vivo assessment of plaque vulnerability. Areas covered: This review article presents the available and emerging imaging modalities introduced to assess plaque morphology and biology, describes the evidence from the first large scale studies that evaluated the efficacy of invasive and non-invasive imaging in detecting lesions that are likely to progress and cause cardiovascular events and discusses the potential implications of the in vivo assessment of coronary artery pathology in the clinical setting. Expert commentary: Invasive imaging, with its high resolution, and in particular hybrid intravascular imaging appears as the ideal approach to study the mechanisms regulating atherosclerotic disease progression; whereas non-invasive imaging is expected to enable complete assessment of coronary tree pathology, detection of high-risk lesions, more accurate risk stratification and thus to allow a personalized treatment of vulnerable patients. ARTICLE HISTORY

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Carotid plaque inflammation on ¹⁸F‐fluorodeoxyglucose positron emission tomography predicts early stroke recurrence

Cited by 213 publications

References 32 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

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Invasive or non-invasive imaging for detecting high-risk coronary lesions?

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Carotid plaque inflammation on 18F‐fluorodeoxyglucose positron emission tomography predicts early stroke recurrence

Cited by 213 publications

References 32 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

The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Invasive or non-invasive imaging for detecting high-risk coronary lesions?

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Carotid plaque inflammation on ¹⁸F‐fluorodeoxyglucose positron emission tomography predicts early stroke recurrence