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(Circulation. 1995;92:1531-1538.)
© 1995 American Heart Association, Inc.
Articles |
Left Heart Obstructive Lesions and Left Ventricular Growth in the Midtrimester Fetus
A Longitudinal Study
From the Department of Cardiology (L.K.H., P.J.S., S.D.C.), Children's Hospital, and the Department of Pediatrics, Harvard Medical School, Boston, Mass; Aldo Castaneda Institute for Congenital Heart Disease (S.P.S.), Clinique de Genolier, Genolier, Switzerland; Hadassah Hospital (A.J.J.T.R.), Cardiology, Ein-Karem, Jerusalem, Israel; and Mount Sinai Hospital (I.A.P.), Department of Pediatrics, Division of Cardiology, New York, NY.
Correspondence to Lisa K. Hornberger, MD, Department of Cardiology, Children's Hospital, 300 Longwood Ave, Boston, MA 02115.
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Abstract |
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Background Isolated case reports that suggest the potential for development of left heart hypoplasia late in gestation provide the only information about the in utero natural history of left heart obstructive lesions.
Methods and Results We reviewed the prenatal and postnatal echocardiograms of 21 fetuses with left heart obstructive lesions, including 15 with serial antenatal study, to elucidate the antenatal natural history of this spectrum of disease and to identify features indicative of postnatal disease severity. Ventricular, atrioventricular valve, and great artery dimensions were measured and growth curves were developed with comparisons to data from 47 normal fetuses. Fetuses were divided into groups according to whether postnatally the left heart was capable (group 1, n=10) or incapable (group 2, n=7) of supporting the systemic circulation in the presence of a patent aortic valve. Group 3 (n=4) included fetuses with aortic atresia. At the initial examination (21.7±3.4 weeks' gestation), left heart dimensions were normal or reduced, with the most diminutive measurements in group 3. Three fetuses in group 2 and most in group 1 had normal initial left heart dimensions. Subsequent growth of left heart structures either paralleled normal growth or was reduced, the latter resulting in the development or progression of left heart hypoplasia. All left heart dimensions grew more slowly in group 2 and group 3 than in group 1 (P<.05). Other prenatal features observed only in groups 2 and 3 included reversed (n=10) or bidirectional (n=1) foramen ovale flow and retrograde distal arch flow (n=9). Initial midtrimester mitral valve and ascending aorta z scores and the growth rates of all left heart structures correlated strongly with postnatal left ventricular end-diastolic dimension (P=.0007 to .03, r=.57 to .82) and could be additional indicators of postnatal disease severity. One group 1 fetus developed severe aortic stenosis late in gestation.
Conclusions The potential for the in utero development or progression in severity of left heart obstruction and hypoplasia in left heart obstructive lesions necessitates serial prenatal study in affected fetuses carried to term.
Key Words: ventricles • lesion • heart disease, congenital
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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For more than a decade, high-resolution ultrasound has made it possible to detect structural and functional cardiovascular abnormalities in the midtrimester human fetus. The prenatal features of most congenital cardiac defects and the postnatal clinical outcome of affected fetuses have been described. There is a paucity of information, however, regarding the natural history of heart defects during the second half of pregnancy. Knowledge of the potential for progression of disease is important not only for appropriate prenatal counseling but also for determining when serial prenatal study is warranted, for planning of postnatal management, and for developing reasonable intrauterine therapy. Furthermore, an understanding of the evolution of heart defects during the second half of gestation should provide insight into the determinants of normal and abnormal cardiac development.
The prenatal detection of left heart obstructive lesions, including hypoplastic left heart syndrome,1 2 3 4 5 coarctation of the aorta,6 7 8 and critical aortic stenosis,9 is well documented in the literature. Isolated case reports, however, provide the only information about the intrauterine evolution of this spectrum of diseases in the second and third trimesters,4 10 11 12 and they suggest a potential for progression in the degree of left heart hypoplasia. Therefore, in the present study, we retrospectively review the prenatal and postnatal echocardiograms of 21 fetuses with left heart obstructive lesions, including 15 with serial antenatal study, to elucidate the natural history of left heart obstructive lesions in the fetus, particularly with respect to left heart growth and the potential for progression in the degree of obstruction. We also attempt to identify prenatal features that could be indicative of the severity of postnatal left heart obstruction and hypoplasia.
