Abstract
ObjectivesThe aim of this study was to evaluate the 18F-sodium fluoride (18F-NaF) coronary uptake compared to coronary intravascular ultrasound (IVUS) in patients with symptomatic coronary artery disease.Background18F-NaF PET enables the assessment of vascular osteogenesis by interaction with surface hydroxyapatite, while IVUS enables both identification and quantification of intra-plaque components.MethodsForty-four patients with symptomatic coronary artery disease were included in this prospective controlled trial, 32 of them (30 patients with unstable angina and 2 patients with stable angina), representing the final study cohort, got additional IVUS. All patients underwent cardiac 18F-NaF PET/CT and IVUS within 2 days. 18F-NaF maximum tissue-to-blood ratios (TBRmax) were calculated for 69 coronary plaques and correlated with IVUS plaque classification.ResultsSignificantly increased 18F-NaF uptake ratios were observed in fibrocalcific lesions (meanTBRmax = 1.42 ± 0.28), thin-cap atheroma with spotty calcifications (meanTBRmax = 1.32 ± 0.23), and thick-cap mixed atheroma (meanTBRmax = 1.28 ± 0.38), while fibrotic plaques showed no increased uptake (meanTBRmax = 0.96 ± 0.18). The 18F-NaF uptake ratio was consistently higher in atherosclerotic lesions with severe calcification (meanTBRmax = 1.34 ± 0.22). The regional 18F-NaF uptake was most likely localized in the border region of intensive calcification. Coronary lesions with positive 18F-NaF uptake showed some increased high-risk anatomical features on IVUS in comparison to 18F-NaF negative plaques. It included a significant severe plaque burden (70.1 ± 13.8 vs. 61.0 ± 13.8, p = 0.01) and positive remodeling index (1.03 ± 0.08 vs. 0.99 ± 0.07, p = 0.05), as well as a higher percentage of necrotic tissue (37.6 ± 13.3 vs. 29.3 ± 15.7, p = 0.02) in positive 18F-NaF lesions.Conclusions18F-NaF coronary uptake may provide a molecular insight for the characterization of coronary atherosclerotic lesions. Specific regional uptake is needed to be determined by histology.
Highlights
The progression of atherosclerosis involves complex pathophysiology, mainly including cell migration, apoptosis, inflammation, and osteogenesis, which drive calcificationprone lesions to become atherosclerotic plaques [1, 2].Calcification is a remarkable biomarker of coronary atherosclerotic plaque burden, and coronary calcification on computed tomography (CT) may be a predictor of clinical disease [3]
A total of 69 coronary atherosclerotic lesions were analyzed from 32 patients who underwent intravascular ultrasound (IVUS) for tissue characterization of coronary plaques, including nonculprit thick-cap mixed atheromatous (n = 21), fibrotic atheromatous lesions (n = 18), calcified atheroma lesions (n = 8), and culprit thincap atheromatous lesions (n = 22) with spotty calcification
Increased 18F-NaF signals were observed in fibrocalcific lesions (n = 8), as well as thin-cap atheroma with spotty calcifications (n = 22) and thick-cap mix atheroma (n = 21)
Summary
The progression of atherosclerosis involves complex pathophysiology, mainly including cell migration, apoptosis, inflammation, and osteogenesis, which drive calcificationprone lesions to become atherosclerotic plaques [1, 2].Calcification is a remarkable biomarker of coronary atherosclerotic plaque burden, and coronary calcification on computed tomography (CT) may be a predictor of clinical disease [3]. Additional evidence has shown that the presence of intraplaque microcalcification or spotty calcification, along with thin, fibrous caps, is associated with a high risk for plaque rupture, which can lead to acute thrombosis and even fatal cardiac events [4,5,6]. The vulnerability of coronary plaques is conventionally assessed using the criteria of luminal stenosis, fibrous cap, lipid core, and severity of calcification by anatomical imaging, such as coronary CT angiography [7], cardiac magnetic resonance imaging (MRI) [8], and non-contrast CT [9]. The extent of coronary calcification could be determined, accurate quantification of various plaque components on conventional CT is still challenging due to limited spatial resolution for microcalcification
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