Impact of epicardial adipose tissue on myocardial function and structure in patients with severe aortic valve stenosis

Abstract Aims Epicardial adipose tissue (EAT) is closely associated with the development of heart failure and adverse myocardial remodelling. In patients with severe aortic valve stenosis (AS) undergoing transcatheter aortic valve replacement (TAVR), increased EAT has been identified as a predictor of adverse outcomes; however, the underlying pathophysiological mechanisms remain unclear. This study aims to explore the effects of increased EAT volumes on myocardial remodelling and dysfunction in patients with severe AS. Methods and results One hundred thirty‐seven patients with severe AS (median age 80 years, 62% male) underwent cardiac magnetic resonance imaging (CMR) prior to TAVR. Myocardial volumes and function as well as EAT volumes were quantified from CMR acquisitions. The cohort was dichotomised at the median EAT volume. Patients with increased EAT volumes above the median (≥46.5 mL/m 2 ) showed impaired left atrial (LA) reservoir strain (Es) as a distinct functional feature compared with patients with lower EAT volumes (11.8% 7.6–16.7 vs. 15.0% 10.9–19.1, P = 0.011), while left ventricular (LV) morphology and function (all P ≥ 0.216), right atrial and ventricular morphology and function (all P ≥ 0.090), as well as tissue characteristics (all ≥ 0.229) were similar between both groups. In a subgroup analysis of the four types of severe AS, the difference was most prominent in patients with low ejection fraction high‐gradient AS. In multivariable regression analyses, EAT was independently associated with impaired LA Es, irrespective of co‐morbidities, ventricular function, tissue characteristics and functional characteristics of AS. Conclusions In patients with severe AS, increased EAT volume is independently associated with impaired LA function but not with other features of biventricular morphology, function or tissue composition. The incremental deterioration of LA function, in addition to the afterload imposed by AS in these patients, could increase vulnerability to heart failure and may require consideration as a therapeutic target beyond TAVR.