Epicardial adipose tissue is associated with extent of pneumonia and adverse outcomes in patients with COVID-19.
Epicardial adipose tissue is associated with extent of pneumonia and adverse outcomes in patients with COVID-19.
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DOI：
10.1016/j.metabol.2020.154436
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发表时间：
2021-03
期刊：
影响因子：
--
通讯作者：
Dey D
中科院分区：
文献类型：
--
作者：
Grodecki K;Lin A;Razipour A;Cadet S;McElhinney PA;Chan C;Pressman BD;Julien P;Maurovich-Horvat P;Gaibazzi N;Thakur U;Mancini E;Agalbato C;Menè R;Parati G;Cernigliaro F;Nerlekar N;Torlasco C;Pontone G;Slomka PJ;Dey D
我们试图检查胸部计算机断层扫描（CT）量化的心外膜脂肪组织（EAT）与2019冠状病毒病（COVID-19）患者的肺炎程度和不良结局的关系。我们对一项前瞻性国际登记研究进行了事后分析，该研究包括109例连续患者（年龄64 ± 16岁; 62%为男性），这些患者均经实验室确诊为COVID-19并进行了非造影胸部CT成像。使用半自动化软件，我们量化了与COVID-19肺炎相关的肺部异常的负担（%）。使用深度学习软件测量EAT体积（mL）和衰减（Hounsfield单位）。主要结局为临床恶化（入住重症监护室、有创机械通气或血管加压药治疗）或院内死亡。在调整患者合并症的多变量线性回归分析中，COVID-19肺炎的总负担与EAT体积（β = 10.6，p = 0.005）和EAT衰减（β = 5.2，p = 0.004）相关。EAT体积与血清乳酸脱氢酶（r = 0.361，p = 0.001）和C反应蛋白（r = 0.450，p < 0.001）水平相关。23例（21.1%）患者在胸部CT后中位3天（IQR 1-13天）发生临床恶化或死亡。在多变量logistic回归分析中，EAT体积（OR 5.1 [95% CI 1.8-14.1]/倍增p = 0.011）和EAT衰减（OR 3.4 [95%CI 1.5-7.5]每增加5个Hounsfield单位，p = 0.003）是临床恶化或死亡的独立预测因子，总肺炎负荷也是（OR 2.5，95% CI 1.4-4.6，p = 0.002）、慢性肺病（OR 1.3 [95% CI 1.1-1.7]，p = 0.011）和心力衰竭病史（OR 3.5 [95% CI 1.1-8.2]，p = 0.037）。从胸部CT量化的EAT指标与COVID-19患者的肺炎程度和不良结局独立相关，支持其在临床风险分层中的使用。心外膜脂肪组织（EAT）体积和衰减与COVID-19肺炎的定量负担相关。EAT体积增加或衰减独立预测临床恶化或死亡。EAT可能有助于增强对COVID-19的全身炎症反应。将EAT测量结果整合到COVID-19风险评分中有可能增强结果预测。
We sought to examine the association of epicardial adipose tissue (EAT) quantified on chest computed tomography (CT) with the extent of pneumonia and adverse outcomes in patients with coronavirus disease 2019 (COVID-19). We performed a post-hoc analysis of a prospective international registry comprising 109 consecutive patients (age 64 ± 16 years; 62% male) with laboratory-confirmed COVID-19 and noncontrast chest CT imaging. Using semi-automated software, we quantified the burden (%) of lung abnormalities associated with COVID-19 pneumonia. EAT volume (mL) and attenuation (Hounsfield units) were measured using deep learning software. The primary outcome was clinical deterioration (intensive care unit admission, invasive mechanical ventilation, or vasopressor therapy) or in-hospital death. In multivariable linear regression analysis adjusted for patient comorbidities, the total burden of COVID-19 pneumonia was associated with EAT volume (β = 10.6, p = 0.005) and EAT attenuation (β = 5.2, p = 0.004). EAT volume correlated with serum levels of lactate dehydrogenase (r = 0.361, p = 0.001) and C-reactive protein (r = 0.450, p < 0.001). Clinical deterioration or death occurred in 23 (21.1%) patients at a median of 3 days (IQR 1–13 days) following the chest CT. In multivariable logistic regression analysis, EAT volume (OR 5.1 [95% CI 1.8–14.1] per doubling p = 0.011) and EAT attenuation (OR 3.4 [95% CI 1.5–7.5] per 5 Hounsfield unit increase, p = 0.003) were independent predictors of clinical deterioration or death, as was total pneumonia burden (OR 2.5, 95% CI 1.4–4.6, p = 0.002), chronic lung disease (OR 1.3 [95% CI 1.1–1.7], p = 0.011), and history of heart failure (OR 3.5 [95% 1.1–8.2], p = 0.037). EAT measures quantified from chest CT are independently associated with extent of pneumonia and adverse outcomes in patients with COVID-19, lending support to their use in clinical risk stratification. Epicardial adipose tissue (EAT) volume and attenuation associate with the quantitative burden of COVID-19 pneumonia. An increasing EAT volume or attenuation independently predicts clinical deterioration or death. EAT may contribute to the augmented systemic inflammatory response to COVID-19. The integration of EAT measurements into COVID-19 risk scores has the potential to enhance outcome prediction.
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影响因子：
5.4
作者：
Goeller, Markus;Achenbach, Stephan;Dey, Damini
通讯作者：
Dey, Damini
影响因子：
25.4
作者：
Guaraldi, Giovanni;Meschiari, Marianna;Mussini, Cristina
通讯作者：
Mussini, Cristina
DOI：
10.1148/ryct.2020200389
发表时间：
2020-10
期刊：
Radiology. Cardiothoracic imaging
影响因子：
--
作者：
Grodecki K;Lin A;Cadet S;McElhinney PA;Razipour A;Chan C;Pressman B;Julien P;Maurovich-Horvat P;Gaibazzi N;Thakur U;Mancini E;Agalbato C;Menè R;Parati G;Cernigliaro F;Nerlekar N;Torlasco C;Pontone G;Slomka PJ;Dey D
通讯作者：
Dey D
影响因子：
8.3
作者：
Franssens, Bas T.;Nathoe, Hendrik M.;Visseren, Frank L. J.
通讯作者：
Visseren, Frank L. J.
影响因子：
3.8
作者：
Lo, Janet;Abbara, Suhny;Grinspoon, Steven K.
通讯作者：
Grinspoon, Steven K.