Estrogen Deficiency and Cardiovascular Disease in Premenopausal Women
For unexplained reasons, young premenopausal women with heart disease have twice the rate of death compared to men of the same age. Animal experiments have shown that stress can reduce ovary function in females monkeys due to reductions in brain hormones. This stress and reduced brain hormone levels lead to low estrogen levels and can cause menstrual cycles to become irregular, leading to reductions in fertility. These monkeys are also more likely to develop heart disease. In order, to better understand this relationship the investigators would like to study estrogen levels in premenopausal women with heart disease.
Premenopausal women who have recently undergone a study of their coronary (heart) arteries will have their blood hormone levels measured over one menstrual cycle. The investigators will correlate the blood hormone levels with coronary angiography results and with other markers of heart disease, such as a test that uses noninvasive, painless ultrasound waves to study the thickness of the arteries in the neck (carotid arteries). In addition blood cholesterol levels, blood sugar levels and other blood tests have been shown to correlate with heart disease will be measured.
Another aim of the study is to evaluate a potential link between environmental stress and hormone levels. Each patient will be given multiple questionnaires to evaluate stress, anxiety and depression and the investigators will be measuring the stress hormone (cortisol) levels in saliva for additional information.
The results of the study will further explore a possible link between low estrogen levels and heart disease in young premenopausal women and help pave the way for larger research studies to define better ways of preventing heart disease in these women.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Estrogen Deficiency and Cardiovascular Disease in Premenopausal Women|
- estrogen deficiency of hypothalamic (central brain) origin [ Time Frame: Baseline and Exit Visits ] [ Designated as safety issue: No ]
Biospecimen Retention: None Retained
Blood Hormone draw for FSH, E2; Urine Pregnancy test; Fasting lipid (cholesterol) panel, fasting insulin and fasting blood glucose levels; Reproductive hormones (FSH, LH, E1, E2, bioE2, PO, freeT, SHBG, DHEA-S); Plasma levels of inflammatory and endothelial function markers including but not limited to hsCRP, serum amyloid, endothelin-1, and ELAM; Fasting Salivary Cortisol (stress hormone).
|Study Start Date:||January 2005|
|Estimated Study Completion Date:||December 2015|
|Estimated Primary Completion Date:||December 2015 (Final data collection date for primary outcome measure)|
Please refer to this study by its ClinicalTrials.gov identifier: NCT00572858
|Contact: Jo-Ann Eastwood, PhD||310-423-9680||EastwoodJ@cshs.org|
|Contact: Ying Mou, PhD||3102487669||Ying.Mou@cshs.org|
|United States, California|
|Cedars-Sinai Women's Heart Center||Recruiting|
|Los Angeles, California, United States, 90048|
|Contact: Ying Mou, PhD 310-248-7669 Ying.Mou@cshs.org|
|Principal Investigator: Noel Bairey-Merz, MD|
|Principal Investigator:||Noel Bairey-Merz, MD||Cedars-Sinai Medical Center|