Why the study?
The association between epicardial adipose tissue thickness and cardiac dysfunction in individuals with severe obesity without known cardiovascular disease was unclear.
Is increased epicardial adipose tissue thickness associated with subclinical cardiac dysfunction in subjects with severe obesity without known cardiac disease?
Is increased epicardial adipose tissue thickness associated with subclinical cardiac dysfunction in subjects with severe obesity without known cardiac disease?
Increased epicardial adipose tissue thickness is independently associated with subclinical cardiac dysfunction (reduced GLS and LASct) in severely obese patients without known cardiovascular disease, suggesting its potential as an early marker.
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EAT thickness may flag early cardiac dysfunction in severe obesity; leaves open its value as a marker pending prospective validation.
AIM: 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. The aim of this study was to 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: 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% (odds ratio 2.8, p = 0.013) and LASct <14% (odds ratio 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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Chin et al. (2023) studied this question.
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