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.