Menopause, Sleep Disruption, T2DM
Conditions
Brief summary
EMPOWER aims to determine the overall effect of menopause and sleep disruption on cardiac remodeling in women with type 2 diabetes.
Detailed description
The EMPOWER prospective cohort study is part of a larger project. This interdisciplinary project will utilize animal models, clinical cohorts, epidemiological datasets and data from randomized control trials to explore the hypothesis that sleep disruption and menopause-induced hormonal changes synergistically increase systemic inflammation and impair incretin signaling, leading to worsened cardiac function, heightened cardiometabolic dysfunction, and accelerated CVD risk. The EMPOWER study aims to determine the cumulative effect of multiple exposures including menopause progression and sleep disruption on subclinical cardiac remodeling in women with T2DM in the perimenopausal transition and if these relationships are moderated by T2DM management, Body Mass Index (BMI), or inflammation.
Interventions
OTHER4 years of clinical evaluations.
The intervention in this study is the additional clinical evaluations for women with type 2 DM and in perimenopause.
Sponsors
Ottawa Heart Institute Research Corporation
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
FEMALE
Age
48 Years to 58 Years
Healthy volunteers
No
Inclusion criteria
* Female Sex * Age range 48-58 years * In menopausal transition phase (pre-menopause or peri-menopause) * Diagnosis of Type 2 Diabetes Mellitus * Have access to and regularly use a smartphone with internet access
Exclusion criteria
* Male Sex * Currently Pregnant * Prior history of total hysterectomy or bilateral oophorectomy * Prior diagnosis of any of the following: Coronary Vascular Disease (CVD) including coronary heart disease, heart failure, congenital heart disease stroke/transient ischemic attack, valvular heart disease, peripheral vascular disease, aortapathy, atrial fibrillation or flutter, other CVD. \- Untreated serious mental illness (e.g, untreated psychosis).
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Reduced septal e' velocity | Baseline to 4 years. | Indicates impaired relaxation of the left ventricle during early diastole; key marker for diastolic dysfunction. Measured by echocardiography. |
| Increased E/e' ratio | Baseline to 4 years. | Indicates elevated left ventricular filling pressure; key marker for diastolic dysfunction. Measured by echocardiography. |
| Increased tricuspid regurgitation (TR) velocity | Baseline to 4 years. | Indicates elevated right ventricular systolic pressure or pulmonary hypertension. Measured by echocardiography. |
| Change in pulmonary artery systolic pressure (PASP) | Baseline to 4 years. | Measures the pressure in the pulmonary artery when the heart beats. Measured by echocardiography. |
| Change in E/A ratio | Baseline to 4 years. | Decrease of E/A ratio below 1 indicates diastolic dysfunction, and an increase of E/A ratio over 2 indicates advance failure. Measured by echocardiography. |
| Change in left atrial size | Baseline to 4 years. | Left Atrial Enlargement (LAE) is abnormal stretching or widening of the upper left heart chamber, typically caused by chronic pressure or volume overload. Measured by echocardiography. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Decline in left ventricular global longitudinal strain (GLS) | Baseline to 4 years. | Detects heart muscle dysfunction. Measured by echocardiography. |
| Decline in left atrial strain | Baseline to 4 years. | Indicates left ventricular diastolic dysfunction, heart failure with preserved ejection fraction, and atrial fibrillation. Measured by echocardiography. |
Contacts
CONTACTCarolyn Van Dam
PRINCIPAL_INVESTIGATORKerri Anne Mullen, Ph.D.
Ottawa Heart Institute Research Corporation
Outcome results
None listed