Cardiovascular Journal of Africa: Vol 30 No 3 (May/June 2019)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 3, May/June 2019 AFRICA 181
Short Communication
An integrated model of materno-foetal cardiac
dysfunction in severe pre-eclampsia
Ismail Bhorat
Abstract
Maternal cardiovascular deterioration in severe pre-eclampsia
is due to a combination of factors in the setting of severe
trophoblastic ischaemia and the outpouring of maternal
cathecolamines, leading to increased left ventricular afterload
and increasing ventricular volumes, resulting in increased
left ventricular stroke work and demand myocardial ischae-
mia. This is the substrate for ventricular arrhythmias. Foetal
cardiac dysfunction is most likely on the basis of the increased
afterload, consequent upon widespread vasoconstriction, due
to angiogenic imbalances.
In this integrated model, chronic trophoblastic ischaemia
is the central role player by releasing vasoactive substan-
ces that induce haemodynamic alterations in the materno-
foetal complex, augmented and modified by ‘latent’ maternal
cardiovascular dysfunction and increased maternal catheco-
lamine secretion on the one hand, and altered foetal signal-
ling mechanisms on the other, all three components of the
materno-placental-foetal complex being in constant interac-
tion with each other. This unified hypothesis may explain
the development of both maternal and foetal morbidity and/
or mortality on a unitary basis in severe, complicated pre-
eclampsia.
Keywords: pre-eclampsia, maternal haemodynamics, foetal cardi-
ac haemodymanics, myocardial performance index, E/A ratio,
foetal cardiac Doppler
Submitted 28/11/17, accepted 20/11/18
Published online 7/2/19
Cardiovasc J Afr 2019; 30: 181–183
DOI: 10.5830/CVJA-2018-071
We present an integrated model of materno-foetal cardiac
dysfunction, based on our studies on maternal and foetal
haemodynamics, as well as other studies in the literature.1-27
Maternal cardiovascular deterioration in the mother in severe
pre-eclampsia is due to a combination of factors, which may
culminate in acute pulmonary oedema and cardiac failure. In
the setting of severe trophoblastic ischaemia, the release of anti-
angiogenic factors and an outpouring of maternal cathecolamines
leads to widespread elevation in systemic vascular resistance
and endothelial cell damage, resulting in a sharp rise in left
ventricular afterload and increasing ventricular volumes, which
result in increased left ventricular stroke work and demand
myocardial ischaemia. This is the substrate for the development
of ventricular arrhythmias, in particular ventricular tachycardia.4
These factors could lead to cardiac failure in severe
pre-eclampsia, either in combination or independently of each
other. This will depend on a number of variables, including
the magnitude of the angiogenic imbalances with resultant
elevation in systemic vascular resistance, the severity of changes
in myocardial relaxation and diastolic filling, gene–environment
interaction, and the presence of pre-existing latent cardiovascular
dysfunction. The overall balance of these interactions could
explain the different pathophysiological pathways that lead to the
onset of cardiac failure if myocardial impairment predominates,
or acute pulmonary oedema in severe pre-eclampsia when the
afterload mismatch is acute and severe, with marked increases
in diastolic filling pressures that transit to the pulmonary
vasculature, which leads to pulmonary vasoconstriction.
In terms of foetal cardiac function, there has been
corroboration, with similar conclusions reached by our
studies18,19 and other related studies20,21 investigating foetal
cardiac haemodynamics in intra-uterine growth restriction
(IUGR) and pre-eclampsia, in that altered cardiac function18-21
was demonstrated, as evidenced by increased myocardial
performance indices and altered transmitral E/A ratios. The
E/A ratio is reflective of diastolic dysfunction, and similar to
the adult haemodynamic changes in pre-eclampsia, significant
diastolic dysfunction was also noted in foetuses in IUGR and
pre-eclampsia. 18-21 Cardiac dysfunction was also noted to worsen
with worsening placental vascular resistance.18-21 In pre-eclampsia
in particular, foetal cardiac dysfunction is most likely on the
basis of the increased afterload consequent upon widespread
vasoconstriction due to angiogenic imbalances.
It is generally accepted that pre-eclampsia is related to
placental maladaptation.22,23 Poor trophoblastic invasion and
utero-placental artery remodelling in pre-eclampsia increases
reactive oxygen species (ROS), hypoxia and endothelial
dysfynction. This defective trophoblastic invasion, with its
resultant ischaemia, favours oxidative stress, consequent
oxidative damage and inflammation.24 Within the trophoblastic
cell, oxidative stress from unbalanced free radical formation
is formed from different sources such as xanthine oxidase
Department of Obstetrics and Gynaecology,
Sub-Department of Foetal Medicine, Nelson R Mandela
School of Medicine, University of Kwa-Zulu Natal, Durban,
South Africa
Ismail Bhorat, MB ChB, FCOG, PhD,