key: cord-0725903-27jqhz98
authors: Kim, In-Cheol; Han, Seongwook
title: Epicardial adipose tissue: fuel for COVID-19-induced cardiac injury?
date: 2020-05-28
journal: Eur Heart J
DOI: 10.1093/eurheartj/ehaa474
sha: e9e6bd4a7373c061a495aa24b4dee0f6b168c907
doc_id: 725903
cord_uid: 27jqhz98

nan

manifestation in COVID-19. Among the possible mechanisms of cardiac injury, ACE2-mediated direct myocardial injury and inflammation are specifically suggested as significant contributors to myocarditis associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections. 1, 2 Epicardial adipose tissue (EAT), located between the myocardium and visceral pericardium, is a unique fat depot with multifaceted features such as local and systemic physiological effects. 3 This tissue has the highest rates of lipogenesis and fatty acid metabolism among the visceral fat depots and displays metabolic, thermogenic, and mechanical properties. Metabolic syndrome, visceral adiposity, and cardiac abnormalities such as coronary artery disease are associated with increased amounts of EAT. 3 Malavazos et al. raised an interesting issue regarding EAT and the incidence of myocardial injury in COVID-19. Since they share similar risk factors and mechanisms related to cardiac inflammation, it can be assumed that patients with cardiac injury would have a higher level of EAT.

The SARS-CoV-2 infection is triggered by binding of the spike protein of the virus to ACE2, which is highly expressed in the heart and lungs. From a previous experiment, ACE2 and the inflammatory cytokines tumour necrosis factor-(TNF) a and interleukin-6 (IL-6) have been demonstrated to be expressed at higher levels in EAT in heart explants removed from obese patients. We may infer that EAT would act as a major contributor for the SARS-CoV-2 entry into the heart and promote an augmented inflammatory response in the myocardium and surrounding structures, causing myocardial complications such as myocarditis and cardiac dysfunction, providing an inflammatory environment by stimulation of inflammatory cells, adipokines, and cytokines. 4 The cascade of inflammatory factors such as TNF-a and IL-6 has been linked to a diminished inotropic effect and decreased cardiac function, resulting in aggravation of hypoxia and a systemic myocardial inflammatory response. 3, 4 Being elderly and being obese are common contributors to EAT and there is an increased chance of SARS-CoV-2 infections in these subjects. 5 The higher prevalence of cardiac injury associated with COVID-19 in these specific populations may be linked to EAT acting as a 'fuel for cardiac inflammation' (Figure 1) .

From the evidence that EAT plays an essential role as a reservoir for SARS-CoV-2 and the related immune amplification, it is plausible to hypothesize that the amount of EAT is associated with the degree of myocardial damage. However, whether there is a direct association between the amount of EAT measured by echocardiography or computed tomography and the severity of the SARS-CoV-2-related cardiac injury has never been investigated. We need to speculate on the role of EAT in the cardiac manifestations related to COVID-19 with utilization of big data from the accumulating global experience.

Conflict of interest: none declared.

COVID-19-related myocarditis in a 21-year-old female patient

Myocardial localization of coronavirus in COVID-19 cardiogenic shock

Local and systemic effects of the multifaceted epicardial adipose tissue depot

Obesity accompanying COVID-19: the role of epicardial fat

Lille Intensive Care COVID-19 and Obesity study group, High prevalence of obesity in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) requiring invasive mechanical ventilation