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

Abstract

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 5 0.04). More AMI patients were active smokers (9/20 vs. 0/7 in stable CAD, P 5 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 5 0.044). Prevalence of excess myocardial 18 F-FDG uptake was similar in both populations (8/20 AMI vs. 3/7 stable CAD, P 5 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.

Molecular Imaging of Vulnerable Coronary Plaque: A Pathophysiologic Perspective

“…The feasibility of using 18 F-FDG for coronary plaque imaging was initially described by Rogers et al (11). We subsequently reported that 12 of 20 patients with recent acute coronary syndromes had increased 18 F-FDG uptake in stented culprit coronary lesions-with a target-to-background ratio greater than 2.0-compared with 1 of 7 in patients with stable coronary artery disease (12). A limitation of coronary imaging with 18 F-FDG is that its uptake by the myocardium frequently cannot be suppressed, despite a high-fat and low-carbohydrate diet (12).…”

Imaging moving heart structures with PET

“…In the case of coronary 18 F-FDG imaging, an additional complication is presented by myocardial activity, which may overlap with plaque activity due to arterial/myocardial motion. 20 Heart motion could be one reason why 18 F-FDG studies investigating coronary plaques have not been strongly conclusive. 18 To partially mitigate blurring due to cardiac motion during Figure 1.…”

“…18,19 In coronary plaque imaging, PET activity originating from very small moving volumes of non-calcified plaques (perhaps as small as a few cubic mm) needs to be quantified with respect to standard uptake value and target-to-background ratio. These measurements will be severely affected by motion of the arteries, effectively reducing both quantified values.…”

Molecular imaging of the atherosclerotic plaque using positron emission tomography

“…30 However, these measures have proved only modestly effective, with background myocardial 18F-FDG activity remaining a significant problem in almost half of patients. 29,30 We believe that this lack of specificity is likely to limit the use of 18F-FDG as a biomarker of coronary artery disease risk and that more macrophage specific tracers are required. The novel radio-ligand 11C-PK11195 holds promise in this regard, targeting a translocator protein specific to human macrophages and demonstrating increased uptake in atherosclerotic plaques that correlates with macrophage infiltration.…”

“…Initial studies were encouraging, with 18F-FDG activity in the proximal vessels and adjacent aorta demonstrating increased activity in patients following acute coronary syndromes compared with those with stable angina. 28,29 However, attempts to examine the coronary vasculature in more detail have been limited by the glycolytic activity of the myocardium, which uses glucose as its predominant energy source and therefore avidly takes up 18F-FDG obscuring any signal in adjacent structures. High-fat, low-carbohydrate diets have been used in an attempt to switch myocardial metabolism to free fatty acid and reduce ventricular uptake.…”