Currently cardiovascular disease (CVD) is the leading cause of death globally accounting for nearly 17.9 million deaths every year. Studies show that CVD affects men and women differently. A significant increase in CVD incidence is marked by the onset of menopause in women compared to age matched males. A commonality seen in CVD is the use of ꞵ-adrenergic receptors (ꞵ-ARs), as studies have shown that estrogen loss exacerbates the signaling of these ꞵ-AR’s. Changes within this signaling molecule can lead to structural and functional modifications in the heart, including systolic or diastolic dysfunction. This leads to the hypothesis that estrogen loss exacerbates cardiac function with acute sympathetic stimulation and hypertrophy, but prolonged stimulation blunts the sympathetic response. Female mice were ovariectomized (OVX) or underwent SHAM surgery at 2.5 months of age. These mice were treated with isoproterenol (ISO) to simulate chronic sympathetic stimulation for 7, 14, 21 and 28 days continuously through mini osmotic pumps 3 months post ovariectomy. Echocardiography parameters were analyzed using diastolic diameter (DD), systolic diameter (SD), fractional shorting (%FS), and ejection fraction (%EF). Preliminary results showed that %FS and %EF did not change in the OVX and ISO groups compared to SHAM at 7, 14, and 28 days. Similar results were observed in the OVX compared to ISO + OVX groups at 7 days. Even though %FS and %EF did not change, the DD increased at all time points in OVX and ISO groups compared to SHAM. When comparing OVX and ISO + OVX, SD decreased at 14 and 21 days. There is however a significant increase in %FS and %EF at 21 days for all treatment groups. These preliminary results give a better insight to heart function over the course of multiple time points, suggesting that estrogen loss combined with chronic sympathetic stimulation significantly exacerbates the function of the heart.

Cardiovascular disease is a worldwide problem for both men and women and accounts for nearly 17.9 million deaths every year. Cardiovascular disease affects men and women differently and has resulted in more deaths in women since the 1980’s. Estrogen status decreases with age and as women go through menopause, it increases the burden of CVD events. Clinical studies have shown that estrogen can have cardioprotective effects via its receptors. These receptors binding causes pleotropic affects in signaling to maintain cardiovascular homeostasis. There are limited studies on estrogen loss in the aging heart over a continuous span. We therefore examined the effects of estrogen loss and its role in cardiac structure and function over time in female mice. This research was a collaborative project by 25 undergraduate students. Studies have shown undergraduate research to be extremely useful in improving undergraduate students’ analytical, communication, statistical knowledge, and other scientific and laboratory skills (Tan et al., 2022). During this lab, students performed various histological staining methods, analysis of echocardiograms, and animal research. Female mice were ovariectomized at 2.5 months of age or underwent a SHAM (mock) surgery. Echocardiography was preformed to examine the cardiac structure and function at 1, 3, 5, 12, and 18 months post ovariectomy. Hearts were removed at each time point and sectioned at 4µm thick. Cardiac hypotrophy was then assessed by histological staining using Wheat Germ Agglutin and myocyte cross-sectional area was measured of the stained images. There was a significant increase in cardiac hypertrophy in the 1-month versus 18-month SHAM and OVX groups. Also, there was a significant increase in cardiac hypertrophy between the SHAM and OVX groups at 1-month, 3-month, and 5-month OVX. Echocardiography results revealed significant increases in the diastolic (DD) and systolic diameter (SD) for the SHAM and OVX group at 1-month versus 18-month. Percent Fractional (%FS), and Ejection Fraction (EF) were significantly higher in the OVX group versus SHAM at 1, 5, and 18-month time points. This work highlights the impact of prolonged estrogen loss on changes in cardiac structure and function in the aging female heart.