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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 29, No 1, January/February 2018

AFRICA

29

reported by Zanstra

et al.

16

Although our study did not find

associations between diastolic blood pressure and obesity with

diastolic dysfunction, women in the pre-eclamptic group had a

significantly higher BMI and diastolic blood pressure than those

in the control group. Additionally, diastolic dysfunction is also a

risk factor for future death.

The Olmsted study described the predictive significance

of left ventricular diastolic dysfunction using multivariable-

adjusted analyses.

19

The hazard ratio for all-cause mortality

was 8.31 (

p

<

0.001) for mild diastolic dysfunction and 10.17

for moderate to severe diastolic dysfunction (

p

<

0.001). At

one year post-delivery, diastolic dysfunction was present in

11.5% of women with pre-eclampsia, in 22.7% of women

with early-onset pre-eclampsia and in 1.9% of women whose

pre-eclampsia developed after 34 weeks. Women with early-onset

pre-eclampsia requiring delivery prior to 34 weeks, irrespective

of the presence of chronic hypertension, were at risk of

developing diastolic dysfunction at one year post-delivery.

Chronic hypertension, therefore, was not an additional risk

factor for diastolic dysfunction at one year in women with early-

onset pre-eclampsia.

This study found that early-onset pre-eclampsia was a risk

factor for diastolic dysfunction, while women who developed

pre-eclampsia after 34 weeks had a risk similar to that of low-risk

parous women (RR 3.41, 95% CI: 1.11–10.5,

p

=

0.04). This may

be explained by the proposed differences in pathophysiology

between early- and late-onset pre-eclampsia.

Redman

et al.

have suggested that pre-eclampsia could

be the result of intrinsic or extrinsic placental causes.

20

In

early-onset pre-eclampsia, factors extrinsic to the placenta

affect the uteroplacental circulation via incomplete spiral artery

remodelling, while in late-onset disease, intrinsic factors affect

the size of the placenta, restricting intervillous perfusion.

20

The placentas of women with early-onset disease differ

significantly from those who develop pre-eclampsia at term.

21

The former group demonstrate placental findings consistent

with insufficiency and vascular lesions, while late-onset disease

is characterised by placental hyperplasia and unimpaired foetal

growth.

21-24

Further evidence suggesting that pre-eclampsia is

more than one disease comes from differences in biochemical

markers, Doppler studies and clinical features of the disease.

25-30

Pre-eclampsia is a known risk factor for future chronic

hypertension. Hypertension and hypertensive heart disease are

one of the key contributors to the burden of non-communicable

cardiovascular disease in Africa. Young African women are bearing

the brunt of this increasing public health problem.

31,32

Several

studies have found that women from sub-Saharan Africa have the

greatest risk of developing pre-eclampsia and eclampsia.

33,34

Nakimuli

et al

., in a study of pre-eclampsia in women

of African ancestry, found that African ancestry was the

second strongest risk factor for pre-eclampsia after chronic

hypertension.

35

African ancestry was also a risk factor for early-

onset pre-eclampsia and poor obstetric outcomes such as foetal

growth restriction and stillbirth.

35

Pregnancy-related deaths from

pre-eclampsia are also three times higher in women of African

ancestry compared with Europeans.

36

Almost 90% of women in

our study were of African origin.

It is estimated that for every woman who dies during

pregnancy or childbirth, 20 others will suffer severe morbidity.

37

Most maternal mortality and morbidity datasets record

information for up to 42 days post-partum. However women

who develop pre-eclampsia during pregnancy, especially those

with early-onset disease, may develop heart failure several years

after pregnancy, resulting in the problem not being adequately

identified and addressed.

The prognosis of women with compromised cardiac function

is poorer than that of men.

18

Women often present with

atypical symptoms, resulting in delayed presentation, delayed

diagnosis and suboptimal care compared to men.

38,39

These

factors highlight the need to identify women at risk of future

cardiovascular disease, with the aim of reducing potential

modifiable risk factors. Blood pressure control, weight loss

and a low-sodium diet are important measures that have

been identified with favourable changes in ventricular diastolic

function.

18

The American Heart Association Guideline on

Lifestyle Management to reduce cardiovascular risk for adults

who would benefit from blood pressure lowering include dietary

modification appropriate to calorie requirements, reduction in

salt intake and three to four sessions of aerobic activity per week

lasting on average 40 minutes per session.

40

This is the first study to evaluate diastolic function in a

pre-eclamptic group of predominantly African population.

Although we did not look at other risk factors for cardiovascular

disease in this population, the study provides valuable information

in identifying a potential group of women at risk of disease at an

early stage. This would provide opportunities for screening and

lifestyle modification.

The strength of this study is that it is one of the first to look

at cardiac diastolic function in an African population where the

rates of hypertension both during and outside of pregnancy were

high. A possible limitation is that most patients were seen for

the first time during pregnancy, with severe acute hypertension.

Only 14.6% of women were known to have chronic hypertension.

It is possible that some women had undiagnosed chronic

hypertension – this is especially likely as the rate of chronic

hypertension postpartum at one year was 54.2%. Some of the

women with undiagnosed chronic hypertension may have had

pre-existing diastolic dysfunction that could have been worsened

by the superimposed pre-eclampsia. A further limitation is that

only a select group of pre-eclamptic women were recruited to

the study.

Conclusion

Women who develop early-onset pre-eclampsia requiring

delivery prior to 34 weeks’ gestation have an increased risk of

cardiac diastolic dysfunction one year after delivery. Diastolic

dysfunction precedes the onset of systolic dysfunction and

Table 3. Cardiac diastolic function at one year

Pre-eclamptic

group,

mean (SD)

Control

group,

mean (SD)

p

-value

Left ventricular ejection

fraction, %

60.54 (7.62)

63.43 (4.88)

0.08

E velocity, m/s

0.98 (0.20)

0.95 (0.14)

0.90

A velocity, m/s

0.70 (0.24)

0.64 (0.05)

0.01

E/A ratio

1.42 (0.39)

1.46 (0.12)

0.74

E-deceleration time (ms)

224.57 (51.00)

225.43 (35.09)

0.08

Lateral e

(cm/s)

10.83 (2.86)

11.80 (1.99)

0.02

E/e

ratio

10.11 (5.32)

9.96 (2.25)

0.11