Preexistingchronic hypertension

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Women with pre-existing hypertension have an increased risk of superimposed pre-eclampsia.

A Canadian study found an incidence of preeclampsia of 21.2% in 337 women with chronic hypertension compared to an incidence of 2.3% in the control population (P <0.01) (Rey and Couturier, 1994). In a study of 169 pregnancies in 156 women with chronic hypertension 34.3% developed superimposed pre-eclampsia (Mabie et al., 1986). More recent studies have confirmed these observations. A large cross-sectional study from South America found that chronic hypertension was associated with a doubling of the risk of pre-eclampsia [RR = 1.99 (95% CI 1.78-2.22)] (Conde-Agudelo and Belizan, 2000a).

This increased risk of pre-eclampsia is related to the degree of hypertension. In a study of 211 women with mild hypertension (diastolic blood pressure 90-110 mmHg) the incidence of superimposed pre-eclampsia was 10% (Sibai etal., 1983). In those women with severe hypertension, defined as a diastolic blood pressure of 110 mmHg or higher before 20 weeks gestation, a study from New Zealand of 155 hypertensive women demonstrated a risk of superimposed pre-eclampsia of 46% compared to 14% for women with mild hypertension [odds ratio 5.2 (95% confidence interval 1.5-17.2)] (McCowan et al., 1996). Both diastolic and systolic hypertension increase the risk of super-imposed pre-eclampsia. In an analysis of risk factors for pre-eclampsia in nulliparous women (Sibai et al., 1997) the odds ratio for a systolic blood pressure in early pregnancy of 120 mmHg or more compared with < 101 mmHg was 2.66. Similarly the odds ratio for a diastolic blood pressure of greater than 60 mmHg compared with less than 60 mmHg was 1.72 (Sibai et al., 1997).

Management

Since severe hypertension carries a higher risk of super-imposed pre-eclampsia than mild hypertension (McCowan etal., 1996), the blood pressure should be optimally controlled prior to pregnancy. A Cochrane review of 19 trials in 2402 women (Abalos et al., 2003) showed that antihypertensive therapy given in pregnancy does not prevent super-imposed pre-eclampsia [RR = 0.99 (95% CI 0.84—1.18)], but it halves the risk of severe hypertension [RR = 0.52 (95% CI 0.41—0.64)] and therefore reduces the risk of dangerous complications such as maternal cerebral hemorrhage.

Traditionally, the drug of choice to treat preexisting hypertension in pregnancy has been methyldopa. However, beta-blockers are becoming more popular, especially in the USA, as a first choice agent in pregnant women with chronic hypertension. Labetalol, in particular, a combined alpha- and beta-blocker, is recommended by the American College of Obstetricians and Gynecologists as a first line therapy for women with pre-existing chronic hypertension (ACOG Practice Bulletin #29, July 2001, Chronic Hypertension in Pregnancy). Beta-blockers have fewer maternal side effects than methyldopa, but their safety in the fetus is not as well established as with methyldopa. There is some concern that beta-blockers may inhibit fetal growth when used long-term (and started in the first trimester) throughout pregnancy, but claims of neonatal hypotension and hypogly-cemia have not been substantiated in the randomized controlled trials performed. There is no evidence for the superiority of any one beta-blocker over the others. Beta-blockers should not be given to women with a history of asthma (Magee et al., 1999).

Second-line drugs for the treatment of hypertension in pregnancy include calcium antagonists (e.g. slow-release nifedipine), and hydralazine. These may be used in conjunction with first-line therapy in those women resistant to monotherapy. Side effects of vasodilators include headache, facial flushing and edema, and may necessitate withdrawal in some patients. Alpha-adrenergic blockers are also safe and can be used as second-or third-line therapy. Diuretics should only be used in pregnancy for the treatment of heart failure and pulmonary edema. They are relatively contrain-dicated in pre-eclampsia because they cause further depletion of an already reduced intravascu-lar volume. The angiotensin-converting enzyme (ACE) inhibitors (e.g. ramipril, enalapril) should not be used in pregnancy because they may cause oligohydramnios, renal failure and hypotension in the fetus. Their use has been associated with decreased skull ossification, hypocalvaria and renal tubular dysgenesis, and there is also a risk of intrauterine death. Any woman on maintenance therapy with an ACE inhibitor should discontinue this (and if necessary switch to methyldopa or labetalol) before pregnancy. The use of these drugs in the first trimester is associated with structural malformations (Cooper et al., 2006). There are few data concerning the newer angiotensin II-receptor blockers agents (e.g. losartan) in pregnancy, but they are similar to the ACE inhibitors and therefore should be avoided (Nelson-Piercy, 2006).

It is acceptable for women to conceive while continuing to take their usual antihypertensive medication, except ACE inhibitors (Cooper et al., 2006). Once pregnancy is confirmed, this can be discontinued. If a woman only requires one antihypertensive agent to control her blood pressure outside of pregnancy, and the blood pressure is < 140/90 mmHg when first seen in pregnancy, it is usually possible to delay the introduction of antihypertensive medication because of the physiological decrease in blood pressure that occurs in early pregnancy. Women with severe hypertension (>170/110) and those requiring more than one agent should be converted directly to one of the first-line drugs.

If hypertension is noted for the first time in the first trimester or early second trimester, it is likely that it is a chronic, pre-existing problem, since pregnancy-induced hypertension (including pre-eclampsia) usually, but not invariably, appears in the second half of pregnancy. Hypertension in any young person should not be attributed to essential hypertension (particularly in the absence of a family history) before secondary causes such as renal or cardiac disease (coarctation of the aorta), and rarely Cushing's syndrome, Conn's syndrome (and other causes of hyperaldosteronism) or phaeochromocytoma have been excluded. Of these, the commonest secondary cause encountered is renal disease, including particularly in women of child-bearing age reflux nephropathy, glomerulonephritis and renal artery stenosis. Therefore, women presenting with hypertension for the first time in early pregnancy should be examined for clues to a possible secondary cause. This should include urinalysis for protein and blood, examination of the femoral pulses (looking for radiofemoral delay suggesting coarctation of the aorta) and a search for renal bruits (possible renal artery stenosis). A simple screen with serum creatinine, urea (to exclude renal impairment), and electrolytes (to exclude hypokalemia which may suggest hyperaldosteronism) should be performed. Urinary catecholamines should be measured in cases suggestive of phaeochromocy-toma (Nelson-Piercy, 2006).

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