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