Advances in the Assessment of Coronary Artery Disease Activity with PET/CT and CTA

Figures

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  Figure 1. Focal 18F-NaF in patients with myocardial infarction and stable angina. Patient with acute myocardial infarction with (A) proximal occlusion (red arrow) of the left anterior descending artery on invasive coronary angiography and (B) intense focal 18F-NaF uptake (yellow-red) at the site of the culprit plaque (red arrow) on PET. Patient with anterior myocardial infarction with (C) culprit (red arrow; left anterior descending artery) and bystander non-culprit (white arrow; circumflex artery) lesions on invasive coronary angiography that were both stented during the index admission. Only the culprit lesion had increased 18F-NaF uptake on PET (D). In a patient with stable angina with previous coronary artery bypass grafting, invasive coronary angiography (E) showed non-obstructive disease in the right coronary artery. Corresponding PET scan (F) showed a region of increased 18F-NaF in the mid-right coronary artery and a region without increased uptake in the proximal vessel. This figure was originally published in the Lancet under the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/) (accessed on 31 December 2022) (Data from [31]).

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  Figure 2. 18F-sodium fluoride positron emission tomography as a marker of disease activity in the coronary arteries is a predictor of fatal or non-fatal myocardial infarction (MI) in patients with established coronary artery disease.18F-NaF PET can be used to measure disease activity across the coronary vasculature and to stratify patients into those with no, low, and high disease activity. Figure 2 is reprinted from [47], with permission from Elsevier.

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  Figure 3. Examples of semi-automated analysis of CTA-derived PCAT attenuation. Two examples of semi-automated PCAT analysis of the right coronary artery using Autoplaque® software (Cedars Sinai Medical Center, Los Angeles, CA, USA). The first case ((A)—longitudinal view, (C)—short-axis view) shows a low PCAT of −94.27 HU, and the second case ((B)—longitudinal view, (D)—short-axis view) shows a high PCAT of −58.23 HU, suggesting increased perivascular inflammatory activity. (E)—schematic representation of the principle of PCAT analysis around the RCA involving a 40-milimeter section of the artery excluding the proximal 10 millimeters.

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  Figure 4. Case illustrations of coronary CTA and assessment of 18F-NaF uptake and PCAT attenuation in high-risk plaques. Patient 1: 53-year-old man with a (A) right coronary arterial (RCA) plaque with positive remodeling (green arrow); (B) focal 18F-sodium fluoride (18F-NaF) uptake with increased target-to-background ratio (TBR) of 1.73; and (C) increased peri-coronary adipose tissue (PCAT) attenuation (mean PCAT density: −76.7 Hounsfield units [HU]). (D) Patient 2: 66-year-old man with a (E) left anterior descending (LAD) lesion with low attenuation plaque (yellow arrow); (F) focal 18F-NaF uptake with increased TBR of 1.87; and increased PCAT attenuation (mean PCAT density: −74.8 HU). (G) Patient 3: 54-year-old human with an LAD lesion with low attenuation plaque (green arrow); (H) focal 18F-NaF uptake with increased TBR of 2.28; and (I) increased PCAT attenuation (mean PCAT density: −73.6 HU). CTA = computed tomography angiography. Figure reprinted from [68], with permission from Elsevier.