Relationship between epicardial adipose tissue thickness and epicardial adipocyte size with increasing body mass index

Abstract

Macroscopic deposition of epicardial adipose tissue (EAT) has been strongly associated with numerous indices of obesity and cardiovascular disease risk. In contrast, the morphology of EAT adipocytes has rarely been investigated. We aimed to determine whether obesity-driven adipocyte hypertrophy, which is characteristic of other visceral fat depots, is found within EAT adipocytes. EAT samples were collected from cardiac surgery patients (n = 49), stained with haematoxylin & eosin, and analysed for mean adipocyte size and non-adipocyte area. EAT thickness was measured using echocardiography. A significant positive relationship was found between EAT thickness and body mass index (BMI). When stratified into standardized BMI categories, EAT thickness was 58.7% greater (p = 0.003) in patients from the obese (7.3 ± 1.8 mm) compared to normal (4.6 ± 0.9 mm) category. BMI as a continuous variable significantly correlated with EAT thickness (r = 0.56, p < 0.0001). Conversely, no correlation was observed between adipocyte size and either BMI or EAT thickness. No difference in the nonadipocyte area was found between BMI groups. Our results suggest that the increased macroscopic EAT deposition associated with obesity is not caused by adipocyte hypertrophy. Rather, alternative remodelling via adipocyte proliferation might be responsible for the observed EAT expansion. ARTICLE HISTORY

Enlarged adipocytes from subcutaneous vs. visceral adipose tissue differentially contribute to metabolic dysfunction and atherogenic risk of patients with obesity

“…However, other studies have failed finding correlation between adipocyte size and visceral mass expansion, as in the case of epicardial thickness. This may be due to the heterogeneity of adipocytes size in VAT from different body sites, or dissimilarities regarding BMI and gender distribution between study populations 20 , 36 .…”

<p>Bone Morphogenetic Protein-2 and Osteopontin Gene Expression in Epicardial Adipose Tissue from Patients with Coronary Artery Disease Is Associated with the Presence of Calcified Atherosclerotic Plaques</p>

“…Despite the small number of subjects, we demonstrated that EAT volume has a positive correlation with BMI, confirming the association observed in previous studies. 42,43 For a long time, the research has been focused on the role of abdominal visceral adipose tissue in cardiovascular diseases. However, due to contiguity with coronary arteries, the EAT could be decisive in the onset, progression, and calcification of atherosclerotic plaque.…”

“…Therefore, EAT may be a potential therapeutic target in cardiovascular disease, and it is necessary to determine the size and the adiposopathy grade of EAT as a risk factor of CAD. 42 In addition, it should be considered that the anatomical location of EAT is related with its secretor pattern. 44 This suggests that not only the EAT per se, but also its anatomical localization is crucial in the artery calcification.…”

Targeting epicardial adipose tissue with exercise, diet, bariatric surgery or pharmaceutical interventions: A systematic review and meta‐analysis

“…A recent study by Aitken-Buck et al 59 has suggested that the expansion of EAT is different from that of the visceral and subcutaneous adipose tissue. It has previously been reported that the primary mechanism of fat depot expansion for visceral and subcutaneous adipose tissue is dependent on adipocyte hypertrophy, but that is not the case with EAT.…”

“…Conversely, the authors suggests hyperplasia to be the primary remodelling mechanism for EAT, but it remains unclear to what extent the physiology and metabolic functions of EAT are affected by this. 59 It is, therefore, expected that visceral, subcutaneous and epicardial fat depots will respond differently to lifestyle or pharmaceutical interventions and a future investigation to explain these differences are warranted.…”