Coronary arterial 18F-FDG uptake by fusion of PET and coronary CT angiography at sites of percutaneous stenting for acute myocardial infarction and stable coronary artery disease.

UNLABELLED

Whether (18)F-FDG PET can detect inflammation in the coronary arteries remains controversial. We examined (18)F-FDG uptake at the culprit sites of acute myocardial infarction (AMI) after percutaneous coronary stenting (PCS) by coregistering PET and coronary CT angiography (CTA).

METHODS

Twenty nondiabetic patients with AMI (median age, 62 y; 16 men and 4 women) and 7 nondiabetic patients with stable coronary artery disease (CAD; median age, 67 y; 4 men and 3 women) underwent (18)F-FDG PET and coronary CTA 1-6 d after PCS of culprit stenoses. After a low-carbohydrate dietary preparation and more than 12 h of fasting, 480 MBq of (18)F-FDG were injected, and PET images were acquired 3 h later. Helical CTA was performed on a dual-source scanner. Stent position on attenuation-correction noncontrast CT and CTA was used to fuse PET and CTA. Two experienced readers masked to patient data independently quantified maximum target-to-background ratio (maxTBR) at each PCS site. A maxTBR greater than 2.0 was the criterion for significant uptake.

RESULTS

Compared with stable CAD patients, more AMI patients exhibited a PCS site maxTBR greater than 2.0 (12/20 vs. 1/7, P = 0.04). More AMI patients were active smokers (9/20 vs. 0/7 in stable CAD, P = 0.03). After adjusting for baseline demographic differences, stent-myocardium distance, and myocardial (18)F-FDG uptake, presentation of AMI was positively associated with a PCS site maxTBR greater than 2.0 (odds ratio, 31.6; P = 0.044). Prevalence of excess myocardial (18)F-FDG uptake was similar in both populations (8/20 AMI vs. 3/7 stable CAD, P = 0.89).

CONCLUSION

Systematic fusion of (18)F-FDG PET and coronary CTA demonstrated increased culprit site (18)F-FDG uptake more commonly in patients with AMI than in patients with stable CAD. However, this approach failed to detect increased signal at the culprit site in nearly half of AMI patients, highlighting the challenging nature of in vivo coronary artery plaque metabolic imaging. Nonetheless, our findings suggest that imaging of coronary artery inflammation is feasible, and further work evaluating (18)F-FDG uptake in high-risk coronary plaques prior to rupture would be of great interest.