In the United States, cardiovascular disease is caused by hypertension. Hypertension also contributes to mortality and morbidity. Globally women have lower diastolic blood pressures than men at all ages and they also have a lower prevalence of hypertension. Although men have a higher incidence of total cardiovascular end points at all ages, hypertensive men and women develop strokes, left ventricular hypertrophy and renal modifiable risk factor that is extremely prevalent in older women.
Hypertension is the main top risk factor for many disorders including coronary heart disease and stroke and contributes to approximately 12.8% of yearly deaths worldwide. The causes of hypertension are numerous and interrelated with various genetic factors and environmental factors. Among them, adiposity is a well-documented modifiable risk factor. Body mass index (BMI), waist circumference (WC) and waist-to-hip (WHR) are the most used anthropometric indices to reflect the total body adiposity or visceral adiposity, and to predict hypertension risk (Dyer et al,1999). However, several recent studies reported that the regional deposition of fat, especially in the upper body segment, is more pathogenic than total body adiposity and visceral abdominal fat (Freedman and Rimm, 1989).
Indispensable hypertension is a heterogeneous disorder; in this case it was not shocking that few gender specific pathogenic factors have been identified. Premenopausal hypertensive women have been shown to have higher resting heart rate, left ventricular ejection time, cardiac index, and pulse pressure compared to age-matched men and has decreased total peripheral resistance and blood volume (Messerli et al, 1987). Minor plasma renin levels have been reported in both pre- and postmenopausal hypertensive women compared to those in men (Lewis, 1996). Nordby and colleagues reported lower serum estradiol levels in hypertensive premenopausal women compared to normotensives (Nordby, Os, Kjeldsen and Eide, 1992).
Obesity is one of the vital aspects of hypertension in women that is worthy of emphasis. Middle aged women are commonly to have obesity than men. In females, it was scientifically proven that body weight has a greater impact on blood pressure than in males (Chaing, Perlman, Epstein, 1969). Although the association between obesity and hypertension is firmly established, the mechanisms involved are not well understood. The relationship of hyperinsulinemia and insulin resistance (both associated with obesity) to hypertension is under investigation by several laboratories. A significant amount of hypertension in women is attributable to obesity, an observation that underscores the importance of dietary modification and exercise in treatment.
From one cross sectional study, it was established that the causes of secondary hypertension in women was the same as in men. Hence, similar care considerations with respect to assessment and treatment are applicable. Parenchymal renal disease should be considered and ruled out with urinalysis and serum creatinine levels. Collagen diseases, such as systemic lupus erythematosis and systemic sclerosis, are more common in women, and the presence of hypertension in patients with these disorders suggests renal involvement. Renovascular hypertension due to fibromuscular dysplasia is primarily a disease of young women. Given the excellent results reported with renal angioplasty (Sos, Pickering, Sniderman et al, 1983), this condition should be ruled out in women under the age of 40 yr with moderate to severe hypertension. It is particularly important to diagnose this disorder before women, because women with renovascular hypertension are more likely to have problematical pregnancies. Similarly, pheochromocytoma, although rare, is associated with considerable maternal morbidity and mortality during women and should be ruled out in young hypertensive women with characteristic symptoms.
Exogenous estrogen, predominantly in the form of oral contraceptive pills, is ansignificant cause of secondary hypertension in women. A review of 24 yr of data suggests that majority women taking oral contraceptives experience a small, but detectable, increase in both systolic and diastolic blood pressure (Woods, 1988). The magnitude of the proliferation varies among populations and also with doses of estrogen and progestin. The Walnut Creek Contraceptive Drug Study, which included 11,672 women, reported an increase in pressure of 5–6 mm Hg systolic and 1–2 mm Hg diastolic in white women and a lesser rise in black women (Ramcharan, Pellegrin and Hoag, 1976). A study conducted in developing countries reported similar average changes after 1 yr of oral contraceptive use (WHO Task Force on Oral Contraceptives, 1989). However, in some centers, marked elevations (10 mm Hg systolic, 6.9 mm Hg diastolic) were reported.
Women taking contraceptives experience or have hypertension 2-3 times more common in women taking oral contraceptives than in women of the same age not taking contraceptives (Royal College of General Practitioners, 1974). Hoag (1976) reported that as the age and body mass of women increases as the risk of hypertension increases. Oral contraceptives currently in use contain lower doses of ethinyl estradiol (20–35 ?g) than those previously used. The available data suggest that there is a correlation between both estrogen and progestin dose and blood pressure (Woods, 1988). Thus, the current incidence of oral contraceptive-induced hypertension may be less than that reported by earlier studies. Nevertheless, recently published data obtained from the Nurses’ Health Study suggests that even oral contraceptives with lower doses of estrogen increase the risk of hypertension, and that the risk increases with duration of use and with increased progestin potency (Ramcharan, Pellegrin and Hoag, 1976).
