Abstract
The use of non-invasive imaging to identify ruptured or high-risk coronary atherosclerotic plaques would represent a major clinical advance for prevention and treatment of coronary artery disease. We used combined PET and CT to identify ruptured and high-risk atherosclerotic plaques using the radioactive tracers (18)F-sodium fluoride ((18)F-NaF) and (18)F-fluorodeoxyglucose ((18)F-FDG). In this prospective clinical trial, patients with myocardial infarction (n=40) and stable angina (n=40) underwent (18)F-NaF and (18)F-FDG PET-CT, and invasive coronary angiography. (18)F-NaF uptake was compared with histology in carotid endarterectomy specimens from patients with symptomatic carotid disease, and with intravascular ultrasound in patients with stable angina. The primary endpoint was the comparison of (18)F-fluoride tissue-to-background ratios of culprit and non-culprit coronary plaques of patients with acute myocardial infarction. In 37 (93%) patients with myocardial infarction, the highest coronary (18)F-NaF uptake was seen in the culprit plaque (median maximum tissue-to-background ratio: culprit 1·66 [IQR 1·40-2·25] vs highest non-culprit 1·24 [1·06-1·38], p<0·0001). By contrast, coronary (18)F-FDG uptake was commonly obscured by myocardial uptake and where discernible, there were no differences between culprit and non-culprit plaques (1·71 [1·40-2·13] vs 1·58 [1·28-2·01], p=0·34). Marked (18)F-NaF uptake occurred at the site of all carotid plaque ruptures and was associated with histological evidence of active calcification, macrophage infiltration, apoptosis, and necrosis. 18 (45%) patients with stable angina had plaques with focal (18)F-NaF uptake (maximum tissue-to-background ratio 1·90 [IQR 1·61-2·17]) that were associated with more high-risk features on intravascular ultrasound than those without uptake: positive remodelling (remodelling index 1·12 [1·09-1·19] vs 1·01 [0·94-1·06]; p=0·0004), microcalcification (73% vs 21%, p=0·002), and necrotic core (25% [21-29] vs 18% [14-22], p=0·001). (18)F-NaF PET-CT is the first non-invasive imaging method to identify and localise ruptured and high-risk coronary plaque. Future studies are needed to establish whether this method can improve the management and treatment of patients with coronary artery disease. Chief Scientist Office Scotland and British Heart Foundation.
Highlights
Coronary atherosclerotic plaque rupture is the principal precipitant of acute myocardial infarction and an important cause of sudden cardiac death
We have recently reported preliminary PET-CT data using the tracer 18F-sodium fluoride (18F-NaF) as a marker of valvular and vascular calcification activity in patients with aortic stenosis.[7,8,9]
Patients Patients were recruited from the Royal Infirmary of Edinburgh between February, 2012, and January, 2013, in three cohorts: 40 patients with acute ST-segment or nonST-segment elevation myocardial infarction,[14 40] patients with stable angina pectoris undergoing elective invasive coronary angiography, and 12 patients
Summary
Coronary atherosclerotic plaque rupture is the principal precipitant of acute myocardial infarction and an important cause of sudden cardiac death. We have recently reported preliminary PET-CT data using the tracer 18F-sodium fluoride (18F-NaF) as a marker of valvular and vascular calcification activity in patients with aortic stenosis.[7,8,9] Other studies have shown the usefulness of 18F-flurodeoxyglucose (18F-FDG) as a surrogate of vascular inflammation and macrophage burden.[6,10,11,12,13] We investigated whether, compared with the current non-invasive gold standard of 18F-FDG, 18F-NaF uptake could identify ruptured and high-risk atherosclerotic plaques in patients with symptomatic coronary and carotid artery disease
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
