Fibroblast activation protein (FAP) is a fibroblast-specific marker expressed in atherosclerosis, associated with endothelial-to-mesenchymal transition and a rupture-prone plaque phenotype. This study aims to evaluate in-vivo fibroblast activation in carotid and coronary atherosclerotic diseases with FAPI PET and its correlation with histological vulnerability and clinical outcome.

Fibroblast activation protein (FAP) is a fibroblast-specific marker expressed in atherosclerosis. Abundant FAP-expressing cells in atherosclerotic plaques co-express endothelial biomarkers involved in endothelial-to-mesenchymal transition. FAP upregulation is also associated with a rupture-prone plaque phenotype with a thin fibrous cap. Positron emission tomography (PET) with 68Ga-FAPI-04 has been demonstrated as a feasible method to image fibroblastic activation in the arterial wall. The current study aims to evaluate in-vivo fibroblast activation in carotid and coronary atherosclerotic diseases with FAPI PET and its correlation with histological vulnerability and clinical outcome.

Inclusion Criteria:

• For the carotid stenosis group: patients with symptomatic carotid stenosis with >50% stenosis on carotid CTA; OR patients with unsymptomatic carotid stenosis with >70% stenosis on carotid CTA
• For CAD group: patients with stable ischemic heart disease OR acute coronary syndrome, including ST-elevation MId, non-ST elevation MI, and unstable angina
• signed informed consent

Exclusion Criteria:

• Pregnancy, lactation, or intention to become pregnant during the study
• Contradiction to MRI or CTA

Patients with carotid stenosis or CAD.