DISCUSSION
In the current study, we aimed to characterize gestational changes in
LVOTO/AS Doppler gradients and LV mechanics in women with LVOTO/AS as
compared to pregnant controls and to assess the relationship with
pregnancy outcomes. In our cohort of asymptomatic women with overall
moderate LVOTO/AS, we found that AV peak gradient, left ventricular size
and left atrial size increased over the course of pregnancy compared to
controls. Although left ventricular function and mechanics were
preserved in this cohort, there were dynamic changes over pregnancy with
a trend to declining LVEF and small increase in GLS over the course of
pregnancy. We also found that in this cohort of women with a range of
LVOTO/AS, left ventricular size parameters, CO, and AV gradients were
significantly increased as compared to controls. Although there was no
overall significant difference in left ventricular function and
mechanics between all LVOTO/AS cases and controls, there was certainly a
lower LVEF and GLS among those with moderate or greater LVOTO/AS as
compared to controls. Pregnancy was well tolerated in all women with
LVOTO/AS in this study with no deterioration in functional status or
cardiac decompensation.
Studies focusing on sequential changes in LV function and mechanics over
the course of normal pregnancies have been limited but would suggest no
significant change occurs. Several older studies have shown that LVEF by
2D echocardiography remained stable during a normal
pregnancy21–24. One study of a healthy pregnant
cohort using 3D echocardiography observed a slight reduction in LVEF in
late pregnancy with return to baseline at
postpartum25. In another study of 36 healthy women,
Sengupta and colleagues showed that global longitudinal and
circumferential strain decreased while the radial strain increased
during pregnancy, and postulated that these counterbalancing changes
served to maintain the overall LVEF26. To our
knowledge, only 2 studies have evaluated gestational changes in AV
Doppler gradient and LV function and mechanics in women with LVOTO/AS.
In a study of 6 women with congenital AS, Samiei et al reported an
increase in the AV peak gradient from first trimester to third trimester
(30.8 ± 12.1 to 38 ± 19.5)9. Left ventricular function
was not evaluated in this study. In a separate study, Tzemos et al.
assessed 10 women with at least moderate congenital AS, and found that
AV peak gradient rose from 59 ± 7 mmHg (prepartum) to 70 ± 9 mmHg
(antepartum)8. This group also assessed left
ventricular mechanics, and found that LVEF and left ventricular
longitudinal strain remained unchanged.
Our larger case control study similarly shows that AV gradients and LV
and LA volumes increase over the course of pregnancy and significantly
more in the LVOTO/AS cases as compared to pregnant controls. This is an
important observation as clinicians should expect that gradients and
cardiac volumes will increase across the spectrum of LVOTO/AS severity
and to a greater degree than seen in pregnancies without structural
heart disease. It is important to note that our cohort consisted of
mostly mild LVOTO/AS (26/34, 76%). Left ventricular function and
mechanics remained in the normal range over the course of LVOTO/AS
pregnancies, although LVEF trended to decline even in this cohort with
milder forms of LVOTO/AS.
Numerous studies outside of pregnancy have demonstrated that increasing
LVOTO/AS and the consequent LVH leads to impaired compliance, high
filling pressures, and eventual replacement of interstitial space with
reactive fibrosis27–31. In patients with AS, left
ventricular GLS has been shown to detect this adverse remodeling before
LVEF declines, and further deteriorates over
time15,16,18,27. These changes certainly can
complicate the hemodynamic adaptations required for an event free
pregnancy.
Pregnancy with pre-existing significant left heart obstruction has been
shown to be associated with increased risk of maternal cardiac events,
as well as adverse obstetrical and fetal/neonatal
outcomes32. Presence of a fixed obstruction and the
reduced ability to augment stroke volume in setting of an increased
physiologic demand of pregnancy is believed to be the mechanism for
decompensation in women with LVOTO/AS10,26,33. Despite
changes in cardiac size and trends to a declining LVEF, there were no
adverse cardiac events in our study’s LVOTO/AS group. This is likely due
to the fact that LV function and mechanics remained in the normal range
over the course of pregnancy for this entire cohort with mostly mild
LVOTO/AS. An important observation is that LV function and mechanics
were significantly lower in the moderate or greater LVOTO/AS group as
compared to milder LVOTO/AS although still in the normal range. This
would suggest that changes in function and mechanics likely play a role
in cardiac decompensation in cases of significant LVOTO/AS with
clinically relevant decline in LV function and mechanics. There was a
trend to increased rate of gestational hypertension which has been
previously documented among women with aortic coarctation. Finally, more
miscarriage and preterm deliveries occurred in the study group, both of
which are common fetal/neonatal complication encountered among woman
with structural heart disease.