Skip to main content
Log in

Should vascular wall 18F-FDG uptake be adjusted for the extent of atherosclerotic burden?

  • Original Paper
  • Published:
The International Journal of Cardiovascular Imaging Aims and scope Submit manuscript

Abstract

Vascular wall 18F-FDG uptake is often used as a surrogate marker of atherosclerotic plaque inflammation. A potential caveat is that vascular wall 18F-FDG uptake is higher simply because more atherosclerosis is present. To determine if the degree of inflammation is high or low relative to the extent of atherosclerosis, vascular wall 18F-FDG uptake may require statistical adjustment for a non-inflammatory marker reflecting the extent of atherosclerosis, e.g. calcification. Adjustments is probably needed if (1) vascular wall 18F-FDG uptake correlates sufficiently strongly with arterial calcification and (2) adjustment for extent of calcification affects determinants of vascular 18F-FDG uptake. This study addresses these questions. 18F-FDG PET/low-dose-CT scans of 99 patients were used. Cardiovascular risk factors were assessed and PET/CT scans were analysed for standardized 18F-FDG uptake values and calcification. ANOVA was used to establish the association between vascular 18F-FDG uptake and calcification. Multiple linear regression (with and without calcification as independent variable) was used to show whether determinants of vascular 18F-FDG uptake were affected by the degree of calcification. 18F-FDG uptake was related to increased calcification in the aortic arch, descending and abdominal aorta. However, 18F-FDG uptake showed considerable overlap between categories of calcification. Age and body mass index were main determinants of vascular 18F-FDG uptake. In multiple regression analyses, most standardized beta coefficients of these determinants were not affected by adjustment for the degree of calcification. Although vascular 18F-FDG uptake is related to total atherosclerotic burden, as reflected by vascular calcification, the association is weak and unlikely to affect the identification of determinants of atherosclerotic inflammation implicating no need for adjustment in future studies.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2
Fig. 3

Similar content being viewed by others

Abbreviations

ANOVA:

Analysis of variance

ASCVD:

American society of cardiovascular disease

BMI:

Body mass index

CT:

Computed tomography

FDG:

Fluorodeoxyglucose

GCA:

Giant cell arteritis

hsCRP:

High sensitivity c-reactive protein

MRI:

Magnetic resonance imaging

PET:

Positron emission tomography

ROI:

Region of interest

SUV:

Standardized uptake value

References

  1. Benjamin EJ, Virani SS, Callaway CW et al (2018) Heart disease and stroke statistics-2018 update: a report from the American Heart Association. Circulation 137(12):e67–e492

    Article  Google Scholar 

  2. Boyle JJ, Bowyer DE, Weissberg PL, Bennett MR (2001) Human blood-derived macrophages induce apoptosis in human plaque-derived vascular smooth muscle cells by Fas-ligand/Fas interactions. Arterioscler Thromb Vasc Biol 21(9):1402–1407

    Article  CAS  Google Scholar 

  3. Falk E (1992) Why do plaques rupture? Circulation 86(6):III30–III42.

    CAS  PubMed  Google Scholar 

  4. Jander S, Sitzer M, Schumann R et al (1998) Inflammation in high-grade carotid stenosis: a possible role for macrophages and T cells in plaque destabilization. Stroke 29(8):1625–1630

    Article  CAS  Google Scholar 

  5. Hansson GK, Libby P, Tabas I (2015) Inflammation and plaque vulnerability. J Intern Med 278(5):483–493

    Article  CAS  Google Scholar 

  6. Tawakol A, Migrino RQ, Bashian GG et al (2006) In vivo 18F-fluorodeoxyglucose positron emission tomography imaging provides a noninvasive measure of carotid plaque inflammation in patients. J Am Coll Cardiol 48(9):1818–1824

    Article  Google Scholar 

  7. Davies JR, Rudd JH, Fryer TD et al (2005) Identification of culprit lesions after transient ischemic attack by combined 18F fluorodeoxyglucose positron-emission tomography and high-resolution magnetic resonance imaging. Stroke 36(12):2642–2647

    Article  Google Scholar 

  8. Figueroa AL, Subramanian SS, Cury RC et al (2012) Distribution of inflammation within carotid atherosclerotic plaques with high-risk morphological features: a comparison between positron emission tomography activity, plaque morphology, and histopathology. Circ Cardiovasc Imaging 5(1):69–77

