By Lynda Williams, Senior medwireNews Reporter
Combined 18F-sodium fluoride (18F-NaF) positron emission tomography–computed tomography (PET–CT) allows physicians to visualize high-risk or ruptured coronary atherosclerotic plaques in patients with myocardial infarction (MI) or stable angina, research shows.
“[This] non-invasive imaging technique has the potential to change how we identify, manage, and treat patients with stable and unstable coronary artery disease,” report Nikhil Joshi (University of Edinburgh, UK) and co-authors in The Lancet.
“Further work is now needed to establish whether 18F-fluoride positron emission tomography will provide a means of improving risk stratification, monitoring disease progression, guiding therapeutic interventions, and assessing novel anti-atherosclerotic therapies.”
18F-NaF uptake was detected in the culprit plaque of 93% of the 40 MI patients who underwent imaging, with a significantly higher median tissue-to-background ratio (TBR) of 1.66 compared with just 1.24 in the highest non-culprit plaque, the team says.
There was also significant focal plaque 18F-NaF uptake in 45% of 40 patients with stable angina, with a TBR of 1.90 compared with just 1.02 for those without. And, 72% of these focal plaques were non-obstructive, defined as less than 70% luminal stenosis, on coronary angiography.
Moreover, intravascular ultrasound showed that focal plaques in the stable angina patients were significantly more likely to have high-risk features like a necrotic core, positive remodeling and/or microcalcification than plaques without uptake, the team reports.
Finally, carotid endartectomy samples taken from nine patients with symptomatic carotid disease showed that the 24 regions with focal 18F-NaF uptake had significantly higher levels of calcification, macrophage infiltration, apoptosis, and necrosis than 15 areas without uptake.
The researchers note that three MI patients did not have culprit plaque 18F-NaF uptake, including two young smokers whose event was thought to have been caused by plaque erosion and thrombosis rather than plaque rupture.
Although the third patient did not have uptake at the culprit lesion in the right coronary artery, there was 18F-NaF plaque uptake in a co-dominant circumflex artery. This raises the “intriguing possibility that 18F-NaF might have a clinical role for patients in whom the culprit lesion is not readily apparent,” Joshi et al write.
In an accompanying comment, Gregory Thomas (Long Beach and University of California, Irvine, USA) and Reka Haraszti (University of Massachusetts, Worcester, USA) question how best to use the information derived from 18F-NaF imaging and its potential impact on coronary artery bypass grafting.
Noting that further research is also required to determine the technique’s benefit in female patients – as the majority of the study participants were male - and those with diabetes, as well as its potential for predicting stroke and transient ischemic attack, the commentators conclude: “Joshi and colleagues and earlier pioneers have identified a new and hopefully fruitful frontier in nuclear cardiology and atherosclerotic coronary imaging.”
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