Epicardial Fat Inflammation in Severe COVID-19.

Abstract

TO THE EDITOR: We read with great interest the paper by Deng et al. ((1)). Obesity increases the risk of coronavirus disease 2019 (COVID-19) morbidity and mortality ((2, 3)). However, Deng et al. suggested that not simply obesity but also visceral adiposity is an independent risk factor for COVID-19 complications in young adults ((1)). Interestingly, visceral fat could serve as a reservoir for the virus and amplify the inflammatory response ((4, 5)). Deng et al. reported computed tomography (CT) data of ectopic fat depots, such as liver fat and epicardial adipose tissue (EAT), in young patients with COVID-19 ((1)). EAT, the visceral fat depot of the heart, has been suggested to play a role in COVID-19 myocardial inflammation ((6-8)). Hence, we retrospectively analyzed EAT from CT scans of patients who were admitted for COVID-19. We collected data from 41 patients with laboratory-confirmed COVID-19 infection who were admitted at the Policlinico San Donato, San Donato Milanese, Milan, University of Milan, Italy, between April 1 and April 9, 2020. A confirmed case of COVID-19 was defined by a positive result on a reverse transcriptase-polymerase chain reaction assay of a specimen collected on a nasopharyngeal swab. Chest CT scan was performed on admission day 1 in patients with suspected or confirmed COVID-19 infection to evaluate the presence of pulmonary embolism. EAT measurement was retrospectively obtained from each CT scan and analyzed according to the clinical and radiological criteria defining COVID-19 severity. EAT and subcutaneous adipose tissue (SAT) density was defined as mean attenuation expressed in Hounsfield units (HU). Patients’ features on admission are reported in Table 1. More than half (54%) of the patients presented clinical and CT signs of pulmonary embolism. Almost two-thirds (26) of the patients had no coronary calcium content (CAC) score, and only two patients had a severe CAC score (> 400). Overall, EAT HU was significantly greater than SAT HU (−95 vs. −118 HU; P < 0.01); mean EAT thickness was 5.5 mm. We then compared EAT attenuation between the four different groups of patients according to COVID-19 severity. EAT attenuation significantly increased with increasing COVID-19 severity, whereas SAT attenuation did not substantially change, as depicted in Figure 1. Patients with severe and critical COVID-19 had significantly greater EAT attenuation than those presenting with mild and moderate COVID-19 (P ≤ 0.01 for all the comparisons; 95% CI: −99 to −69 HU). Results were substantially similar when EAT HU was calculated with or without contrast. CT-measured EAT thickness was similar among the groups of COVID-19 severity. EAT HU was significant correlated (r = −0.45; P < 0.05) with high-sensitivity troponin T levels, while there was no significant correlation with interleukin-6 levels (r = 0.05; P = 0.76). Moreover, EAT HU was significantly correlated with peripheral oxygen saturation (r = −054; P < 0.05) and body temperature (r = −0.43; P < 0.05). EAT attenuation reflects inflammatory changes within the fat depot ((9)). In our analysis, EAT showed imaging signs of increased inflammation in patients with severe and critical COVID-19. CT-measured EAT attenuation was consensually greater with higher degree of COVID-19 severity. Remarkably, EAT attenuation was similar to that observed in coronary artery disease despite most of these patients with COVID-19 having no history of coronary artery disease and no CAC. Deng et al. ((1)) found not quite statistically significant differences in CT-EAT attenuation between patients with moderate and severe COVID-19. However, in our study, patients were older and more critical than those evaluated by Deng et al. ((1)). Hence, the lower prevalence of patients with severe COVID-19 in the study by Deng et al. may explain the lack of statistically significant difference in CT-EAT attenuation. Also, elderly participants were more likely to have myocardial inflammation and injury ((1)). Notably, we found that SAT attenuation, unlike EAT, did not progress with the severity of COVID-19. This could be somehow consistent with Deng et al. who found no difference in SAT thickness between moderate and severe patients. Although our analysis presents with some limitations, cardiac imaging, particularly CT-measured EAT attenuation, could play a diagnostic and prognostic role in patients with COVID-19 with obesity ((10)). The authors declared no conflict of interest.