Until recently cardiovascular disease in women has been a largely neglected and poorly understood issue, in part related to the misconception of a lower incidence among females compared with males, underrepresentation of females in clinical trials and observational studies until recently, and nontraditional presentation of symptoms in many females. Women have been typically viewed as largely protected from cardiovascular disease until menopause, and thereafter a rise in prevalence has been recognized, presumably related to hormonal decline. Hormonal replacement therapy (HRT) has been viewed as a useful prophylactic approach to ward off such events after menopause as well as to minimize menopausal symptoms. However, recent studies have yielded conflicting results regarding the protective effects of estrogen administration in preventing myocardial infarction and stroke.1–3 Indeed, the results of the Women’s Health Initiative have been interpreted as showing a neutral effect of estrogen administration in women in the 50 to 59 age decile and an adverse cardiovascular effect in older subjects.1 Whereas different pharmacological regimens may have been used in these replacement trials, the impact of these regimens on known risk factors for cardiovascular disease, such as blood pressure, lipoprotein profiles, insulin sensitivity, endothelin, C- reactive proteins, and other vasoactive substances, has not been carefully investigated. The relationship between estrogen and progesterone administration in the form of oral contraceptives and blood pressure, a major risk factor for stroke and cardiovascular disease, has been recognized for 4 decades.4 Population studies have documented a small but significant rise in systolic blood pressure in women receiving oral contraceptives in the 1970s, but only a small proportion of such women demonstrated a rise into the hypertensive range. Whereas epidemiologists remind us repeatedly that a …