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Methods |
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Study Population
All fetuses studied initially before 30 weeks of gestation and subsequently carried to term with the prenatal diagnosis of a left heart obstructive lesion(s) at Children's Hospital, Boston, between March 1987 and July 1994 were identified. Fetuses diagnosed with mitral or aortic valve obstruction or hypoplasia and those with coarctation of the aorta (or a combination of left heart obstructive lesions) were included. Those with left heart obstructive lesions associated with conoventricular abnormalities such as double-outlet right ventricle or associated with malaligned atrioventricular canal defects were not included in this study. Also, fetuses with aortic and mitral atresia in whom the severely diminutive left ventricle and aorta could not be visualized in the midtrimester were excluded. The postnatal clinical outcomes were reviewed.
Echocardiographic Examinations and
Measurements
Prenatal and postnatal studies were performed with an
Acuson 128 or Hewlett-Packard 77020 or Sonos 1000 system with 5- or
7.5-MHz transducers. Studies included four-chamber views and long-
and short-axis views of the ventricles, ventricular
outflow tracts, great arteries, and aortic arch. Spectral Doppler
and color flow mapping were used to identify abnormal blood flow
patterns and velocities, including the direction of ductus arteriosus
and foramen ovale flow, and to determine patency and degree of
obstruction of the ventricular inflow and outflow tracts.
All images were recorded on videotape for off-line
analysis.
The following measurements were made from the echocardiograms
(Fig 1
): (1) end-diastolic left
ventricular and right ventricular diameters
measured just below the atrioventricular valve from a
short-axis view, immediately before closure of the
atrioventricular valves (defined as end
diastole); (2) end-diastolic left and right
ventricular long-axis dimensions measured in a
four-chamber view from the level of the
atrioventricular valve annulus to the endocardium of
the apex; (3) mitral and tricuspid valve annulus diameters during
diastole in a four-chamber view; (4) ascending aorta
diameter above the aortic root, during ventricular systole;
and (5) main pulmonary artery diameter midway between the
pulmonary valve and the bifurcation, also during
ventricular systole. Measurements were made in most of the
studies at the time of the prenatal examination. The studies were
reviewed and the data were collected by one reviewer (Dr Hornberger),
who was blinded to the clinical outcome of all except one of the
affected fetuses.
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With the use of the postnatal echocardiograms in the abnormal fetuses, the left ventricular end-diastolic volume was measured with a modified biplane Simpson algorithm and indexed to body surface area. In our laboratory, the lower limit of normal of indexed left ventricular end-diastolic volume in infants is considered to be 46 mL/m2.13
After the measurements were made, fetuses were divided retrospectively into three groups according to clinical outcome and the severity of left heart obstruction. Fetuses were included in group 1 if the left heart was sufficient to sustain the systemic circulation and the infant was not ductus arteriosus dependent either before or after intervention. Fetuses were included in group 2 if the aortic valve was patent but the left heart was incapable of supporting the systemic circulation, necessitating single ventricle palliation. Fetuses were in group 3 if there was aortic atresia diagnosed prenatally and confirmed at birth.
Calculations and Statistical Analysis
Left and right heart
measurements from the initial
midtrimester examinations were converted to z scores using
data from 105 prenatal studies performed in 47 fetuses of normal
pregnancies without cardiac or noncardiac abnormalities. z
scores for left and right heart structures in the three groups were
compared with the normal data with the use of single-group
t test (assuming a population mean of 0) and with each other
by ANOVA. The differences between groups were identified with an
unpaired Student's t test.
Growth curves were developed for fetuses with serial antenatal studies using regression analysis. Growth rates for the left and right heart structures were calculated from the regression analysis and were compared for the three groups with ANOVA. Mann-Whitney rank sum test was then used to compare growth rates of left heart structures between individual groups.
To identify features that correlate with the severity of postnatal left ventricular hypoplasia, correlation analysis was used to compare indexed postnatal left ventricular end-diastolic volume with a number of parameters measured from the earliest prenatal echocardiogram, including ratios of the measurements of left heart to right heart structures and the z score for the initial left and right heart structure measurements. Growth rates of left heart structures were also compared with postnatal indexed left ventricular end-diastolic volume by linear regression analysis.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Twenty-one fetuses were included in the study. The reasons for referral for fetal echocardiography were a discrepancy in ventricular or great artery size on a level I ultrasound in 18, a family history of congenital heart disease in 2 (including one with a family history of hypoplastic left heart syndrome), and drug exposure in 1. The estimated gestational age by biparietal diameter and femur length at the initial prenatal study was 21.7±3.4 (±SD) weeks. The mean time from the initial study to the postnatal follow-up was 16.7±3.7 weeks (range, 6 to 22 weeks), and the mean interval to follow-up in the serially studied fetuses was 7.3±2.3 weeks. Fifteen fetuses had two or more prenatal studies, and 6 had only one prenatal study. All 15 fetuses with prenatal follow-up were studied after September 1991, when we routinely began to serially study fetuses with left and right heart obstructive lesions in utero and prospectively measure left and right heart dimensions.
