Discussion

We have shown that, obese pregnant women have a different haemodynamic profile, altered cardiac geometry and impaired diastolic indices compared to pregnant women with normal BMI. This is the first study to present longitudinal data of cardiac function using 2D echocardiography in obese pregnant women. In particular, we found that women with obesity have higher SBP, DBP, HR, SV and CO with lower PVR. They also demonstrate higher PWT, RWT, LV mass and LV mass index with impaired diastolic indices including lower E/A ratio, TDI E’ lateral, TDI E’ medial and higher E/E’ ratio suggesting, suboptimal cardiac geometry, haemodynamic and diastolic function. In addition, we have a novel finding of a reduction in MAPSE between the second and third trimester in the obese group and lower TAPSE in this group compared to the normal BMI pregnant women, indicating possible impaired function in pregnant women with obesity.
Our haemodynamic findings in the obese group are consistent with literature of non-pregnant obese individuals. 5Obesity is associated with increased plasma volume expansion and CO due to excess body mass, with a concomitant decrease in natriuresis.28 The raised CO leads to glomerular hyperfiltration and in turn raised distal tubular sodium delivery. 28Complex mechanisms lead to the upregulation of the renin-aldosterone-angiotensin system and stimulation of the sympathetic nervous system, which can result in increased sodium reabsorption, plasma volume expansion and arterial hypertension. 28, 29 Heart rate is known to be raised in obese individuals due to autonomic impairment, defined by a reduction in parasympathetic activity and relative predominance of the sympathetic nervous system.5, 30 Maternal PVR decreased with gestation in both groups, in accordance with normal pregnancy physiology as peripheral vasodilation leads to a fall in systemic vascular resistance7, and was lower in the obese, compared to the normal BMI group. Obese individuals have an expanded intravascular volume to meet the elevated metabolic requirements and as PVR is proportional to MAP and CO, an elevated CO, seen in our obese group, will result in PVR reduction. 31, 32
We found a significant increase in LV mass and RWT across gestation in both groups, probably due to physiological myocardial hypertrophy needed to support the increased CO in pregnancy.8, 33Maternal LA diameter, IVS, LVEDD, PWT, RWT, LV mass, LV mass index and LV hypertrophy prevalence were all significantly higher in the obese group. Pregnancy itself is a hyperdynamic state and even in normal pregnancy a small proportion of “healthy” pregnant women (5-6%) will have LV hypertrophy, defined by LV mass index>95g/m2 and RWT>0.42.8 Here we report that obese pregnant women have an even more marked hyperdynamic circulation, probably, in order to cope with the metabolic demands of increased adipose tissue and fat-free mass, which can lead to LV dilation, increased wall stress and compensatory LV hypertrophy. Furthermore, hyperinsulinemia and hyperleptinaemia, seen in obese individuals, could also be involved in the pathogenesis of LV hypertrophy seen in this population.5, 34, 35
With regard to cardiac function, we found a reduction in diastolic indices, including E/A ratio and TDI E’ at the lateral mitral annulus, with gestation in both groups. 8 It is conceivable that the physiological maternal myocardial hypertrophy reduces LV compliance, leading to a reduction in early diastolic filling and a greater need for atrial contraction which can result in an increased A-wave and reduced E/A ratio. 8, 36 When comparing the groups, the E/A ratio and TDI E’ lateral and medial were higher and E/E’ ratio lower in the obese group. 37, 38 Obesity associated LV hypertrophy leads to impaired relaxation and early filling abnormalities which are compensated by augmented atrial contribution; these findings represent an early index of cardiac dysfunction even when systolic performance is maintained. 39 We found no difference in ejection fraction between groups, which is consistent with obese individuals outside pregnancy. 5, 40 Mitral annular plane systolic excursion assesses longitudinal function and gives an indication of systolic function 41 and in normal pregnancy, lateral and septal MAPSE have been reported to be reduced at term. 8 We found that women with obesity have a reduction in MAPSE between the second and third trimester, which could indicate early cardiac decompensation in this group. Right heart function, as assessed by TDI s’ and TAPSE, were lower in obese compared to normal BMI women, in accordance with findings outside the setting of pregnancy, suggesting suboptimal right heart function in obesity.42
The relationship between obesity and hypertension outside and during pregnancy is well documented. 43, 44 Obesity increases the risk of hypertensive disorders compared to normal BMI pregnant women and it has been reported that this risk doubles with each 5 to 7 unit increase in pre‐pregnancy BMI. 45 It is conceivable that maternal obesity induced insulin resistance can be associated with reduced cytotrophoblast migration and uterine spiral artery remodelling, which leads to placental hypoxia and ischemia, which in turn can result in the release of anti-angiogenic and inflammatory factors into the maternal circulation promoting endothelial dysfunction, reduction in nitric oxide production, increase in oxidative stress and finally the development of PE. 46 More recently, it is thought that the maternal cardiovascular system plays a pivotal role in the pathophysiology of PE; the risk factors for PE are cardiovascular in nature, cardiovascular signs and symptoms predominate the clinical picture of PE and cardiovascular morbidity persists for decades after PE. 13, 46 In accordance with this notion, higher early pregnancy maternal BP, maternal hyperdynamic circulation with high CO and low resistance have been described prior to the onset, as well as, during the clinical phase of late PE.23, 47, 48With regard to cardiac geometry, it has been reported that 50% and 20% of pregnant women destined to develop PE have evidence of cardiac remodelling, with higher RWT, and concentric hypertrophy, respectively. Additionally, diastolic function has also been shown to be reduced prior to the onset of PE. 49, 50 We have found that obese pregnant women have features of a hyperdynamic circulation with higher BP and CO, lower PVR, LV hypertrophy and reduced diastolic indices; characteristics that may render these women more susceptible to the development of hypertensive disorders during pregnancy and explain their high prevalence in obese pregnant women. 10