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SA JOURNAL OF DIABETES & VASCULAR DISEASE
RESEARCH ARTICLE
VOLUME 16 NUMBER 1 • JULY 2019
7
often calcium channel blockers are more rapidly effective in these
circumstances and are a good choice of treatment for the limited
period for which they will be required.
One of the most important aspects of managing the postpartum
pre-eclamptic is that of counselling. Pre-eclampsia has been
shown to be a marker of long-term risk. Specifically, there is an
association between hyperinsulinaemia, dyslipidaemia and the risk
of pre-eclampsia. These underlying metabolic disorders are also risk
factors for early onset vascular disease (both coronary artery and
cerebrovascular disease).
47
Consequently, women with early onset
pre-eclampsia are at risk of vascular arterial disease in later life.
Attention therefore needs to be paid to primary prevention of these
conditions through regular screening, and treatment for metabolic
disorders. The second long-term consequence of pre-eclampsia is
that of an increased risk of renal failure.
48
This risk correlates with
the number of pre-eclamptic pregnancies a woman may have and
indicates a need to pay attention to aspects of care in later life
that may have a renal protective effect, specifically the early and
adequate treatment of hypertension.
Chronic hypertension in pregnancy
Chronic hypertension during pregnancy may be divided into
two groups: uncomplicated chronic hypertension and chronic
hypertension with superimposed pre-eclampsia. The latter group
requires management according to the principles outlined above,
whereas the former requires out-patient care, often with an altered
approach to therapeutic intervention. Chronic hypertension is
defined as blood pressure of 140/90 mmHg or more on two
occasions before 20 weeks of gestation or persisting beyond 12
weeks after delivery.
Chronic hypertension with superimposed
pre-eclampsia
The risk of developing superimposed pre-eclampsia is estimated to
be between 10 and 25%.
49
The possibility of decreasing this risk
merits consideration. The development of pre-eclampsia cannot be
averted by controlling blood pressure and there is no therapy that
has any major impact on the risk of developing superimposed pre-
eclampsia. However, there is some evidence that the use of low-dose
aspirin, given as a daily dose of 57 to 81 mg of aspirin, may reduce
the risk of pre-eclampsia developing in about 10% of women who
are at risk of the disease.
50
It is not clear why aspirin is effective, and
initial theories related to altered prostanoid metabolism have been
discounted, with more recent speculation focused on the possible
interaction between aspirin and the production of pro-inflammatory
cytokines.
51
Aspirin given in this dose is safe and has no effect on the
foetus. Despite the modest effect on the incidence of the disease, it
remains recommended therapy in women who are at risk.
The second strategy used to reduce the occurrence of pre-
eclampsia is based on the prophylactic administration of large
doses of oral calcium. Meta-analysis of the studies conducted
to date indicate that calcium administered in doses of up to one
gram three times a day may significantly reduce the occurrence
of pre-eclampsia and may also reduce the development of severe
hypertension.
52
The criticism of this data arises from the observation
that the two single largest studies in the meta-analysis failed to
reach statistical significance. Despite these reservations, calcium
supplementation is widely accepted practice during pregnancy
where there is a suspected risk of pre-eclampsia.
Interventions that are not of benefit in preventing pre-
eclampsia include bedrest, the use of anti-oxidant vitamins and
antihypertensive therapy itself.
Given the imperfect prophylactic measures aimed at preventing
pre-eclampsia, care of pregnant women with chronic hypertension
requires appropriate precautions to ensure that the development of
superimposed disease is detected early in its development because
of the attendant risks of foetal and maternal morbidity and
mortality. Knowing who will develop superimposed pre-eclampsia
before it becomes clinically manifest would be useful information.
The clinical phenotype of pre-eclampsia arises fromchanges at the
level of the foetoplacental unit and any early signs of intra-uterine
growth restriction or abnormal uterine artery Doppler velocimetry
may precede the onset of the clinical disease.
49
The hallmark of
superimposed pre-eclampsia is, however, the development of
proteinuria. The difficulty with this is knowing when the proteinuria
is a consequence of underlying pre-eclampsia rather than due to
renal disease caused by longstanding hypertension or a priori renal
disease with secondary hypertension (in many communities HIV-
associated nephritis may be a major differential diagnosis).
This distinction may not be easily made on a clinical basis and
where a diagnosis of pre-eclampsia enters the differential diagnosis,
the patient deserves in-patient care andmanagement for presumptive
pre-eclampsia until an alternative diagnosis can be made. The natural
history of pre-eclampsia sometimes facilitates the distinction between
pre-eclampsia and renal disease as a cause for proteinuria because
pre-eclampsia tends to worsen as the pregnancy continues, whereas
the chronically hypertensive patient has an indolent condition that
changes little with the passage of time.
The recent interest in biomarkers may provide an alternative
way of diagnosing which hypertensive conditions have a placental
origin. Angiogenic and anti-angiogenic factors [placental growth
factor and the soluble receptor for vascular endothelial growth
factor (sFlt)] have been shown to be good predictors of placental
disease and may provide a ready means of discriminating between
various types of hypertensive disease in pregnancy, specifically
identifying those most at risk of adverse outcome.
53
Uncomplicated chronic hypertension
Uncomplicated chronic hypertension does not usually affect the
pregnancy outcome to any significant degree. The drugs used to
treat hypertension outside pregnancy may need to be revised and
alternatives introduced in order to protect the foetus.
Physiological changes during pregnancy have an impact on
chronically hypertensive women as well. Specifically, they will
vasodilate during the second trimester, leading to a fall in blood
pressure and a reduction in the requirement for treatment at this
point in the pregnancy. As the volume expansion during pregnancy
continues and peaks at about 32 weeks’ gestation, the need for
treatment may increase again. The goals of treatment also may
need to be revised during pregnancy.
Outside pregnancy, the aim of treatment is prevention of end-
organ damage to the heart, vasculature and kidneys. The use of
diuretics with ACE inhibitors is common and the goal of therapy is
normotensive blood pressure. This strategy does not apply during
pregnancy because the drugs may harm the foetus, and placental
perfusion (in theory) may be adversely affected by antihypertensive
drugs that diminish perfusion pressure.
Diuretics, although used to treat cardiac conditions during