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Bariatric Surgery Reduces Epicardial Adipose Tissue and is Associated with Improved Cardiac Function
Jie Fen Chin1,2, Yaar S Aga3,4, Sabrina Abou Kamar4
1Sint Franciscus Gasthuis, Rotterdam, Netherlands. j.chin@franciscus.nl.
Background:
Epicardial adipose tissue (EAT) has garnered interest due to its important role in obesity-related heart failure with preserved ejection fraction. However, while bariatric surgery is known to both improve cardiac function and reduce EAT, the presence of any relation between these two remains unclear. This study aims to investigate the association between EAT changes and improvement of cardiac dysfunction following bariatric surgery.
Methods:
This prospective cohort study enrolled subjects aged 35-65years with a body mass index ≥ 35 kg/m² who underwent bariatric surgery, excluding those with known cardiac disease. Conventional transthoracic echocardiography and strain analyses were conducted before and one-year post-surgery. Improvement in cardiac function was defined as a composite outcome requiring improvement in three domains: systolic function (ejection fraction or global longitudinal strain), diastolic function (E/e'ratio or septal e'velocity), and cardiac remodeling (left atrial volume index or left ventricular mass index).
Results:
In the 142 patients who completed one year follow-up, a significant reduction in EAT of 31% was observed (pre-surgery:4.9 ± 1.5 mm, post-surgery:3.4 ± 1.1 mm; p < 0.001). Linear regression revealed that a one-millimeter reduction in EAT thickness was independently associated with improvements in global longitudinal strain (%)(β-coefficient:0.48; 95%CI:0.06-0.90; p = 0.027) and septal e'(cm/s)(β-coefficient:0.28; 95%CI:0.02-0.54; p = 0.035). Furthermore, a one-millimeter reduction in EAT thickness increased the odds of cardiac improvement by 58% (OR:1.58: 95%CI:1.15-2.24: p = 0.007).
Conclusion:
EAT reduction post-bariatric surgery was associated with LV function improvement one-year after bariatric surgery in individuals with obesity without established cardiac disease. Our results underscore the potential role of EAT as a marker of functional heart disease in obesity.
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