Key result
Menopausal estrogen decline is hypothesized to contribute to HFpEF pathogenesis.
Why the study?
Because HFpEF carries an annual mortality of 10% to 30% without specific treatments and predominantly affects women, a better understanding of underlying mechanisms like menopause-related estrogen decline is needed.
Does menopause-related estrogen decrease contribute to the pathogenesis of HFpEF?
This review hypothesizes that the decline of estrogen at menopause contributes to the pathogenesis of HFpEF, potentially explaining the higher prevalence of this condition in women.
Answers are grounded in this paper and cite their sources.
Supports estrogen-HFpEF hypothesis in postmenopausal women; should not yet change practice pending prospective validation.
Heart failure (HF) is a complex condition affecting >40 million people worldwide. It is defined by failure of the heart to pump (HF with reduced ejection fraction) or by the failure of the heart to relax, resulting in reduced filling but with preserved ejection fraction (HFpEF). HFpEF affects approximately 50% of patients with HF, most of whom are women. Given that the annual mortality ranges from 10% to 30% and as there are no treatments specifically directed for HFpEF, there is a need for better understanding of the underlying mechanisms of this condition. We put forward the hypothesis that the decline of estrogen at menopause might contribute to the pathogenesis of HFpEF and we highlight potential underlying mechanisms of estrogen action, which may attenuate the development of HFpEF. We also discuss areas in which additional research is needed to develop new approaches for prevention and treatment of HFpEF.
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Sabbatini et al. (2020) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Estrogen was evaluated. The decline of estrogen at menopause is hypothesized to contribute to the pathogenesis of heart failure with preserved ejection fraction (HFpEF), highlighting a need for further research.
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