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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Related Experiment Video

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In vivo alpha-V beta-3 integrin expression in human aortic atherosclerosis.

William S Jenkins1, Alex T Vesey2, Anna Vickers2

  • 1British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK williamjenkins@doctors.net.uk.

Heart (British Cardiac Society)
|August 19, 2019
PubMed
Summary
This summary is machine-generated.

Positron emission tomography (PET) radiotracer 18F-fluciclatide effectively visualizes alpha-V beta-3 (αvβ3) integrin expression in human aortic atherosclerosis. This imaging approach shows potential for assessing plaque vulnerability and disease activity in atherosclerosis.

Keywords:
atherosclerosiscomputed tomographyintegrinpositron emission tomography

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Area of Science:

  • Cardiovascular Imaging
  • Molecular Imaging
  • Nuclear Medicine

Background:

  • Intraplaque angiogenesis and inflammation are key drivers of atherosclerosis, mediated by the alpha-V beta-3 (αvβ3) integrin pathway.
  • Assessing these processes in human aortic atherosclerosis is crucial for understanding disease progression and vulnerability.

Purpose of the Study:

  • To investigate the applicability of the αvβ3-integrin receptor-selective positron emission tomography (PET) radiotracer 18F-fluciclatide for assessing human aortic atherosclerosis.
  • To correlate 18F-fluciclatide uptake with established measures of atherosclerotic burden and disease activity.

Main Methods:

  • Forty-six subjects with stable or unstable atherosclerotic disease underwent PET and CT imaging after 18F-fluciclatide administration.
  • Ex vivo analysis of carotid endarterectomy samples (autoradiography, immunohistochemistry) evaluated vascular 18F-fluciclatide binding.
  • In vivo kinetic modeling and static imaging quantified thoracic aortic 18F-fluciclatide uptake, correlated with CT-derived measures of atherosclerotic burden.

Main Results:

  • 18F-Fluciclatide uptake co-localized with αvβ3 integrin expression, inflammation, and angiogenesis markers.
  • In vivo uptake correlated significantly with aortic wall thickness (r=0.57), plaque volume (r=0.56), and calcium score (r=0.37).
  • Patients with recent myocardial infarction showed greater aortic 18F-fluciclatide uptake compared to those with stable disease.

Conclusions:

  • In vivo αvβ3 integrin expression in human aortic atheroma correlates with plaque burden and is elevated in patients with recent myocardial infarction.
  • 18F-fluciclatide PET imaging offers a potential method for quantifying αvβ3 integrin expression.
  • This technique may aid in assessing plaque vulnerability and disease activity in atherosclerosis.