ESTRADIOL CONCENTRATIONS IN PREMENOPAUSAL WOMEN WITH CORONARY HEART-DISEASE

Background Because of the beneficial effects of estrogen, premenopausa l women are normally protected against coronary heart disease (CHD) an d are at lower risk for myocardial infarction; consequently, CHD occur s very rarely in menstrually active women. Given this background, the aim of the present study was to test the hypothesis that decreased con centrations of estrogen are associated with CHD in premenopausal women . Methods Fourteen premenopausal women with CHD were investigated and compared with a healthy control group comparable for age and cardiovas cular risk factors. Relevant characteristics of patients and controls were assessed: age, blood pressure, body mass index, total cholesterol and high-density lipoprotein cholesterol, triglycerides, former pregn ancies, ovariectomy and related surgical interventions, smoking histor y and former use of oral contraceptives. To ensure the premenopausal s tatus of the participants, the regularity of the menstrual cycle and t he follicle-stimulating hormone concentrations were also assessed. Pla sma estradiol and progesterone and urine estrone concentrations (24 h urine collection) were measured at day 6 after estimated ovulation to assess the relative increase in plasma estradiol and progesterone duri ng the second half of the menstrual cycle. Results Compared with the c ontrol group, premenopausal women with CHD had significantly lower con centrations of plasma estradiol (408.9 +/- 141 pmol/l and 287.8 +/- 10 9 pmol/l respectively; P = 0.0228) and total estrogen (2061 +/- 693 pg /mu mol creatinine and 1607 +/- 448 pg/mu mol creatinine respectively; P = 0.025) in the urine. However, the progesterone concentrations wer e not significantly different between the groups. These findings might be explained by a partial ovarian dysfunction, as the patient group h ad a significantly higher number of tubal sterilizations (eight compar ed with one). Conclusion Our data provide support for the hypothesis t hat decreased concentrations of estradiol might be an additional patho genetic factor for the development of CHD in menstrually active premen opausal women.