key: cord-1030576-sdw3kbmg
authors: Sevilla, Teresa; Aparisi-Sanz, Álvaro; Aristizábal-Duque, Cristhian; Gómez-Salvador, Itziar; Baladrón, Carlos; Román, Alberto San
title: Epicardial adipose tissue attenuation in admitted patients with the COVID-19
date: 2021-07-21
journal: Rev Esp Cardiol (Engl Ed)
DOI: 10.1016/j.rec.2021.07.006
sha: 28fff3cc4d84a7a6797befcd6bbfc889e9776bed
doc_id: 1030576
cord_uid: sdw3kbmg

nan

To the Editor,

Since the outbreak of the acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus disease 2019 (COVID-19) pandemic has spread worldwide and has caused almost 4 million deaths while more than 171 million people have contracted the virus 1 year later. 1 It has been previously reported that obesity increases the risk of COVID-19 complications. 2 Obesity not only indicates increased subcutaneous adipose tissue, but is also associated with increased visceral ectopic fat, including epicardial adipose tissue (EAT). It is known that increased visceral fat distribution promotes chronic proinflammatory, prothrombotic, and vasoconstrictive states 2 and it has been linked to a worse prognosis in COVID-19 patients. 3 Due to its local and systemic effects, EAT has been proposed as a leading actor in myocardial inflammation in COVID-19. 4, 5 Chest computed tomography (CT) examination allows quantification of adipose tissue and assessment of its metabolic activity by measuring its radiodensity or attenuation with a quantitative scale: Hounsfield units (HU). It has been proven that CT attenuation measured in HU can distinguish the metabolic activity of adipose tissue; highly active adipose tissue is characterized by more positive HUs, and hence greater tissue densities. 6 Our aim was to investigate the association of EAT attenuation with the clinical outcomes of COVID-19 infection. We retrospectively analyzed EAT attenuation in chest CT scans performed in 75 patients admitted to our hospital due to COVID-19 infection between March and May 2020. The decision to perform the CT scans was made clinically by the treating physician. We compared EAT attenuation values of COVID-19 patients with those of controls individually matched for age and sex. All controls were identified from a prospectively collected database of 3792 patients who underwent a cardiac CT scan in our hospital. The eligibility criteria for controls included 256 patients undergoing the test due to chest pain that were reported as normal (Agatston score= 0, normal epicardial coronary arteries and no other pathology seen on the CT scan). After randomly matching for age and sex, we obtained J o u r n a l P r e -p r o o f 46 pairs to compare. The study was performed in accordance with the institutional review board of our center, and there was no requirement for informed consent due to the retrospective and observational study design. CT images were analyzed using a state-of-the-art workstation tool (AW Server, General Electric Healthcare, USA). EAT was considered as all tissue with a HU threshold between −190 to −30 contained within the parietal pericardium. EAT attenuation was measured as the mean of 3 values obtained by manually drawing 3 regions of interest: 1 anterior to the great vessels, 1 in the pericoronary fat, and 1 anterior to the right ventricle.

Baseline characteristics of the study cohort were mean age 71 ± 11 years, 56% male patients, and median in-hospital stay of 15 days. Comorbidities were frequent: 55% of patients had hypertension, 27% had a history of cancer, and 25% had diabetes mellitus. A total of 42.7% of patients was overweight and 18.7% obese. Ten patients required intensive care, all of them with mechanical ventilation and 18 patients died (24%). COVID-19 patients had significantly higher EAT attenuation than controls (−91 HU vs −105 HU, P < .001, figure 1A ). In our population of cases, we found no differences in EAT attenuation in patients with different cardiovascular risk factors or comorbidities. Regarding the laboratory results, we found no correlation between EAT and any markers (including inflammatory, troponin and D-dimers). EAT attenuation was higher among patients with bacterial coinfection and in those requiring intensive care, mechanical ventilation, and vasopressor support. We found no differences between survivors and nonsurvivors (figure 1B).

The main factors associated with higher mortality included age, hypertension, dyslipidaemia, prior cancer, baseline hemoglobin, total white cell count, D-dimers, troponin, C-reactive protein, and lactate dehydrogenase levels. Table 1 summarizes their relationship with EAT attenuation values.

Our COVID-19 patients had higher EAT attenuation values than controls. Among COVID-19 patients, EAT attenuation was higher in cases with a complicated clinical course: in hemodynamically unstable patients and among those requiring intensive care and mechanical ventilation. These findings are compatible with the hypothesis that EAT could act as a contributor to SARS-CoV-2 entry into the heart Correcciones a la figura: Cambiar guiones por signos menor, cambiar comas por puntos, y poner espacios a ambos lados de "±" y "=".

WHO Coronavirus Disease (COVID-19) Dashboard. Available at

Obesity and Mortality Among Patients Diagnosed With COVID-19: Results From an Integrated Health Care Organization

The role of visceral adiposity in the severity of COVID-19: Highlights from a unicenter cross-sectional pilot study in Germany

Epicardial adipose tissue: fuel for COVID-19-induced cardiac injury?

Does epicardial fat contribute to COVID-19 myocardial inflammation?

Differential computed tomographic attenuation of metabolically active and inactive adipose tissues