Introduction
Obesity has nearly tripled since 1975 and the World Health Organisation
estimate that in 2016, 650 million adults (13%) had obesity.1 In the UK, this epidemic is perpetuated and in 2020,
60% of women were overweight and 29% obese. Many of these woman are of
childbearing age and go on to have high risk pregnancies.2 Obesity outside
pregnancy has several effects on the cardiovascular system as every 100g
of fat deposited increases the cardiac output (CO) by 30–50 ml/minute
and this high volume load can lead to left ventricle (LV) dilation with
subsequent hypertrophy, impaired LV relaxation and compliance resulting
in diastolic dysfunction. 3, 4 Furthermore, conduction
and contractility can be compromised when fat deposition occurs in the
myocardial tissue and in severe sustained obesity, systolic dysfunction
can also ensue. 5, 6
Normal pregnancy is associated with significant maternal cardiovascular
and haemodynamic changes that are needed to support fetal growth, with
systemic vasodilation leading to reduced peripheral vascular resistance
and increased stroke volume (SV) and CO. 7 In
addition, there is physiological eccentric cardiac remodelling with
increased LV mass and reduced diastolic reserve with evidence of
dysfunction in around 25% of women at term. 8 Obesity
in pregnancy is associated with an increased risk of hypertensive
disorders, gestational diabetes (GDM), venous thromboembolism,
dysfunctional/prolonged labour, caesarean section and even, mortality.9 In particular, booking BMI>35
kg/m2 doubles the risk of pre-eclampsia (PE) and there
is a dose dependent relationship with morbidly obese women having the
highest incidence; around five‐fold higher than normal BMI women.10, 11 Pre-eclampsia has been associated with maternal
cardiovascular compromise and echocardiographic studies have
demonstrated significant cardiac dysfunction both in the pre-clinical
and clinical phase of the disease. 12, 13 However,
studies of the effect of obesity on the maternal cardiovascular system
are limited. A cross-sectional study at term (n=40) found that morbidly
obese pregnant women (BMI≥35 kg/m2) had higher CO,
lower resistance, altered geometry and a degree of diastolic and
systolic dysfunction , compared to pregnant women with
BMI<30kg/m2. 14 The only
longitudinal study (n= 232) has demonstrated that women with obesity
start in a state of high volume/low resistance which gradually moves to
volume overload with decreased CO and disappearance of low vascular
resistance in the third trimester. However, this study assessed
haemodynamic function using impedance cardiography and therefore did not
examine the maternal cardiac geometry or function. 15The aim of the current study was to provide novel longitudinal data of
the maternal cardiovascular profile (including haemodynamic function,
cardiovascular geometry and systolic and diastolic function) in obese
pregnant women, compared to women with normal BMI, using a two
dimensional echocardiography which is considered the gold standard.16 We hypothesised that the women with obesity will
have a suboptimal cardiovascular profile.