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.