The appliance of the proliferation in blood pressure or of the advance of overt hypertension due to oral contraceptives remains uncertain. Intensifications in body weight, plasma volume, exchangeable sodium, plasma insulin, insulin resistance and hepatic synthesis of angiotensinogen have been reported to be involved. Experimental evidence favors a role for the renin-angiotensin system in the hypertension induced by estrogen (WHO Task Force on Oral Contraceptives, 1989). In a rat model of oral contraceptive hypertension, administration of estrogen alone (ethinyl estradiol) caused hypertension and an increase in angiotensinogen and angiotensin II levels (33). The hypertension induced by estrogen responded to angiotensin-converting enzyme inhibitor treatment. Progestin administration alone also increased blood pressure, although the elevation in blood pressure was of lesser magnitude, of shorter duration, and associated with increased sodium retention.
In observation of the above contemplations, a judiciousmethod to oral contraceptive use is to monitor blood pressure at least every 6 months. If blood pressure rises, then a decision to discontinue the pill should be based on the degree of hypertension, the potential hazards of women, and the overall cardiovascular risk profile. Although it is preferable to avoid oral contraceptives in individuals with elevated blood pressure, this modality of contraception can be considered in carefully selected individuals when the risks of women appear greater than the risks of mild hypertension.
Hormone replacement therapy (HRT) and hypertension, the effects of HRT on blood pressure are not as clear-cut as the effects of oral contraceptive pills. An association between estrogen therapy in postmenopausal women and hypertension was first reported in the 1970s and 1980s (34–37), and until recently many physicians considered hypertension to be a contraindication to HRT. The mechanism of the increase in blood pressure was attributed to increased angiotensinogen generation as well as increased sodium retention (Crane and Harris, 1978). In fact, estrogen preparations (e.g. Premarin and ethinyl estradiol) with a greater ability to stimulate hepatic synthesis of angiotensinogen have been shown to raise blood pressure to a greater extent than those preparations that have a modest effect on angiotensinogen (natural estradiol and transdermal estrogen) (Akkad, Halligan, Abrams, Al-Azzawi, 1997). However, the hypertensive effect of postmenopausal estrogen therapy is not as consistently observed as that of oral contraceptive pills. One difference that may account for the more common association of increases in blood pressure with oral contraceptive pills is the dose. The dose of ethinyl estradiol in contraceptive pills is more potent than the doses of conjugated estrogens that are given to postmenopausal women. The effects of synthetic progestins on blood pressure have not been extensively studied in postmenopausal women. Preliminary evidence suggests that they cause increases in blood pressure by increasing sodium retention (Oelkers, Schoneshofer, Blumel, 1974).
Data from newly published prospective clinical trials suggest that the risk of hypertension is because HRT is low, and some studies have even documented a decrease in blood pressure in patients treated with HRT (42–44). The Postmenopausal Estrogen/Progestin Interventions Trial evaluated cardiovascular risk factors in 875 normotensive postmenopausal women, aged 45–64 yr, accidentally assigned to treatment with a diversity of different regimens of HRT. At 3 yr of follow-up, there were no differences in systolic or diastolic blood pressure in any of the treatment groups compared to that in the placebo group. The patients in this clinical trial were normotensive to commence and it is not known whether hypertensive women would be more likely to develop increases in blood pressure while taking HRT. A recent prospective study of 75 hypertensive women treated with HRT failed to demonstrate an increase in blood pressure after 12 months of follow-up (Lip, Beevers, Churchill and Beevers, 1994), but data on larger numbers of patients are needed to determine whether HRT is a risk factor for blood pressure elevation in hypertensive postmenopausal women. A concern with respect to the existing data is that reporting mean changes in blood pressure in a population may mask individuals who have a blood pressure increase with HRT. This was demonstrated by a recent study of ambulatory blood pressure monitoring in normotensive women receiving either transdermal or oral estrogen, which showed that although the group as a whole did not have a rise in blood pressure, as many as one third of the individuals had a 4-mm Hg increase in diastolic blood pressure after 6 months of therapy (Akkad, Halligan, Abrams and Al-Azzawi, 1997).
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