Patient-Level Perivascular Adipose Tissue Density Aggregation and Plaque Progression

脂肪组织 化学 病理 医学 炎症 弹性蛋白 细胞外基质 内皮 纤维帽 动物模型
作者
Sang‐Eun Lee,Ji Min Sung,Daniele Andreini,Mouaz Husayn Al-Mallah,Matthew Jay Budoff,Filippo Cademartiri,Kavitha M. Chinnaiyan,Jung Hyun Choi,Eun Ju Chun,Edoardo Conte,Ilan Gottlieb,Martin Hadamitzky,Yong Jin Kim,Byoung Kwon Lee,Jonathon A. Leipsic,Erica Maffei,Hugo Marques,Pedro de Araújo Gonçalves,Gianluca Pontone,Peter Howard Stone
出处
期刊:Jacc-cardiovascular Imaging [Elsevier BV]
被引量:1
标识
DOI:10.1016/j.jcmg.2026.08.018
摘要

BACKGROUND: Perivascular adipose tissue (PVAT) density on coronary computed tomography angiography (CTA) reflects pericoronary inflammation, but measurements adjacent to existing plaques may be confounded by local inflammatory signaling from the plaque itself-a form of reverse causation. Whether systematically comparing patient-level PVAT aggregation approaches (including measurements restricted to plaque-free segments) can identify a more robust inflammatory biomarker has not been evaluated. OBJECTIVES: The authors aimed to compare the predictive performance of 4 patient-level PVAT aggregation approaches for coronary plaque progression. METHODS: From the PARADIGM serial coronary CTA registry, 412 patients with baseline coronary plaque who underwent serial coronary CTA at identical tube voltages were included (mean age: 61.1 ± 9.3 years; 61.7% male; mean interval: 3.2 ± 1.2 years). Four patient-level PVAT measures were compared: proximal right coronary artery (pRCA), whole-coronary, plaque-free, and plaque PVAT. Multivariable regression models were constructed for annualized plaque volume (PV) progression with adjustment for clinical risk factors and imaging covariates. RESULTS: Annualized increases in pRCA PVAT (β = 0.804; P = 0.033), whole-coronary PVAT (β = 1.142; P = 0.022), and plaque-free PVAT (β = 1.419; P = 0.007) were each independently associated with total PV progression, whereas plaque PVAT did not reach significance (β = 0.755; P = 0.083). For noncalcified PV progression, plaque-free PVAT was the only significant measure (β = 1.086; P = 0.026). None of the 4 baseline PVAT measures were significantly associated with plaque progression (all P > 0.50). Pairwise comparisons revealed no significant differences among the 4 measures. CONCLUSIONS: Changes in pRCA, whole-coronary, and plaque-free PVAT were each independently associated with total PV progression. For noncalcified PV progression, plaque-free PVAT change was the only significant measure. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).
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