68Ga-FAPI PET/MR for Atherosclerosis

  • STATUS
    Recruiting
  • End date
    Aug 30, 2023
  • participants needed
    100
  • sponsor
    Peking Union Medical College Hospital
Updated on 17 September 2021
carotid atherosclerosis

Summary

A thin-cap fibroatheroma with a large necrotic core and macrophage infiltration marks the vulnerable plaque. Fibroblast activating protein (FAP) is an active serine protease, which can degrade type I collagen, potentially thinning the fibrous cap. Thus we speculate that atherosclerotic plaque could be imaged with 68Ga-FAPI PET/MR.

Description

A thin-cap fibroatheroma with a large necrotic core and macrophage infiltration marks the vulnerable plaque. Fibroblast activating protein (FAP) is an active serine protease, which can degrade type I collagen, potentially thinning the fibrous cap. Previous ex vivo analysis of human aortic atheromata revealed that FAP was expressed in atherosclerotic plaques, and higher FAP expression was detected in thin fibrous caps than thick caps. Constitutive Fap deletion in atherosclerosis-prone mice models could reduce plaque formation and improve plaque stability with increased fibrous cap thickness. Thus we speculate that atherosclerotic plaque could be imaged with 68Ga-FAPI PET/MR.

Details
Condition Atherosclerotic Cardiovascular Disease, Arteriosclerosis, Atherosclerosis
Treatment 68Ga-FAPI
Clinical Study IdentifierNCT05036759
SponsorPeking Union Medical College Hospital
Last Modified on17 September 2021

Eligibility

Yes No Not Sure

Inclusion Criteria

intracranial or carotid atherosclerosis patients
signed informed consent

Exclusion Criteria

pregnancy, breastfeeding
contradictions of MRI
unstable vital signs
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