Focal arterial inflammation precedes subsequent calcification in the same location: A longitudinal FDG-PET/CT study

Amr Abdelbaky, Erin Corsini, Amparo L. Figueroa, Sara Fontanez, Sharath Subramanian, Maros Ferencik, Thomas J. Brady, Udo Hoffmann, Ahmed Tawakol

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)747-754
Number of pages8
JournalCirculation: Cardiovascular Imaging
Volume6
Issue number5
DOIs
StatePublished - Sep 2013
Externally publishedYes

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Arteritis
Calcium
Blood Vessels
Thoracic Wall
Positron-Emission Tomography
Aorta
Arteries
Odds Ratio
Research Personnel
Databases
Confidence Intervals
Inflammation

Keywords

  • Arterial inflammation
  • Positron-emission tomography
  • Vascular calcification

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Radiology Nuclear Medicine and imaging

Cite this

Focal arterial inflammation precedes subsequent calcification in the same location : A longitudinal FDG-PET/CT study. / Abdelbaky, Amr; Corsini, Erin; Figueroa, Amparo L.; Fontanez, Sara; Subramanian, Sharath; Ferencik, Maros; Brady, Thomas J.; Hoffmann, Udo; Tawakol, Ahmed.

In: Circulation: Cardiovascular Imaging, Vol. 6, No. 5, 09.2013, p. 747-754.

Research output: Contribution to journalArticle

Abdelbaky, A, Corsini, E, Figueroa, AL, Fontanez, S, Subramanian, S, Ferencik, M, Brady, TJ, Hoffmann, U & Tawakol, A 2013, 'Focal arterial inflammation precedes subsequent calcification in the same location: A longitudinal FDG-PET/CT study', Circulation: Cardiovascular Imaging, vol. 6, no. 5, pp. 747-754. https://doi.org/10.1161/CIRCIMAGING.113.000382
Abdelbaky, Amr ; Corsini, Erin ; Figueroa, Amparo L. ; Fontanez, Sara ; Subramanian, Sharath ; Ferencik, Maros ; Brady, Thomas J. ; Hoffmann, Udo ; Tawakol, Ahmed. / Focal arterial inflammation precedes subsequent calcification in the same location : A longitudinal FDG-PET/CT study. In: Circulation: Cardiovascular Imaging. 2013 ; Vol. 6, No. 5. pp. 747-754.
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abstract = "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.",
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AU - Fontanez, Sara

AU - Subramanian, Sharath

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AU - Tawakol, Ahmed

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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.

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