153 Epicardial adipose tissue volume and density is associated with cardiac dysfunction in asymptomatic people with type 2 diabetes

Background

Type 2 diabetes (T2D) is associated with several perturbations of cardiac structure and function, which are precursors to the development of heart failure. Excess accumulation of epicardial adipose tissue (EAT) may contribute to cardiac dysfunction in individuals with T2D. Lipid-laden adipocytes have a lower computed tomography (CT) attenuation and can be readily identified using cardiac CT. Using a multimodality cardiac imaging approach, we aimed to assess the association of total and low attenuation EAT volume with early markers of cardiac dysfunction in people with T2D.

Methods

Prospective case-control study, in which participants with and without T2D and no known cardiovascular disease, underwent comprehensive cardiovascular phenotyping including multiparametric cardiac magnetic resonance imaging (MRI), echocardiography and non-contrast cardiac CT. EAT volume was measured from CT scans using a deep learning method and volumes indexed to body surface area. Total EAT was defined according to CT adipose tissue attenuation range of -30 to -190 Hounsfield Units (HU) and low attenuation EAT as -90 to -190 HU. Left ventricular (LV) volumes, function and strain measurements were derived from cardiac MRI images and diastolic function also assessed using echocardiography. Markers of early cardiac dysfunction in those with T2D were assessed for associations with EAT in T2D participants using multivariable linear regression analyses.

Results

Two hundred and fifty-four participants were included: demographic, anthropometric and imaging variables are displayed in Table 1. Subjects with T2D had increased LV concentric remodelling (higher LV mass/volume ratio), diastolic dysfunction (lower circumferential peak early diastolic strain rate (PEDSR) and average E/e’) and reduced systolic function (global longitudinal strain, GLS) compared with controls. Total and low attenuation indexed EAT volumes were 1.6-fold and 2-fold higher, respectively, in participants with T2D compared to controls (Figure 1). After adjustment for age, gender, ethnicity, insulin resistance, systolic blood pressure and waist/hip ratio, total and low attenuation indexed EAT volume were independently associated with LV mass/volume ratio (total indexed EAT volume: ß= 0.002, p = 0.02, low attenuation indexed EAT volume: : ß= 0.004, p= 0.01) and LV GLS (total indexed EAT volume: ß= -0.02, p <0.01, low attenuation indexed EAT volume: ß= -0.04, p= 0.02) in subjects with T2D, but not indices of diastolic dysfunction.

Conclusion

Total and low attenuation EAT volumes are higher in individuals with T2D, and excess EAT accumulation is independently associated with early markers of cardiac dysfunction. Further studies into the underlying mechanisms of this interaction may facilitate the development of interventions targeted at EAT, which could mitigate against the development of heart failure in people with T2D.

Conflict of Interest

None