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Effect of hormonal contraceptives and postmenopausal hormone therapy on blood pressure

Jan Basile, MD
Michael J Bloch, MD, FACP, FASH, FSVM, FNLA
Section Editors
George L Bakris, MD
Norman M Kaplan, MD
Deputy Editors
Daniel J Sullivan, MD, MPH
John P Forman, MD, MSc


Combined oral contraception — Chronic use of oral contraceptives at contemporary doses will slightly increase the systemic blood pressure (BP) in most women and may have other adverse effects on cardiovascular risk. Early epidemiologic studies using high-dose estrogen found a mean elevation in BP of 3 to 6/2 to 5 mmHg, with approximately 5 percent of women developing overt hypertension [1]. A subsequent prospective cohort study of over 68,000 women on lower doses of estrogen demonstrated that, as compared with women who had never used oral contraceptives, the age-adjusted relative risk of developing hypertension was 1.5 for current use and 1.1 for past use [2]. Development of hypertension is more likely to occur in patients who developed hypertension during a prior pregnancy or who have a family history of hypertension. Although the rise in BP is usually mild, some women will have more significant increases in BP, and hypertensive emergencies may very rarely occur [3]. Cessation of therapy typically leads to a return of the BP to baseline, but resolution may take many months.

A newer progestin, drospirenone, has antimineralocorticoid diuretic effects and, when given as part of combined oral contraceptive therapy, appears to blunt the BP-increasing effect of estrogen [4-6].

Dose dependence and mechanisms — Both estrogen and progesterone appear to contribute to BP elevation in a dose-dependent fashion. The 5 percent incidence of hypertension reported in 1988 was largely derived from studies of high-dose therapy in which the estrogen dose was generally 50 to 150 mcg and the progestin dose was 1 to 4 mg. However, current preparations contain less than 35 mcg of estrogen, and many preparations (often known as ultra-low dose) contain less than 20 mcg of estrogen.

The mechanisms responsible for the hypertensive effect of oral contraceptives are incompletely understood [1]. The renin-angiotensin system (RAS) may be involved since estrogen stimulates the hepatic production of renin substrate (angiotensinogen) [7], but the interaction among estrogen and progesterone and the RAS are complex. Activation of the sympathetic nervous system may also be involved. However, no changes in muscle sympathetic nerve activity or systemic hemodynamics were found between young women taking an oral contraceptive and women with natural menstrual cycles [8].

Cardiovascular consequences — The main concern with an oral contraceptive-induced rise in BP is the development of persistent hypertension and the corresponding risk of subsequent premature cardiovascular disease. In a meta-analysis of 14 independent studies published from 1980 to 2003, the relative risk of stroke and myocardial infarction was increased twofold in current users of "low-dose" oral contraceptives (defined as less than 50 mcg of ethinyl estradiol) [9]. A statistically significant increase in risk for ischemic stroke was also seen with both second- and third-generation oral contraceptive formulations, while a trend toward an enhanced risk for myocardial infarction was noted among third-generation low-dose oral contraceptive users. However, it appears that the absolute (rather than relative) increase in risk is low and is mainly confined to women over the age of 35 years or those who have other risk factors for atherosclerotic events (particularly smoking) [10]. However, past rather than current use of oral contraceptives may not be associated with an increased risk of subsequent cardiovascular events [11].

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Literature review current through: Nov 2017. | This topic last updated: Oct 26, 2016.
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