PET Radiotracer Identifies Atherosclerotic Inflammation

A new study describes a novel positron emission tomography (PET) radiotracer that can quickly and non-invasively identify life-threatening atherosclerotic plaques.

Developed by researchers at the Munich Technical University and Klinikum rechts der Isar, gallium-68 (Ga-68)-pentixafor binds with nanomolar affinity to the CXC chemokine receptor type 4 (CXCR4, also known as fusin), which is present on the surface of inflammatory cells in atherosclerotic plaques. For the study, the researchers imaged seven atherosclerotic rabbits and five controls in vivo on a PET-MRI system after injection of 15 MBq/kg of 68Ga-pentixafor.

One hour later, strong signals were detected with PET-MRI in atherosclerotic plaques of the abdominal aorta and right carotid artery, as compared to normal control arteries. The uptake in the vessel wall on radiographies was located in the macrophage-rich regions of atherosclerotic plaques, and correlated with the intensity of CXCR4 expression. The researchers also confirmed (with a small number of human patients) that the radiotracer detected atherosclerotic plaques located in their carotid arteries. The study was published in the March 2017 issue of The Journal of Nuclear Medicine.

“Ga-68-pentixafor binds more specifically to inflammatory cells than F-18-fluorodeoxyglucose and does not require the patient to fast for six hours before imaging,” said lead author Fabien Hyafil, MD, PhD, of Klinikum Rechts der Isar. “This new radiotracer will strongly facilitate the imaging of inflammation in atherosclerotic plaques with PET, and hopefully support the early detection and treatment of atherosclerosis, thus preventing heart attack or stroke.”

Atherosclerotic plaques fall into two broad categories - stable and unstable. While stable atherosclerotic plaques, which tend to be asymptomatic, are rich in extracellular matrix (ECM) and smooth muscle cells, unstable plaques are rich in macrophages and foam cells, and the ECM separating the lesion from the arterial lumen is usually weak and prone to rupture, causing thromboembolism. In the extreme, the emboli can cause myocardial infarction (MI) when lodged in cardiac arteries, or a stroke when reaching the brain.