Vincent Heart Center, Indianapolis, Indiana. Hypertension s for 1 in 5 deaths among American women, posing a greater burden for women than men, and is among their most important risk factors for death, development of cardiovascular and other diseases. Hypertension affects women in all phases of life, with specific characteristics relating to risk factors and management for primary prevention of hypertension in teenage and young adult women, hypertension in pregnancy, use of oral contraceptives and assisted reproductive technologies, pregnancy, lactation, menopause, hormone replacement, hypertension in elderly women, and issues of race and ethnicity.
All are detailed in this review, as is information relative to women in clinical trials of hypertension and medication issues.
The overarching message is that effective treatment and control of hypertension improves cardiovascular outcomes. But many knowledge gaps persist, including the contribution of hypertensive disorders of pregnancy to cardiovascular disease risk, role of hormone replacement, blood pressure targets for elderly women, etc.
Hypertension HTN s for about 1 in 5 deaths of U. More women than men with HTN develop adverse pathophysiologic consequences such as left ventricular hypertrophy, diastolic dysfunction, heart failure [HF, with preserved ejection fraction HFpEF ], increased arterial stiffness, diabetes, chronic kidney disease 1 — 5. Control of HTN reduces CVD-related adverse outcomes that contribute to poor quality of life, disability, healthcare resource consumption 6.
Among adult Americans, HTN occurs in more women than men 4 ; and after age 60, the prevalence is becomes higher in women than men and this gap widens with aging, related to the large proportion of older women, possibly access to medication, and ethnicity issues Figure 1. Yet, debate remains that optimal BP targets have not been established by the highest level of evidence, particularly for older women 7. Older women are more likely to have multiple comorbidities such as HTN, diabetes, and physical inactivity 89. Estimates for the 18 and over category were age-adjusted by the direct method to the U.
Common risk factors include obesity, physical inactivity, increased salt intake, diabetes, and alcohol use. Evidence suggests that multiple sex-specific processes also mediate HTN development among women e. Regular, mild-to-moderate aerobic activity in women is associated with 5—8 mmHg BP reduction 1619independent of weight loss 8.
Prospective studies document decreased alcohol intake associated with BP decreases, independent of weight loss Modest sodium blkfemale reduction is associated with lower BP 23 — 25 ; reduction from for to low level, with diet, reduces SBP in women with and without HTN in many ethnic groups The lower incidence of HTN in premenopausal women versus age-matched men 26 raises consideration of sex hormones.
Emerging data propose that brain SNS activity is impacted by obesity, neuroinflammation, and stress. Research is needed to fill knowledge gaps in this area. PE portends future HTN risk. Postulated mechanisms for HTN development with prior PE include endothelial dysfunction, inflammation, and a hypercoagulable state Although there are limitations, associations appear strong.
It is unclear whether normal BP after delivery indicates resolution of this process but vascular changes likely persist. These women warrant close BP-monitoring and aggressive risk factor modification.
The impact of six risk factors in women and hypothetical population-attributable risk were examined to estimate the percentage of new HTN cases Obesity had the greatest impact, but all factors were associated with HTN risk in varying degrees both in isolation and in combination. These data support a multi-pronged approach to BP management in women including working toward normal BMI, diet favoring fruits and vegetables, restricting salt and fat, regular physical exercise, limiting alcohol and non-narcotic analgesics, with adequate folic acid intake.
Evidence indicates that adult HTN has antecedents during childhood and teen years contributing to early development of CVD e. Although beyond the scope of this document, this area is well summarized elsewhere Obesity alone contributes to primary HTN in adolescents, especially among minorities Also important is family history of HTN In general, the younger the age of presentation, the more likely there is a secondary cause for HTN, including parent-related factors obesity, HTN, smoker in close proximityextreme postnatal weight gain, sedentary behavior, and obstructive sleep apnea OSA.
OSA has also been associated with blkfemale BP and lack of nocturnal dip in children It is prudent to evaluate adolescents and young adults with HTN for secondary causes to prevent long-term CV complications Table 1 Clinical features may suggest a specific etiology of secondary hypertension. Although most adults have essential HTN, the opposite is true in children and young adults, so an age-based blkfemale is recommended In teenagers, especially girls, secondary causes may relate to renal artery obstruction, usually fibromuscular dysplasia. Hyperaldosteronism should be suspected in those with hypokalemia Pheochromocytoma should be suspected with episodic HTN that may be associated with for, sweating, and palpitations For heart disease, e.
Turner syndrome and variants is the most common genetic abnormality of young women and is associated with an increased risk of adverse CV, cerebral and renal problems, with HTN playing a pathophysiologic role Multifocal FMD : String of be in the mid to distal portion of the artery. Focal FMD : a concentric or tubular stenosis. Race and ethnicity have an association with HTN in young women, but are not readily identified as most studies involve adults.
There may be important social and environment issues.
This occurs at a very young age and is accelerated during adolescence Non-Hispanic black women are more likely to have HTN when they become pregnant, and even if normotensive at start, have a higher incidence of HTN during pregnancy It is difficult to assess socioeconomic factors for HTN in young adults. Younger adults without access to blkfemale or insurance, or below poverty level, are less likely to take medications as prescribed and may reduce financial burdens by taking fewer medications less frequently or not at all, which for result in worse outcomes Eclampsia is diagnosed when seizures occur.
