European heart journal. Cardiovascular Imaging · 2025
Association between inflammatory biomarkers, chronic stress, and pericoronary adipose tissue attenuation obtained with coronary CT.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Albertini Tobia, Dörner Marc, Giannopoulos Andreas A, von Känel Roland, Benz Dominik C, Mikail Nidaa, de Wilde Daniel, Voegel Clarissa D, Binz Tina M, Kaufmann Philipp A, Gebhard Catherine, Buechel Ronny R, Pazhenkottil Aju P
Аннотация
AIMS: Pericoronary adipose tissue (PCAT) attenuation is a novel imaging biomarker of coronary inflammation associated with an increased risk of coronary artery disease (CAD). However, no studies have examined the relationship between chronic stress and PCAT. This study aimed to evaluate the intersection between chronic stress, inflammatory biomarkers, coronary plaque features, and PCAT attenuation.
METHODS AND RESULTS: A total of 98 participants without known CAD were included. PCAT attenuation, total plaque volume (TPV) quantification, and vulnerable plaque features were assessed by coronary CT angiography and chronic stress was measured by hair cortisol concentration (HCC) and vital exhaustion questionnaire. Regression models were used to analyse associations of PCAT with the inflammatory biomarkers interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α), TPV, vulnerable plaque features, and coronary stenosis. Moderating analyses were performed to test whether chronic stress modulated the association between inflammatory biomarkers and PCAT attenuation. PCAT attenuation was significantly associated with IL-6 (mean difference 1.05, 95% CI 0.21-1.89, P = 0.014), TNF-α (mean difference 0.60, 95% CI 0.06-1.13, P = 0.027), and a greater TPV (mean difference 3.51, 95% CI 0.02-7.00, P = 0.048), but not vulnerable plaque features or coronary stenosis. HCC (interaction term -0.12, 95% CI -0.22 to -0.02, P = 0.019) and vital exhaustion (interaction term 0.13, 95% CI 0.01-0.25, P = 0.024) moderated the relationship between IL-6, but not TNF-α, and PCAT attenuation.
CONCLUSION: This study suggests that circulating inflammatory biomarkers are associated with PCAT attenuation, which was further correlated with TPV. Chronic stress may moderate the relationship between inflammatory cytokines and PCAT attenuation.
METHODS AND RESULTS: A total of 98 participants without known CAD were included. PCAT attenuation, total plaque volume (TPV) quantification, and vulnerable plaque features were assessed by coronary CT angiography and chronic stress was measured by hair cortisol concentration (HCC) and vital exhaustion questionnaire. Regression models were used to analyse associations of PCAT with the inflammatory biomarkers interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α), TPV, vulnerable plaque features, and coronary stenosis. Moderating analyses were performed to test whether chronic stress modulated the association between inflammatory biomarkers and PCAT attenuation. PCAT attenuation was significantly associated with IL-6 (mean difference 1.05, 95% CI 0.21-1.89, P = 0.014), TNF-α (mean difference 0.60, 95% CI 0.06-1.13, P = 0.027), and a greater TPV (mean difference 3.51, 95% CI 0.02-7.00, P = 0.048), but not vulnerable plaque features or coronary stenosis. HCC (interaction term -0.12, 95% CI -0.22 to -0.02, P = 0.019) and vital exhaustion (interaction term 0.13, 95% CI 0.01-0.25, P = 0.024) moderated the relationship between IL-6, but not TNF-α, and PCAT attenuation.
CONCLUSION: This study suggests that circulating inflammatory biomarkers are associated with PCAT attenuation, which was further correlated with TPV. Chronic stress may moderate the relationship between inflammatory cytokines and PCAT attenuation.