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Figure 1

From: Ex vivo 18F-fluoride uptake and hydroxyapatite deposition in human coronary atherosclerosis

Figure 1

18F-Fluoride binding in ex vivo coronary artery specimens. (A) Total activity of 18F-fluoride (MBq/mL) following 20 min incubation in hydroxyapatite plotted against dose of 18F-fluoride (kBq) per milligram of hydroxyapatite. Scatchard plot of bound/free versus bound 18F-fluoride (inset). (B) Hydroxyapatite and other calcium-derived minerals were incubated with 18F-fluoride for 20 min after which unbound supernatant was removed and the solid particles were analysed by micro positron emission tomography. Data shown is from at least three replicates and shown as the mean ± standard deviation. (C) Micro-computed tomography defined regions of myocardium (CT number < 100) from coronary plaque (CT number > 300). Calcification had high CT attenuation on micro-computed tomography (CT number > 1000). Quantitative 18F-fluoride positron tomography was analysed on hybrid images. (D) Non-specific binding in the surrounding myocardium was higher than background activity (median 14.9 [interquartile range 9.6–27.4] versus 0.30 [interquartile range, 0.09–1.3] kBq/mL respectively, p < 0.0001). Signal in coronary artery segments was tenfold higher (p < 0.0001) than myocardium (non-calcified plaque median 158.1 [interquartile range, 121.7–234.8] kBq/mL and calcified plaque median 149.8 [interquartile range, 85.3–207.3] kBq/mL). CaPi calcium bisphosphate, CaPyr calcium pyrophosphate, CaOx calcium oxalate, HAP hydroxyapatite, WL window level, WW window width. *Indicates p < 0.0001

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