Radioisotope ID’s high-risk, ruptured coronary plaques

PET-CT using the radioisotope ¹⁸F-sodium fluoride (¹⁸F-NaF) identified high-risk and ruptured plaques in patients with stable and unstable coronary heart disease, according to a study published online Nov. 11 in The Lancet.

Nikhil V. Joshi, MD, of The Centre for Cardiovascular Science at the University of Edinburgh in the U.K., and colleagues compared ¹⁸F-NaF with the current gold standard radioactive tracer, ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) PET-CT, to determine if ¹⁸F-NaF uptake could identify high-risk or ruptured atherosclerotic plaque in patients with symptomatic coronary and carotid artery disease.

The study included three patient groups who were recruited between 2012 and 2013. Joshi et al enrolled 40 patients with STEMI, a comparator group of 40 patients with stable angina who were undergoing elective coronary angiography and nine patients undergoing carotid endarterectomy for symptomatic carotid artery disease.

Patients in the STEMI and angina groups underwent ¹⁸F-NaF and ¹⁸F-FDG PET-CT, CT coronary angiography and CT calcium scoring. Ex-vivo PET-CT scans were done on atherosclerotic plaques obtained during the carotid endarterectomy procedures.

The primary endpoint was a comparison of ¹⁸F-NaF ratios for the culprit and nonculprit lesions in patients with acute MI.

In the STEMI group, increased ¹⁸F-NaF uptake was seen in the culprit plaque of 93 percent of the patients. “By contrast, coronary ¹⁸F-FDG uptake was commonly obscured by myocardial uptake and where discernible, there were no differences between culprit and non-culprit plaques,” they wrote.

The ex-vivo PET-CT showed that plaque rupture was present in each of the nine patients with high ¹⁸F-Na uptake in the rupture sites. The sites with increased uptake had more active calcification, macrophage infiltration, cell death and necrotic core compared with tissue sections with no uptake.

“This technique holds major promise as a means of identifying high-risk and ruptured plaque, and potentially informing the future management and treatment of patients with stable and unstable coronary artery disease,” they proposed.   

Joshi et al suggested that ¹⁸F-NaF PET-CT might offer a better predictor of cardiovasacular risk than calcium scoring and recommended prospective trials with a larger patient population to see if increased uptake of the radioactive tracer translates into future adverse events.

“If the results prove confirmatory then this technique has the potential to fundamentally alter the way we treat coronary artery disease: moving us away from the current framework based on lesion severity and ischaemia to one focused on plaque metabolism and inflammation,” they wrote.

In an accompanying editorial, Gregory Thomas, MD, of Long Beach Memorial Medical Center in Irvine, Calif., and Reka A. Haraszti, MD, of the University of Massachusetts Medical School in Worchester, called for more research. “Just because a plaque at risk for rupture can be identified does not mean that we know what to do with this information,” they emphasized.

The¹⁸F-NaF PET-CT technique may prove useful as a tool for measuring plaque changes from pharmacological treatments and devices, Thomas and Haraszti added, or to explore whether most MIs are caused by the rupture of nonobstructive plaque.