Key result
Epicardial fat expansion during menopause contributes to inflammation, LV remodeling, and HFpEF pathogenesis.
Why the study?
Postmenopausal women are overrepresented in HFpEF, and the menopause transition provides an opportunity to evaluate the role of epicardial adipose tissue expansion in HFpEF pathogenesis.
Highlights the potential role of epicardial adipose tissue expansion during the menopause transition in the pathogenesis of HFpEF, suggesting CT imaging as a useful evaluation tool.
Postmenopausal women are overrepresented in the preserved ejection heart failure population. Expansion of visceral and epicardial adipose tissue during the menopause transition leads to local and low-grade systemic inflammation that in turn contributes to left ventricular concentric remodeling, diastolic dysfunction and the development and progression of preserved ejection fraction. In contrast to visceral adipose tissue imaging, epicardial adipose tissue can be inexpensively imaged on low radiation coronary calcium score computerized tomography examination. The menopause transition provides a unique time frame to evaluate the contribution of epicardial adipose tissue expansion to the pathogenesis of preserved ejection heart failure.
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Museedi et al. (2024) conducted a review in Heart failure with preserved ejection fraction. Menopause transition and epicardial adipose tissue expansion was evaluated. Expansion of epicardial adipose tissue during the menopause transition contributes to local inflammation, left ventricular remodeling, and the pathogenesis of preserved ejection fraction heart failure.
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