1337383 - Epicardial adipose tissue association with adverse biomarkers and mortality in aortic stenosis: A Cardiovascular Magnetic Resonance Study

Epicardial adipose tissue (EAT) is an active type of visceral fat situated between the pericardium and the myocardium. EAT can be accurately quantified non-invasively by computed tomography (CT) and cardiovascular magnetic resonance (CMR) imaging. CMR has a high sensitivity to the off-resonance properties of fat and allows fat-water separation imaging to accurately detect and quantify EAT^[1], without the exposure to ionizing radiation that comes with CT. CMR also allows accurate detection of myocardial fibrosis using late gadolinium enhancement (LGE-CMR) and is therefore a valuable part of routine assessment of aortic stenosis (AS). Current literature proposes that EAT has cardioprotective properties and therefore may be of value as a prognostic predictor in those with AS^[2–5]. We aimed to investigate the relation of EAT indexed to myocardial mass and prognosis in AS and its correlation with peripheral blood biomarkers.

Methods:

We included 119 consecutive patients with Aortic Stenosis (AS) who had undergone LGE-CMR on a 1.5T Siemens magnet. Left ventricular function, volume, mass, myocardial fibrosis, aortic valve severity and EAT volume were quantified. The volume of EAT was determined blinded to clinical data using a dedicated software (CVI 42, Circle Cardiovascular Imaging, Calgary, Canada). EAT was assessed both in the short-axis (SAX) views for all slices in diastole to render a 3D model of overall adipose and then indexed to myocardial mass. Survival status was acquired from the Office of National Statistics.

Results:

Over a mean follow up of 4.2 ± 2.4 years, 61 (51%) patients died. The main finding of this study was that a higher volume of EAT was not significantly associated with mortality in patients with AS when indexed to myocardial mass (HR 0.646, 95% CI 0.135-3.097, p=0.585). In addition, volume of EAT was not significantly associated with body surface area, valve area, ejection fraction and late gadolinium enhancement (LGE), suggesting that EAT volume is not correlated with the presence of myocardial fibrosis (figure 1). Finally, EAT volume was not significantly associated with any of the prognostic biomarkers analysed including high-sensitivity troponin, N-terminal pro hormone brain natriuretic peptide (NT-proBNP), BNP, osteoprotegerin, suppression of tumorigenicity 2 (ST2), C-reactive protein (CRP) or Lipoprotein (a) (figure 2).

Conclusion:

Our findings demonstrate that increased EAT volume is not significantly associated with mortality in a cohort of patients with AS. Whilst there is no conclusive evidence surrounding the potential role of EAT in AS, it is clear that this is a dynamic organ that requires further larger collaborative research to investigate the effect EAT has in those with AS, as well as other major cardiovascular diseases.