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. 2022 Apr;46(4):866-873.
doi: 10.1038/s41366-021-01050-7. Epub 2022 Jan 11.

Epicardial adipose tissue thickness is associated with increased COVID-19 severity and mortality

Roopa Mehta #  1   2 , Omar Yaxmehen Bello-Chavolla #  3 , Leonardo Mancillas-Adame  4 , Marcela Rodriguez-Flores  5 , Natalia Ramírez Pedraza  6 , Bethsabel Rodríguez Encinas  6 , Carolina Isabel Pérez Carrión  7 , María Isabel Jasso Ávila  7 , Jorge Carlos Valladares-García  7 , Pablo Esteban Vanegas-Cedillo  7 , Diana Hernández Juárez  7 , Arsenio Vargas-Vázquez  8   9 , Neftali Eduardo Antonio-Villa  8   9 , Monica Chapa-Ibarguengoitia  4 , Paloma Almeda-Valdés  8   7 , Daniel Elias-Lopez  8   7 , Arturo Galindo-Fraga  10 , Alfonso Gulias-Herrero  11 , Alfredo Ponce de Leon  10 , José Sifuentes-Osornio  10   11 , Carlos A Aguilar-Salinas  12   13   14
Affiliations

Epicardial adipose tissue thickness is associated with increased COVID-19 severity and mortality

Roopa Mehta et al. Int J Obes (Lond). 2022 Apr.

Abstract

Background: Increased adiposity and visceral obesity have been linked to adverse COVID-19 outcomes. The amount of epicardial adipose tissue (EAT) may have relevant implications given its proximity to the heart and lungs. Here, we explored the role of EAT in increasing the risk for COVID-19 adverse outcomes.

Methods: We included 748 patients with COVID-19 attending a reference center in Mexico City. EAT thickness, sub-thoracic and extra-pericardial fat were measured using thoracic CT scans. We explored the association of each thoracic adipose tissue compartment with COVID-19 mortality and severe COVID-19 (defined as mortality and need for invasive mechanical ventilation), according to the presence or absence of obesity. Mediation analyses evaluated the role of EAT in facilitating the effect of age, body mass index and cardiac troponin levels with COVID-19 outcomes.

Results: EAT thickness was associated with increased risk of COVID-19 mortality (HR 1.18, 95% CI 1.01-1.39) independent of age, gender, comorbid conditions and BMI. Increased EAT was associated with lower SpO2 and PaFi index and higher levels of cardiac troponins, D-dimer, fibrinogen, C-reactive protein, and 4 C severity score, independent of obesity. EAT mediated 13.1% (95% CI 3.67-28.0%) and 5.1% (95% CI 0.19-14.0%) of the effect of age and 19.4% (95% CI 4.67-63.0%) and 12.8% (95% CI 0.03-46.0%) of the effect of BMI on requirement for intubation and mortality, respectively. EAT also mediated the effect of increased cardiac troponins on myocardial infarction during COVID-19.

Conclusion: EAT is an independent risk factor for severe COVID-19 and mortality independent of obesity. EAT partly mediates the effect of age and BMI and increased cardiac troponins on adverse COVID-19 outcomes.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. Adipose tissue compartments and COVID-19 mortality.
Boxplots comparing transformed levels of epicardial fat thickness, pericardial fat, subthoracic fat and body-mass index (BMI), according to severe vs. non-severe COVID-19 (IVM, A–D) or COVID-19 mortality (E–H).
Fig. 2
Fig. 2. Epicardial adipose tissue and COVID-19 mortality risk.
Post-estimation simulation of the risk of epicardial fat thickness transformed by repeated out-of sample 10-fold cross-validation adjusted for age, gender, comorbid conditions and BMI (A) stratified in non-obese (B) and obese (C) cases with confirmed COVID-19.
Fig. 3
Fig. 3. Causal mediation models.
Diagrams of causal mediation models evaluating the role of epicardial adipose tissue (EAT) thickness as a mediating factor of the impact of body-mass index (BMI, A) on severe COVID-19 and mortality (COVID-19 outcome). Diagrams also show cardiac troponins (B) and Fibrinogen (C) as mediators of the association between EAT and COVID-19 outcomes.
See this image and copyright information in PMC

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