Association between epicardial adipose tissue and cardiac dysfunction in subjects with severe obesity

Background

Epicardial adipose tissue (EAT) plays a role in obesity‐related heart failure with preserved ejection fraction. However, the association of EAT thickness with the development of cardiac dysfunction in subjects with severe obesity without known cardiovascular disease is unclear.

Aims

Determine the association between EAT thickness and cardiac dysfunction and describe the potential value of EAT as an early marker of cardiac dysfunction.

Methods and results

Subjects with BMI ≥35 kg/m² aged 35 to 65 years, who were referred for bariatric surgery, without suspicion of or known cardiac disease, were enrolled. Conventional transthoracic echocardiography and strain analyses were performed. A total of 186 subjects were divided into tertiles based on EAT thickness, of whom 62 were in EAT‐1 (EAT <3.8 mm), 63 in EAT‐2 (EAT 3.8–5.4 mm), and 61 in EAT‐3 (EAT >5.4 mm). Parameters of systolic and diastolic function were comparable between tertiles. Patients in EAT‐3 had the lowest global longitudinal strain (GLS) and left atrial contractile strain (LASct). Linear regression showed that a one‐unit increase in EAT thickness (mm) was independently associated with a decrease in GLS (%) (β‐coefficient − 0.404, p = 0.002), and a decrease in LASct (%) (β‐coefficient − 0.544, p = 0.027). Furthermore, EAT‐3 independently predicted cardiac dysfunction as defined by a GLS < 18% (OR 2.8, p = 0.013) and LASct<14% (OR 2.5, p = 0.045).

Conclusions

Increased EAT thickness in subjects with obesity without known cardiac disease was independently associated with subclinical cardiac dysfunction. Our findings suggest that EAT might play a role in the early stages of cardiac dysfunction in obesity before this may progress to overt clinical disease.

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