Hypertension and cardiovascular disease risk in women


Section Editor(s): Wenger, Nanette K.; Drinkwater, Barbara L.

Medicine & Science in Sports & Exercise:
Roundtable Discussion

    Systolic blood pressure rises with age in women, but a plateau is reached for diastolic blood pressure after age 60 yr(19). More than 20% of U.S. women have high blood pressure, and, in the Hypertension Detection and Follow-up Program, the rates of mild, moderate, and severe hypertension (defined as diastolic blood pressures of 90-104, 105-114, and ≥115 mm Hg, respectively) were 2.1, 3.7, and 7.1 times greater in black compared with white women(11). The prevalence of isolated systolic hypertension(≥160 mm Hg), which increases with age, is also higher in black women(21,23). The pathogenesis of hypertension remains unexplained in over 95% of patients. Factors incriminated include overactivity of the sympathetic nervous system, renal factors, high sodium intake, imbalance between vasodilator (nitric oxide) and vasoconstrictor (endothelin, angiotensin II) factors, genetic factors, obesity, increased activity of vascular growth factors, abnormality of resistance vessels, diabetes mellitus, and insulin resistance (18).

    Androgens increase renal and hepatic angiotensinogen mRNA, and exert a trophic effect on the heart muscle and enhance vascular contractility(3). Estrogen and progesterone receptors are present in blood vessels (2) and estrogen increases hepatic angiotensinogen release, but does not produce cardiac trophic changes(6); acting via endothelial derived relaxation factor, it produces vasodilation (7).

    The influence of menopause on blood pressure is surrounded with controversy. No rise in blood pressure with menopause was observed in the Framingham longitudinal study (10). In contrast, higher systolic and diastolic blood pressures in post menopausal women were reported in a cross-sectional study, which adjusted for age and body mass(22).

    Hypertension is the most important risk factor, after age and smoking, for cardiovascular disease in women, others being physical inactivity, diabetes mellitus, and abnormal blood lipid levels. Hypertension is associated with premature death in both genders. The relative risk of fatal and nonfatal stroke increases with a rise in systolic and diastolic blood pressures. Hypertension also increases morbidity and mortality from coronary heart disease in both white and black women and is an important cause of heart failure at elderly age, even when left ventricular systolic function is relatively well preserved. After adjusting for age, blood cholesterol level, and smoking, a 7.5-mm Hg increase in usual diastolic blood pressure was associated with a 29% increase in coronary heart disease risk(15).

    Use of contraceptive pills (synthetic estrogens) has been occasionally associated with an increase in blood pressure; some women are especially sensitive (24). In postmenopausal women, hormonal replacement treatment usually does not produce any significant change in blood pressure. No relationship of blood pressure to rise in estrogen, progesterone or other hormone levels has been documented in either preeclampsia or eclampsia of pregnancy or pregnancy-associated hypertension. Insulin resistance has been linked to hypertension; but, in the absence of obesity and carbohydrate intolerance, its influence on coronary heart disease in women is uncertain (17).

    Dynamic aerobic exercise increases systolic and lowers diastolic blood pressure, whereas isometric exercise increases both systolic and diastolic blood pressures. An abnormal increase in blood pressure during exercise has been reported in borderline hypertensive individuals, but the rate of rise in blood pressure is similar to that observed in normotensive subjects(5). Resting blood pressure level and cardiac hypertrophy at young age are better indicators of subsequent hypertension. Exercise improves well-being and enhances insulin sensitivity. Regular aerobic physical activity of moderate intensity decreases systolic and diastolic blood pressures by an average of 10 mm Hg (1). Brisk walking for 30-45 min or low-intensity exercise at least 3-4 times a week is at least as effective in lowering blood pressure than regular aerobic exercise(1). Exercise training reduces sympathetic outflow activity; this is probably the mechanism for exercise-induced blood pressure reduction (8). Effects of dynamic exercise on hemodynamics are different in younger and older persons (14), but this has not been well studied in women. An abnormal rise in systemic vascular resistance and decrease in cardiac output may account for reduced effort tolerance at elderly age; antihypertensive drug treatment may be required prior to instituting an exercise program in older patients.

    In women with severe hypertension, control of blood pressure is associated with a reduction in the incidence of stroke and heart failure(9,21). In mild to moderate hypertension, weight control with diet and an increase in physical activity produce a modest reduction in blood pressure. When nonpharmacologic efforts fail, drug therapy is indicated and has to be individualized. Although recent drug trials have included women, sample sizes have been too small to adequately address the impact of treatment on cardiovascular mortality. The published data, however, clearly show that compared with placebo, pharmacologic treatment of mild and moderate hypertension produces a 40%-50% reduction in fatal and nonfatal stroke rates (12,16).

    In a study comparing referred care to a stepped care approach, at 5-yr follow-up, there was a 16.9% reduction in overall mortality in black women and a nonsignificant increase in mortality of 2.1% in white women in the stepped care group (12). However, with longer followup, there was a decrease in mortality with the stepped care approach in both black and white women, although the benefit was greater in black women(13). There was a significant reduction in fatal and nonfatal stroke rates in the stepped care group.

    In isolated systolic hypertension, treatment with a diuretic alone or in combination with atenolol produced a significant reduction in stroke rate in both genders (4). Nonfatal coronary events were also reduced in the overall group, but gender-specific data were not available(4).

    In elderly hypertensive patients, including women, the combined incidence of fatal and nonfatal stroke, and fatal and nonfatal myocardial infarction was significantly lower in patients treated with a diuretic or diuretic-beta-blocker combination, as compared with placebo(20).

    Thus, on the basis of available outcome data, recommended first-line pharmacologic treatment of hypertension is either a low-dose diuretic or a beta-blocker, or their combination. Unlike many other drugs, beta-blocker use in elderly patients does not produce postural hypotension. Some have concern with adverse metabolic effects of diuretic drugs. When these agents are contraindicated or not tolerated, treatment with a calcium channel blocker or ACE inhibitor should be tried.

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    Section Description

    Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors

    Nanette K. Wenger: Preventive Coronary Interventions for Women

    Udho Thadani: Hypertension and Cardiovascular Disease Risk in Women

    Steven N. Blair: Physical Inactivity and Cardiovascular Disease Risk in Women

    Ronald T. Burkman: Oral Contraceptive Use and Coronary and Cardiovascular Risk

    Margo A. Denke: Lipids, Estrogen Status, and Coronary Heart Disease Risk in Women

    Caren Solomon: Diabetes Mellitus and Risk of Cardiovascular Disease in Women

    Murray Freedman: Postmenopausal Hormone Replacement Therapy and Cardiovascular Disease Risk

    This mongraph is based on the proceedings of an ACSM Roundtable entitled“Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors,” held June 21-22, 1994, in Indianapolis, Indiana.

    The Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors Roundtable was funded through a grant from Wyeth-Ayerst Laboratories.

    ©1996The American College of Sports Medicine