    Article  Google Scholar 

  9. Silvera SS, Aidi HE, Rudd JH et al (2009) Multimodality imaging of atherosclerotic plaque activity and composition using FDG-PET/CT and MRI in carotid and femoral arteries. Atherosclerosis 207(1):139–143

    Article  CAS  Google Scholar 

  10. Iwatsuka R, Matsue Y, Yonetsu T et al (2018) Arterial inflammation measured by (18)F-FDG-PET-CT to predict coronary events in older subjects. Atherosclerosis 268:49–54

    Article  CAS  Google Scholar 

  11. Figueroa AL, Abdelbaky A, Truong QA et al (2013) Measurement of arterial activity on routine FDG PET/CT images improves prediction of risk of future CV events. JACC Cardiovasc Imaging 6(12):1250–1259

    Article  Google Scholar 

  12. Bucerius J, Duivenvoorden R, Mani V et al (2011) Prevalence and risk factors of carotid vessel wall inflammation in coronary artery disease patients: FDG-PET and CT imaging study. JACC Cardiovasc Imaging 4(11):1195–1205

    Article  Google Scholar 

  13. Eisen A, Tenenbaum A, Koren-Morag N et al (2008) Calcification of the thoracic aorta as detected by spiral computed tomography among stable angina pectoris patients: association with cardiovascular events and death. Circulation 118(13):1328–1334

    Article  Google Scholar 

  14. Hoffmann U, Massaro JM, D'Agostino RB Sr, Kathiresan S, Fox CS, O'Donnell CJ (2016) Cardiovascular event prediction and risk reclassification by coronary, aortic, and valvular calcification in the Framingham Heart Study. J Am Heart Assoc 5(2):e003144

    Article  Google Scholar 

  15. Ben-Haim S, Kupzov E, Tamir A, Israel O (2004) Evaluation of 18F-FDG uptake and arterial wall calcifications using 18F-FDG PET/CT. J Nucl Med 45(11):1816–1821

    PubMed  Google Scholar 

  16. Blomberg BA, de Jong PA, Thomassen A et al (2017) Thoracic aorta calcification but not inflammation is associated with increased cardiovascular disease risk: results of the CAMONA study. Eur J Nucl Med Mol Imaging 44(2):249–258

    Article  Google Scholar 

  17. Derlin T, Toth Z, Papp L et al (2011) Correlation of inflammation assessed by 18F-FDG PET, active mineral deposition assessed by 18F-fluoride PET, and vascular calcification in atherosclerotic plaque: a dual-tracer PET/CT study. J Nucl Med 52(7):1020–1027

    Article  Google Scholar 

  18. Quirce R, Martinez-Rodriguez I, Banzo I et al (2016) New insight of functional molecular imaging into the atheroma biology: 18F-NaF and 18F-FDG in symptomatic and asymptomatic carotid plaques after recent CVA. Preliminary results. Clin Physiol Funct Imaging 36(6):499–503

    Article  CAS  Google Scholar 

  19. Goff DC Jr, Lloyd-Jones DM, Bennett G et al (2014) 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 63(25):2935–2959

    Article  Google Scholar 

  20. Ridker PM, Danielson E, Fonseca FA et al (2009) Reduction in C-reactive protein and LDL cholesterol and cardiovascular event rates after initiation of rosuvastatin: a prospective study of the JUPITER trial. Lancet 373(9670):1175–1182

    Article  CAS  Google Scholar 

  21. Lensen KDF, van Sijl AM, Voskuyl AE et al (2017) Variability in quantitative analysis of atherosclerotic plaque inflammation using 18F-FDG PET/CT. PLoS ONE 12(8):e0181847

    Article  Google Scholar 

  22. Rominger A, Saam T, Wolpers S et al (2009) 18F-FDG PET/CT identifies patients at risk for future vascular events in an otherwise asymptomatic cohort with neoplastic disease. J Nucl Med 50(10):1611–1620

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Karel-Jan D. F. Lensen.

Ethics declarations

Conflict of interest

The authors declare that they have no conflict of interest.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Supplementary file1 (DOCX 14 kb)

Supplementary file2 (DOCX 14 kb)

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Lensen, KJ.D.F., Voskuyl, A.E., Comans, E.F.I. et al. Should vascular wall 18F-FDG uptake be adjusted for the extent of atherosclerotic burden?. Int J Cardiovasc Imaging 36, 545–551 (2020). https://doi.org/10.1007/s10554-019-01744-0

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10554-019-01744-0

Keywords

Navigation