A total of 41 prenatal studies were reviewed. In 31 of the 41 antenatal studies, all seven of the cardiovascular measurements could be made, and in the remaining studies, two or more measurements could be made. All af-fected fetuses had complete postnatal echocardiographic examinations.
Prenatal and Postnatal Anatomy and Outcome
The prenatal and
postnatal anatomy and clinical outcome
for all of the cases are summarized in Table 1.
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Ten of
the 21 fetuses were included in group 1. Of these 10, 6 had
coarctation of the aorta, 5 of whom had surgical repair at 
2 months
of age. One of the 6 with coarctation had significant valvar aortic
stenosis, which was successfully balloon dilated at 6 months of
age. Three had a mitral valve abnormality as the primary lesion, and
none had surgical or medical intervention; however, 1 fetus died at 2
weeks of age from apnea secondary to significant central nervous system
disease. One fetus in group 1 had isolated severe aortic
stenosis and underwent successful balloon valvuloplasty at 2
weeks of age. Nine of 9 fetuses in whom postnatally the left
ventricular end-diastolic volume could be
determined had some degree of left ventricular hypoplasia
with an indexed left ventricular
end-diastolic volume of 18 to 31 mL/m2.
Group 2 consisted of
7 fetuses, including 5 with severe aortic
stenosis and 2 with significant mitral valve obstruction and
only mild aortic outflow obstruction. Of the 7, 6 underwent stage I
palliation (Norwood operation); 4 of whom died in the postoperative
period, and 1 died of sepsis while awaiting stage I palliation. All 7
had moderate or severe left ventricular hypoplasia with an
indexed left ventricular end-diastolic
volume of 16 mL/m2.
Four fetuses with aortic atresia were included in group 3. Three underwent stage I palliation, 2 of whom died in the postoperative period; 1 died without surgical intervention.
Left and Right Heart Size in the Midtrimester
At the initial
prenatal examination, all except 2 of the fetuses
had some discrepancy in right and left ventricular or great
artery size with larger right heart structures. Most of the left heart
dimensions in group 1 at the initial examination had z
scores that were more than -2, although for the group left
ventricular short-axis, mitral valve, and ascending
aortic dimensions were significantly smaller than normal (Table
2). In group 2, the initial left heart dimensions were
within the normal range in 3 of 7 fetuses. In contrast, in group 3 all
left heart dimensions were more than 2 SD below the mean at the initial
examination, with the exception of the ascending aortic diameter in 1
fetus. Groups 1 and 2 differed only in the diameter of the ascending
aorta on the initial examination. Mean z scores for left and
right heart dimensions and left-to-right heart ratios from the
initial midtrimester examinations are given for groups 1, 2, and 3 in
Table 2.
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Initial right heart dimensions for all groups tended to be above the mean values observed in the normal fetuses (z scores >0), although most were within 2 SD of the mean. There were no significant differences in z scores for initial right heart measurements among the three groups, and right heart dimensions for all three groups did not differ significantly from normal.
Growth of Left and Right Heart Structures
Growth curves for
left heart structures from individual fetuses in
groups 1, 2, and 3 are shown in Fig 2 with the 5th
through 95th percentiles of the normal fetuses demonstrated by the
shaded area. Growth curves for left ventricular length were
similar to those for left ventricular short axis, and
therefore only the short-axis diameter curves are shown. Growth of
the left and right heart structures best fit a linear regression model
in the fetuses with serial prenatal measurements. Correlation
coefficients were 
.83 in 79 of 84 regression analyses
performed using the serial measurements.
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Growth of left heart
structures in most of the fetuses either
paralleled normal growth or was slower than normal, the latter
resulting in the development of or progression in severity of left
heart hypoplasia. For group 1 fetuses, growth of left heart structures
was often normal or only mildly reduced, whereas for most left heart
structures in the group 2 fetuses there was progressive hypoplasia with
slower growth of the structure than predicted from the normal fetal
values (Fig 3). Growth of the left ventricle and the
ascending aorta was uniformly abnormal in the group 3 fetuses,
resulting in severe hypoplasia of these left heart structures at
birth.
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As shown in Table 3, there were statistically
significant differences in growth rates of left ventricular
dimensions and ascending aortic diameter for all three groups when
compared by ANOVA, with the slowest growth rates in the group 3 fetuses
(P.008). Rates of growth of all left heart structures were
significantly slower in group 2 fetuses than in group 1 fetuses
(P<.05), with the most significant difference in the rate
of growth of the mitral valve annulus (P=.001).
