The median Perivascular Adipose Tissue-Fat Attenuation Index (FAI) was significantly higher in patients with carotid webs and atherosclerosis (-51.77 HU) compared to those without (-59.32 HU, p=0.03).
Is Perivascular Adipose Tissue-Fat-Attenuation Index (PVAT-FAI) associated with symptomatic presentation or atherosclerosis in patients with carotid webs?
Perivascular inflammation assessed by FAI is associated with atherosclerosis but not symptomatic presentation in patients with carotid webs.
Absolute Event Rate: 0% vs 0%
Introduction: The risk of stroke from carotid webs (CaW) seems to be linked to their morphological characteristics. While metabolic factors may also influence the likelihood of symptomatic presentation, this aspect remains unexplored. Perivascular Adipose Tissue-Fat-Attenuation Index (PVAT-FAI) assessed via CTA has emerged as a biomarker of inflammation, predicting coronary atherosclerosis progression. We aim to evaluate the occurrence and implications of peri-vascular inflammation in CaW via FAI analysis. Methods: Retrospective cross-sectional analysis of a prospective CaW database between 2022-2025 at two CSCs. FAI were obtained in Hounsfield unit(HU) of fat from the region of interest(ROI) from CTAs. FAI values range from -190 to -30 HU (lipid rich–less inflammation; more aqueous–more inflammation). CTA-DICOM image (axial) in 3D-Slicer was used. A semi-automated method for contrasted carotid lumen ( Fig1A/1B) and vessel wall segmentation (10 slices /6.2mm) at the web level (Fig1C/1D) was used. The vessel’s average diameter was obtained (centerline extraction method - Fig1E) for the perivascular area to extend the ROI radially (Fig1F). The PVAT region is exported to obtain HU values using RStudio. T-test and generalized linear regression models were used. Results: 40 patients met the inclusion criteria, of which 20 are consecutive symptomatic and 20 asymptomatic/incidental carotid webs. The overall median FAI was -57.95 HU (IQR: -62 to -48.15). Of the 40 cases 16(40%) had co-existent atherosclerotic changes at level of web by CTA. The median FAI for patients with atherosclerosis was significantly higher than for patients with no atherosclerosis (-51.77 IQR: -58.39 to -45.94 vs -59.32 IQR: -64.88 to -50.82;p=0.03). The median FAI for asymptomatic webs was -57.49 (IQR: -62 to -48.15), comparable to symptomatic carotid webs (-58.35 IQR: -61.76 to -48.77;p=0.9). The median FAI for patients in symptomatic and asymptomatic webs without associated atherosclerosis were comparable (-59.32 IQR: -65.28 to -48.77 vs -59.56 IQR: -63.93 to -55.49;p=0.9). There is no significant relationship between FAI and symptomatic webs while adjusting for atherosclerosis and age (p=0.7). Conclusion: Perivascular inflammation was commonly observed in CaW patients. Since FAI constitutes a non-invasive biomarker for local inflammation, this study suggests a potential pathophysiological metabolic role in the development of ischemic events in CaW. Further studies are warranted.
Yelam et al. (Thu,) reported a other. The median Perivascular Adipose Tissue-Fat Attenuation Index (FAI) was significantly higher in patients with carotid webs and atherosclerosis (-51.77 HU) compared to those without (-59.32 HU, p=0.03).
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