TY - JOUR
T1 - Focal arterial inflammation precedes subsequent calcification in the same location
T2 - A longitudinal FDG-PET/CT study
AU - Abdelbaky, Amr
AU - Corsini, Erin
AU - Figueroa, Amparo L.
AU - Fontanez, Sara
AU - Subramanian, Sharath
AU - Ferencik, Maros
AU - Brady, Thomas J.
AU - Hoffmann, Udo
AU - Tawakol, Ahmed
N1 - Copyright:
Copyright 2013 Elsevier B.V., All rights reserved.
PY - 2013/9
Y1 - 2013/9
N2 - Background-Arterial calcium (Ca) deposition has been identified as an active inflammatory process. We sought to test the hypothesis that local vascular inflammation predisposes to subsequent arterial calcium deposition in humans. Methods and Results-From a hospital database, we identified 137 patients (age, 61±13 years; 48.1% men) who underwent serial positron-emission tomography/computed tomography (1-5 years apart). Focal arterial inflammation was prospectively determined by measuring 18F-flourodeoxyglucose uptake (using baseline positron-emission tomography) within predetermined locations of the thoracic aortic wall and was reported as a standardized uptake value. A separate, blinded investigator evaluated calcium deposition (on the baseline and follow-up computed tomographic scans) along the same standardized sections of the aorta. New calcification was prospectively defined using square root-transformed difference of calcium volume score, with a cutoff value of 2.5. Accordingly, vascular segment was classified as either with or without subsequent calcification. Overall, 67 (9%) of aortic segments demonstrated subsequent calcification. Baseline median (interquartile range) standardized uptake value was higher in segments with versus without subsequent calcification (2.09 [1.84-2.44] versus 1.92 [1.72-2.20], P=0.002). This was also true in the subset of segments with Ca present at baseline (2.08 [1.81-2.40] versus 1.86 [1.66-2.09], P=0.02), as well as those without (2.17 [1.87-2.51] versus 1.93 [1.73-2.20], P=0.04). Furthermore, across all patients, subsequent Ca deposition was associated with the underlying 18F-flourodeoxyglucose uptake (inflammatory signal), measured as standardized uptake value (odds ratio [95% confidence interval]=2.94 [1.27-6.89], P=0.01) or target-to-background ratio (2.59 [1.18-5.70], P=0.02), after adjusting for traditional cardiovascular risk factors. Conclusions-Here, we provide first-in-man evidence that arterial inflammation precedes subsequent Ca deposition, a marker of plaque progression, within the underlying location in the artery wall.
AB - Background-Arterial calcium (Ca) deposition has been identified as an active inflammatory process. We sought to test the hypothesis that local vascular inflammation predisposes to subsequent arterial calcium deposition in humans. Methods and Results-From a hospital database, we identified 137 patients (age, 61±13 years; 48.1% men) who underwent serial positron-emission tomography/computed tomography (1-5 years apart). Focal arterial inflammation was prospectively determined by measuring 18F-flourodeoxyglucose uptake (using baseline positron-emission tomography) within predetermined locations of the thoracic aortic wall and was reported as a standardized uptake value. A separate, blinded investigator evaluated calcium deposition (on the baseline and follow-up computed tomographic scans) along the same standardized sections of the aorta. New calcification was prospectively defined using square root-transformed difference of calcium volume score, with a cutoff value of 2.5. Accordingly, vascular segment was classified as either with or without subsequent calcification. Overall, 67 (9%) of aortic segments demonstrated subsequent calcification. Baseline median (interquartile range) standardized uptake value was higher in segments with versus without subsequent calcification (2.09 [1.84-2.44] versus 1.92 [1.72-2.20], P=0.002). This was also true in the subset of segments with Ca present at baseline (2.08 [1.81-2.40] versus 1.86 [1.66-2.09], P=0.02), as well as those without (2.17 [1.87-2.51] versus 1.93 [1.73-2.20], P=0.04). Furthermore, across all patients, subsequent Ca deposition was associated with the underlying 18F-flourodeoxyglucose uptake (inflammatory signal), measured as standardized uptake value (odds ratio [95% confidence interval]=2.94 [1.27-6.89], P=0.01) or target-to-background ratio (2.59 [1.18-5.70], P=0.02), after adjusting for traditional cardiovascular risk factors. Conclusions-Here, we provide first-in-man evidence that arterial inflammation precedes subsequent Ca deposition, a marker of plaque progression, within the underlying location in the artery wall.
KW - Arterial inflammation
KW - Positron-emission tomography
KW - Vascular calcification
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U2 - 10.1161/CIRCIMAGING.113.000382
DO - 10.1161/CIRCIMAGING.113.000382
M3 - Article
C2 - 23833282
AN - SCOPUS:84884481891
SN - 1941-9651
VL - 6
SP - 747
EP - 754
JO - Circulation: Cardiovascular Imaging
JF - Circulation: Cardiovascular Imaging
IS - 5
ER -