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Fig
3a
through 3d includes prenatal and postnatal
echocardiographic images obtained in a fetus with
severe aortic stenosis in the midtrimester associated with a
dilated, poorly contractile left ventricle (case 17). Despite
normal-sized left heart dimensions on the initial examination,
growth of these structures was significantly reduced, resulting in
moderate-to-severe left heart hypoplasia at birth.
Rates of growth of
the right ventricular
short-axis diameter and length, the tricuspid valve annulus, and
the main pulmonary artery diameter did not differ significantly
among groups when compared by ANOVA (Table 3).
Indicators of Postnatal Disease Severity
Several antenatal
indexes were identified that correlated with the
degree of left ventricular hypoplasia at birth. Regression
equations, correlation coefficients, and probability values for initial
dimensions and growth rates versus indexed postnatal left
ventricular end-diastolic volume are
presented in Table 4. From the initial
examination, the mitral valve and ascending aorta diameter z
score and the ratio of the ascending aorta to main pulmonary
artery diameter correlated with the indexed postnatal left
ventricular end-diastolic dimension.
Midtrimester left ventricular dimensions, however, did not
correlate with postnatal left ventricular
end-diastolic volume. A strong correlation between the
postnatal left ventricular end-diastolic
dimension and the rates of growth for all left heart structures was
observed. Rates of tricuspid valve, right ventricle, and
pulmonary artery growth showed no correlation.
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In addition to differences in left heart growth, several in utero features were more commonly observed in groups 2 and 3 than in group 1 at the initial midtrimester examination. Blood flow in the distal aortic arch was retrograde in all of the fetuses of group 3 and in 5 of the fetuses of group 2, whereas it was antegrade in group 1 fetuses. The two group 2 fetuses with antegrade distal arch flow both had mitral stenosis as the primary obstructive lesion with only mild aortic outflow obstruction, and both had ventricular septal defects. All of group 3 and 6 of 7 group 2 fetuses had left-to-right atrial flow through the foramen ovale. One fetus from group 2 had bidirectional flow through the foramen. In contrast, there was only right-to-left atrial flow through the foramen ovale in the group 1 fetuses. The direction of foramen ovale flow and distal arch flow remained unchanged at follow-up in all serially studied fetuses.
Endocardial fibroelastosis was suspected in 3 group 2 fetuses in whom the left ventricular endocardial surface was echogenic. In all 3, the left ventricular function appeared qualitatively depressed in the presence of severe aortic valve stenosis. None of the group 1 or group 3 fetuses had evidence of endocardial fibroelastosis, although 1 group 1 fetus with severe aortic stenosis had qualitatively depressed left ventricular function late in gestation.
Mild mitral regurgitation was observed in 3 group 2 fetuses at the initial prenatal examination and only later in gestation in the group 1 fetus with severe aortic stenosis.
Despite the presence of left ventricular inflow and outflow obstruction, the presence of a gradient detected by spectral Doppler was unusual. Only 1 group 2 fetus with a thickened and hypoplastic mitral valve and aortic stenosis had a gradient through the mitral valve (peak, 9 mm Hg; mean, 3 mm Hg). Two of the 21 fetuses had gradients through the left ventricular outflow by continuous wave Doppler. In 1 group 2 fetus with mild aortic outflow obstruction at birth, there was a gradient of 10 to 15 mm Hg at the initial prenatal examination. In the group 1 fetus with severe valvar aortic stenosis at birth, a gradient of 25 mm Hg was initially detected during the second prenatal examination at 28 weeks.
Progression of Left Heart Obstruction
An increasing gradient
was detected by continuous wave Doppler
in only the group 1 fetus with postnatally confirmed severe valvar
aortic stenosis (Fig 4). On the initial
examination at 17.5 weeks of gestation, a bicommissural aortic valve
was suspected; however, there was no detectable gradient. At the
28-week follow-up study, there was a 25 mm Hg gradient detected
across the aortic valve, and by 36 weeks the gradient had increased to
64 mm Hg. Postnatally, the infant (case 10) was diagnosed with severe
valvar aortic stenosis and underwent successful balloon
valvuloplasty at 2 weeks of age.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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In Utero Features of Left Heart Obstruction
We have presented a series of in utero left heart obstructive lesions, including a spectrum of abnormalities of the mitral valve, left ventricular outflow tract and aortic valve, and the aortic arch with prenatal and postnatal follow-up. We found left heart obstructive lesions in the fetus to be associated with a discrepancy in left and right ventricular and great artery size with larger right heart structures and, in many, hypoplasia of one or more left heart structures. Regardless of the severity of obstruction, left heart obstructive lesions were not usually associated with a detectable gradient by Doppler at the level of left ventricular inflow or outflow in utero. In more severe obstruction, however, foramen ovale flow was either reversed, from left atrium to right atrium or bidirectional, and in many, distal arch flow was retrograde from the ductus arteriosus. The antenatal natural history of left heart obstructive lesions through the second half of gestation was characterized in many by reduced left heart growth, particularly in those with more severe obstruction in the midtrimester, resulting in the development or progression in severity of left heart hypoplasia.
