Abstract
Obesity has been conceptualized as a highly heterogeneous condition. We aim to investigate chamber-specific effects of obesity on the heart and relevant outcomes. A total of 2944 symptom-free individuals (age: 47.5 ± 10.0 years), free of known cardiovascular diseases were classified into four categories based on body mass index (BMI) (as normal-weight (NW) vs. overweight/obese (O)) and metabolic status (metabolically-healthy (MH) vs. unhealthy (MU)). Epicardial adipose thickness (EAT) using echocardiography method. Speckle-tracking based atrio-ventricular (LA/LV) deformations including global longitudinal strain (GLS) and peak atrial longitudinal strain (PALS) were also analyzed. MUNW had higher cardiometabolic risks and more impaired diastolic and GLS/PALS than MHNW phenotype. Both MHO and MUO phenotypes exhibited worst atrial functions. Greater EAT was independently associated with worse GLS and PALS after correcting for various anthropometrics, LV mass and LA volume, respectively, with unfavorable LA effects from EAT being more pronounced in the NW phenotypes (both p interactions < 0.05). During a median follow-up period of 5.3 years, BMI/EAT improved the reclassification for atrial fibrillation (AF) incidence (p for net reclassification improvement < 0.05) mainly in the NW phenotypes (p interaction < 0.001). Categorization of clinical obesity phenotypes based on excessive visceral adiposity likely provides increment prognostic impacts on atrial dysfunction, particularly in non-obese phenotypes.
Highlights
Obesity and its associated cardiometabolic disorders are well-established clinical risks for heart failure (HF) [1,2] and atrial fibrillation (AF) [3]
We further examined the associations of various adiposity/anthropometric measures with abnormal left ventricle (LV) strain (GLS < 18%), left atrium (LA) volume index (LAVi > 34 mL/m2 based on American Society of Echocardiography (ASE) guideline) [25], or LA strain (PALS < 23%) [26]
EAT index (EATi) of metabolically unhealthy normal weight” (MUNW) was significantly higher than both O phenotypes (Table 2)
Summary
Obesity and its associated cardiometabolic disorders are well-established clinical risks for heart failure (HF) [1,2] and atrial fibrillation (AF) [3]. AF is a known risk factor for HF with preserved ejection fraction (HFpEF), an HF phenotype of emerging clinical significance [4]. At least two distinct obesity phenotypes have been established: (i) an excessive body mass (defined by a large body mass index (BMI)); and (ii) an excessive ectopic fat deposition (subcutaneous or visceral adiposity). An excessive epicardial adipose tissue (EAT) has been recognized as a distinctive HFpEF phenotype in extremely obese subjects and was shown to exert adverse biological effects on the atrium, thereby leading to a higher AF risk [13,14]. It is possible that chamber-specific myocardial dysfunctions (atrial or ventricular) may differ among these obesity phenotypes, resulting in differential cardiovascular outcomes (i.e., AF or HF)
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