OBJECTIVES: 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: From a hospital database, we identified 137 patients (age=61Â±13, 48.1% Male) patients who underwent serial PET/CT (1 to 5 years apart). Focal arterial inflammation was prospectively determined by measuring FDG uptake (using baseline PET) within pre-determined locations of the thoracic aortic wall, and reported as a standardized uptake value (SUV). A separate, blinded investigator evaluated calcium deposition (on the baseline and follow-up CT scans) along the same, standardized sections of the aorta. New calcification was prospectively defined using square root transformed difference of calcium volume score (CVS), with a cut-off value of 2.5. Accordingly, vascular segment were classified as either with- or without- “subsequent calcification”.
RESULTS: Overall, 67(9%) of aortic segments demonstrated subsequent calcification. Baseline median (IQR) SUV was higher in segments with- vs. without subsequent calcification (2.09[1.84, 2.44] vs. 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] vs. 1.86[1.66, 2.09], p=0.02), as well as those without (2.17[1.87, 2.51] vs. 1.93[1.73, 2.20], p=0.04). Moreover, across all patients, subsequent Ca deposition was associated with the underlying FDG uptake (inflammatory signal), measured as SUV [OR (95%CI) = 2.94 (1.27 – 6.89), p =0.01] or TBR [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. Brandon Coleman Jersey