Abstract 13257: Impact of Epicardial Adipose Tissue and Its Distribution on Cardiac Function in Patients With Diastolic Dysfunction

Background: Epicardial adipose tissue (EAT) was identified as an important risk factor for diastolic dysfunction and affects cardiac structural remodeling. However, within this patient group the impact of increased EAT and its regional distribution on cardiac function is yet unclear.

Methods: 68 patients with exertional dyspnea (NYHA≥II), preserved ejection fraction (EF≥50%) and diastolic dysfunction (E/e’≥10) underwent rest and stress right heart catheterization (RHC), transthoracic echocardiography and cardiac magnetic resonance (CMR). EAT volumes were depicted from CMR short-axis stacks. First, the impact of increased total EAT was analyzed. Second, we investigated the association of ventricular and atrial EAT with impaired strain at rest and during exercise stress of the adjacent chambers in multivariable regression analysis.

Results: Patients with high EAT had higher HFA-PEFF and H2FPEFF-Scores as well as nt-proBNP levels (p<0.048). Furthermore, they were diagnosed with manifest heart failure with preserved ejection fraction (HFpEF) more frequently (low EAT: 37% vs. high EAT: 64%; p=0.029) and had signs of adverse remodelling indicated by higher T1-times (p<0.001).While both groups had no differences in biventricular volumetry and left ventricular mass (p>0.074), functional analysis in high EAT patients revealed impaired atrial strain at rest and during exercise stress, while ventricular strain was impaired during exercise stress only.The assessment of regional EAT revealed an independent association of higher ventricular and atrial EAT with functional impairment of the adjacent chambers.

Conclusion: Patients with diastolic dysfunction and increased EAT show more pronounced signs of diastolic functional failure and structural remodeling. Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular of the atria. Our results indicate that regionally increased EAT directly induces atrial functional failure, which represents a distinct pathophysiological feature in HFpEF.