The Role of Estrogen in Cardiac Metabolism and Diastolic Function

Shumin Li; Anisha A. Gupte

doi:10.14797/mdcj-13-1-4

January 1, 2017Methodist DeBakey Cardiovascular JournalOpen Access

The Role of Estrogen in Cardiac Metabolism and Diastolic Function

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Why the study?

Does estrogen replacement improve left ventricular diastolic function in postmenopausal women and animal models?

Structured PICO

Does estrogen replacement improve left ventricular diastolic function in postmenopausal women and animal models?

P

Population

Postmenopausal women with heart failure with preserved ejection fraction (HFpEF) and animal models of left ventricular diastolic dysfunction (LVDD)

I

Intervention

Estrogen (E2) replacement therapy and estrogen receptor (ERa, ERb, GPR30) agonists

C

Comparator

Estrogen deficiency (menopause or ovariectomy)

O

Outcome

Left ventricular diastolic function and underlying mechanistic pathways (mitochondrial function, cardiac remodeling, hypertrophy, calcium homeostasis)

Targeting restoration of estrogen and its signaling provides novel therapeutic strategies for managing and treating diastolic heart failure in postmenopausal women.

Implication

Estrogen loss may contribute to HFpEF in postmenopausal women; animal data leave open any therapeutic role pending human studies.

Abstract

Heart failure with preserved ejection fraction (HFpEF) has similar prevalence and prognosis as HF with reduced EF, but there is no approved treatment for HFpEF. HFpEF is common in postmenopausal women, which suggests that the absence of estrogen (E2) plays a role in its pathophysiology. With the country's growing elderly population, the prevalence of HFpEF is rapidly increasing. This has triggered a renewed urgency in finding novel approaches to preventing and slowing the progression of HFpEF. In this review, we address the role of E2 in left ventricular diastolic function and how it impacts women with HFpEF as well as animal models. We also discuss the primary potential mechanisms that represent critical nodes in the mechanistic pathways of HFpEF and how new treatments could be developed to target those mechanisms.