Impact of epicardial adipose tissue on cardiac function and morphology in patients with diastolic dysfunction

Abstract

AimsThis study aimed to identify the impact of increased epicardial adipose tissue (EAT) and its regional distribution on cardiac function in patients with diastolic dysfunction.Methods and resultsSixty‐eight patients with exertional dyspnoea (New York Heart Association ≥II), preserved ejection fraction (≥50%), and diastolic dysfunction (E/e′ ≥ 8) underwent rest and stress right heart catheterization, transthoracic echocardiography, and cardiovascular magnetic resonance (CMR). EAT volumes were depicted from CMR short‐axis stacks. First, the impact of increased EAT above the median was investigated. Second, the association of ventricular and atrial EAT with myocardial deformation at rest and during exercise stress was analysed in a multivariable regression analysis. Patients with high EAT had higher HFA‐PEFF and H2FPEFF scores as well as N‐terminal prohormone of brain natriuretic peptide levels (all P < 0.048). 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). No differences in biventricular volumetry and left ventricular mass (all P > 0.074) were observed. Patients with high EAT had impaired atrial strain at rest and during exercise stress, and impaired ventricular strain during exercise stress. Regionally increased EAT was independently associated with functional impairment of the adjacent chambers.ConclusionsPatients with diastolic dysfunction and increased EAT show more pronounced signs of diastolic functional failure and adverse structural remodelling. Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular in the atria. Our results indicate that regionally increased EAT directly induces atrial functional failure, which represents a distinct pathophysiological feature in HFpEF.

New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review

“…In this study, the LV eccentricity was not related to body mass index, subcutaneous fat, visceral fat, or pulmonary vascular resistance and exercise did not modify the cardio-mechanical interaction [103]. Patients with diastolic dysfunction and increased EAT show more pronounced signs of diastolic functional failure and adverse structural remodeling [104]. Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular in the atria, indicating that regionally increased EAT directly induces atrial functional failure [104] (Figure 1).…”

“…more pronounced signs of diastolic functional failure and adverse structural remodeling [104]. Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular in the atria, indicating that regionally increased EAT directly induces atrial functional failure [104] (Figure 1). Recently, it has been shown that in HFpEF patients obesity and epicardial adiposity are associated with hemodynamic signs of pericardial constraint [106], and 73% of them had a square root sign [106].…”

“…Patients with diastolic dysfunction and increased EAT show more pronounced signs of diastolic functional failure and adverse structural remodeling [104]. Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular in the atria, indicating that regionally increased EAT directly induces atrial functional failure [104] (Figure 1). more pronounced signs of diastolic functional failure and adverse structural remodeling [104].…”

“…Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular in the atria, indicating that regionally increased EAT directly induces atrial functional failure [104] (Figure 1). more pronounced signs of diastolic functional failure and adverse structural remodeling [104]. Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular in the atria, indicating that regionally increased EAT directly induces atrial functional failure [104] (Figure 1).…”

Novel Therapeutics for Type 2 Diabetes Mellitus—A Look at the Past Decade and a Glimpse into the Future

“…The beneficial effects of GLP-1 RAs on HFpEF could be related to the alteration of epicardial adipose tissue (EAT) [132]. Evidence suggests that individuals with diastolic dysfunction have increased epicardial adipose tissue, which could lower peak oxygen consumption and worsen exercise tolerance [133]. Using liraglutide over 6 months, EAT thickness was significantly reduced from 9.6 to 6.26 mm versus no change in the metformin arm [134].…”