Coronary, aortic and carotid artery inflammation by 18F-fluorodeoxyglucose positron emission tomography in acute and chronic coronary artery disease

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) can detect arterial inflammation in individuals with atherosclerosis, but the associations among different vascular territories for 18F-FDG uptake are not known. Purpose We explored any possible correlation between arterial inflammation quantified by 18F-FDG PET in the aorta, carotid arteries, and coronary arteries in patients presenting with acute coronary syndrome (ACS), or chronic coronary artery disease (CAD). Methods Prospectively, we performed hybrid computed tomography angiography and 18F-FDG PET in 43 patients (26 ACS and 17 chronic CAD) at 6.6 ± 5.7 days following invasive coronary angiography. 18F-FDG PET was performed 90 minutes after injection of 302.2 ± 28.4 MBq 18F-FDG. Arterial 18F-FDG uptake was measured in the thoracic aorta, carotid arteries, and coronary arteries, and expressed as the target-to-background ratio (TBR; the ratio between arterial maximal standardized uptake value normalized to blood pool mean standardized uptake value) in the whole artery, and in the most diseased segment (MDS). Results Mean age was 64.9 ± 9.1 years, 90.7% males. The whole artery 18F-FDG uptake was higher in the aorta than in the carotid arteries (median TBR 2.23, interquartile range [0.36] vs. 1.88 [0.42], p < 0.001); whereas uptake in the coronary arteries was lower than in the aorta or carotid arteries (1.13 [0.23], p < 0.001 both). Similarly, 18F-FDG uptake in the aortic MDS was higher than in the carotid MDS (2.75 [0.62] vs. 2.25 [0.63], p < 0.001); whereas 18F-FDG uptake in the coronary MDS was the lowest (1.40 [0.33], p < 0.001 both). These findings were consistent in both ACS and chronic CAD patients. The whole artery 18F-FDG uptake of the aorta and carotid arteries correlated in patients with ACS (r = 0.58, p = 0.002), but not in patients with chronic CAD (r = 0.21, p = 0.3). There was no correlation between the whole artery 18F-FDG uptake in the coronary arteries and either the aorta or carotid arteries in the whole cohort (r=-0.16, p = 0.2, r = 0.01, p = 0.9, respectively), in patients with ACS (r = 0.06, p = 0.7, r=-0.01, p = 0.9, respectively), or in those with chronic CAD (r=-0.4, p = 0.1, r=-0.09, p = 0.7, respectively). Conclusions In patients with ACS or chronic CAD, large arteries had higher 18F-FDG uptake than the coronary arteries. The intensity of 18F-FDG uptake in the coronary arteries did not correlate with that in the carotid arteries or the aorta, indicating that disease activity differs between large arteries and coronary arteries.