Chronic hypertension with superimposed PE-eclampsia : when a woman with chronic HTN develops increased BP with new onset proteinuria or other evidence of end-organ dysfunction characteristic of PE. Defining HTN during pregnancy is based on general population thresholds despite a 10—15 mmHg SBP reduction in most normotensive pregnant women toward end of first trimester. Chronic HTN prevalence has increased as women have delayed pregnancy. HTN can be misdiagnosed as gestational HTN for women who first present for prenatal care in the second trimester, as this may be their first medical visit since childhood.
When BP is persistently elevated after the 12 th week postpartum, diagnosis of chronic HTN is made It disproportionately affects African Americans and is more prevalent at extremes of reproductive age range or in women with underlying CV risk factors e. PE is a syndrome with a spectrum of progressive and multi-systemic disorders.
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All women with PE, without severe features, must be monitored closely during labor for progression to severe disease, which can occur suddenly. Screening for PE is recommended by BP measurement at each pregnancy visit The cause of PE involves inadequate cytotrophoblastic invasion of uterine myometrium with placental hypoperfusion and generalized maternal endothelial dysfunction.
Sequential changes in circulating angiogenic and antiangiogenic factors appear in PE development 53 — Immediate risks of PE to the mother include pulmonary edema, cerebral hemorrhage, renal and hepatic failure, disseminated intravascular coagulation, and progression to eclampsia Given the prevalence of HTN disorders of pregnancy, it is important to have consensus on definitions, however, definitions vary The U. This finding may help identify women who should be included in a postpartum cardiovascular risk management program.
Furthermore, women with For who become pregnant should not be treated with angiotensin-converting enzyme ACE inhibitors, angiotensin receptor blockers ARBsblkfemale direct renin inhibitors. Intravenous magnesium sulfate is used to manage severe PE or eclampsia. A systematic review and meta-analysis of antihypertensive treatment on pregnancy outcomes complicated by chronic HTN 59 concluded that antihypertensive therapy reduces risk of severe HTN but there is a paucity of data to guide antihypertensive agent choice, except for avoiding ACE inhibitors, ARBs, or direct renin inhibitors as noted above.
However, beta blockers are useful.
A randomized controlled trial of labetalol versus nifedipine for chronic HTN in pregnancy 60 reported that both agents controlled BP to target. No difference in treatment effect was observed in 73 black women; but a mean 4 mmHg reduction in DBP occurred with labetalol versus nifedipine in 49 non-black women. Due to the expected BP decline over the first and second trimesters, it is reasonable to stop or reduce antihypertensive medications when a woman with chronic HTN becomes pregnant, with plans to restart therapy if BP rises in the second or third trimester There are no randomized trials supporting any therapy goals in HTN pregnant women, therefore there are no specified treatment goals.
The decision to treat HTN during pregnancy should include consideration of risks and benefits for both mother and fetus. All antihypertensive drugs cross the placenta; evidence supporting appropriate treatment for pregnant women is limited due to lack of controlled trials examining efficacy and safety So, there are no FDA risk category A antihypertensive drugs for pregnancy.
Hydrochlorothiazide and chlorthalidone are category B and nifedipine, labetalol, and hydralazine are category C Methyldopa, although only an antihypertensive category B agent, has been widely used in pregnancy and with fetal safety Lifestyle changes are recommended, but trials supporting effectiveness are limited Pre-eclamptic women have up to 4-fold increased risk for developing chronic HTN and IHD risk is doubled at year follow-up blkfemale The metabolic stress of pregnancy and lactation may for underlying CVD, which then manifests as PE However, endothelial dysfunction plays a central pathogenetic role in PE and may persist for years postpartum There are no recommendations for duration of postpartum BP monitoring with pregnancy-related HTN, save for annual BP measurement but without goals or attention to other traditional risk factor ascertainment.
Women who would benefit from periodic, close BP monitoring and aggressive CV risk factor modification may miss the opportunity of early detection and HTN treatment.
Sex differences exist in HTN; postmenopausal women have pronounced increases in both systolic BP and pulse pressure versus blkfemale men Several studies support a positive relationship between menopause and HTN. One such study with 5-year follow-up reported a rise only in SBP in a cohort of peri- and post-menopausal women compared with age and BMI matched premenopausal women and men.
Decrease in arterial compliance with aging was proposed responsible for this rise in SBP Different studies suggest the apparent relationship between menopause and HTN is explained by other factors including age and BMI Another study, after controlling for age, found no difference between pre- and postmenopausal women in HTN or CV risk.
The women were evaluated twice separated by 16 years, and the higher SBP and CV morbidity and mortality in postmenopausal women was ed for by age The BP rise after menopause also clearly involves other factors, which include genetic predisposition, aging, obesity, arterial for, etc.
HTN is most likely a multi-genetic disorder with each gene contributing only modestly to BP elevation. It is possible that menopause might provide a trigger for expression of certain genetic susceptibilities resulting in genetic influences that mediate HTN in women A study evaluating the relationship between BP extremes, with 35 loci having physiological roles in BP regulation, identified several gene-by-gender interactions. In women, polymorphism at the 1-adrenergic receptor and 2A-adrenergic receptor contributed to elevated BP, and in men polymorphism of 2-adrenergic receptor and angiotensinogen were associated with elevated BP Gene-environment interactions have been shown including BMI and salt intake 81 ,