Results:

In 37 (93%) patients with myocardial infarction, the highest coronary ¹⁸F-NaF uptake was seen in the culprit plaque (median maximum tissue-to-background ratio: culprit 1.66 [interquartile range (IQR) 1.40–2.25] vs. highest nonculprit 1.24 [1.06–1.38], p < 0.0001). By contrast, coronary ¹⁸F-FDG uptake was commonly obscured by myocardial uptake, and where discernible, there were no differences between culprit and nonculprit plaques (1.71 [1.40–2.13] vs. 1.58 [1.28–2.01], p = 0.34). Marked ¹⁸F-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. Eighteen (45%) patients with stable angina had plaques with focal ¹⁸F-NaF uptake (maximum tissue-to-background ratio 1.90 [IQR, 1.1–2.17]) that were associated with more high-risk features on intravascular ultrasound than those without uptake: positive remodeling (remodeling 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).