Abstract
Background: Excessive visceral adipose tissue, a marker of abnormal metabolic process, has recently been shown to exert effects on cardiac struture and function. However, data regarding regional fat burden on left atrial (LA) mechanics and contractile function in subjects with heart failure and preserved ejection fraction (HFpEF) remained elusive. Methods: Totally studied 48 heart failure patients with preserved left ventricular ejection fraction (HFpEF) from heart failure (HF) outpatient clinics. Another 58 hypertensives and 26 normal volunteers were recruited from health evaluation center at the same time of patients enrollment. Myocardial deformation imaging from all directions, cardiac twist and left atrial (LA) strain analyzed. Global epicardial (EAT), thoracic peri-aortic (TAT) adipose tissue and regional inter-atrial fat burden (IAF, in thickness) were quantified by multi-detector Computed Tomography (MDCT) (Sensation 16, Siemens Medical Solutions, Forchheim, Germany) off-line analysis (Aquarius 3D Workstation, TeraRecon, San Mateo, CA, USA). Metabolic risk scoring (MS) was calculated by NCEP ATP III score. Results: Compared to hypertensives and normal group, patients with HFpEF tended to have higher LV mass index and LA diameter though similar LVEF (all p<0.05) observed. In addition, EAT, TAT and IAF all correlated with MS (trend p<0.05), and were all significantly higher in HFpEF group (ANOVA p<0.05), which were accompanied by significantly reduced LV deformation from all three directions and cardiac twist as well as lower LA strain (all p<0.05). In a multivariate model adjusting for age, gender, body mass index, blood pressure, MS and LV mass, for each increased standard deviation of IAF were independently associated with reduced LA strain (ß coef: -0.35, p=0.018). Conclusions: Fat pad surrounding inter-atrial region in relation to metabolic abnormalities may influence left atrial mechanical function in terms of atrial deformation. Our data suggested that such excessive regional adipose burden may partly play a role in the pathogenesis of early stage heart failure.
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