In Utero Left Heart Growth
In the newborn, left ventricular
inflow and outflow
obstructive lesions, including coarctation of the aorta, are frequently
associated with hypoplasia of left heart
structures.14 15 16 17 18
The severity of left heart hypoplasia, including dimensions of inflow,
outflow, and left ventricular size, is an important
determinant of the medical and surgical management and clinical outcome
of these infants.17 19 20 21
For some infants with severe
left heart obstruction, particularly with a diminutive left ventricle
incapable of supporting the systemic circulation, single-ventricle
palliation or cardiac transplantation are the surgical
options,22 23 whereas in others, an aortic
valvuloplasty
or repair of coarctation of the aorta can result in a two-ventricle
outcome. For some of these newborns, no medical or surgical
intervention is necessary initially but may be required later in
life.
The ability to predict the postnatal severity of left heart hypoplasia in the midtrimester fetus requires knowledge of the patterns of left heart growth in utero with this spectrum of disease. In our series, the size of left heart structures in left heart obstructive lesions in the second trimester was either normal or small for gestational age. Fetuses with less severe disease and 3 of 11 with more severe left ventricular inflow or outflow obstruction had normal or only mildly hypoplastic left heart dimensions at the initial midtrimester examination, indicating normal or only mildly reduced left heart growth in the first half of gestation. In 4 fetuses with patent left ventricular inflows and outflows but with severe obstruction and in fetuses with aortic atresia and mitral atresia, however, the left heart dimensions were very hypoplastic on the initial midtrimester examination, suggesting that abnormal left heart growth had occurred earlier in gestation, perhaps shortly after embryogenesis was complete.
In the presence of left heart obstructive lesions, growth of left heart structures through the second half of pregnancy in many fetuses was reduced, resulting in the development or progression in severity of left heart hypoplasia. We found left heart growth to be most reduced through the second and third trimesters in fetuses with more severe obstruction in the midtrimester. However, when severe aortic outflow obstruction developed late, as observed in 1 fetus in the present study, or when there was only mild left ventricular inflow or outflow obstruction, in utero growth of left heart structures was normal or only mildly reduced.
In contrast to left heart structures, tricuspid valve, right ventricle, and main pulmonary artery dimensions were normal in the midtrimester in most of the fetuses, and subsequent growth of right heart structures at follow-up was similar despite the severity of left heart obstruction.
Development of Left Heart Hypoplasia
Based on our
observations, it appears that left heart hypoplasia
can develop or progress in the second and third trimester in
association with left ventricular outflow and inflow
obstruction, as suggested in the 1970s by Lakier et al,24
subsequently demonstrated in late-trimester fetal
lambs,25 and recently described in isolated human fetal
case reports.4 10 11 12
Although the specific mechanism of
impairment of left heart growth in the presence of left heart
obstruction remains speculative, it is most likely the effect of
several structural and hemodynamic abnormalities that
result in a reduction in blood flow through the mitral valve, the left
ventricle, and the aorta. During fetal life, the foramen ovale and
ductus arteriosus play a key role in equalizing intracardiac and great
artery pressures. Any rise in left atrial pressure in utero, for
example, results in a reduction of right-to-left atrial flow
through the foramen ovale and even a reversal of flow in more severe
disease, as observed in the present series. Blood diverted toward
the right heart and through the ductus arteriosus serves to maintain an
adequate cardiac output. Potential causes of elevated left atrial
pressure antenatally include the presence of left
ventricular inflow obstruction and increased left
ventricular filling pressures from decreased systolic
and/or diastolic function secondary to outflow obstruction
or primary myocardial disease.11 Premature restriction or
closure of the foramen ovale, observed in 1 of our fetuses, also
reduces left heart flow and may result in left heart
hypoplasia.26 27 However, this phenomenon may also be
a
secondary event associated with elevated left atrial pressures. The
degree of postnatal left heart hypoplasia is probably determined at
least in part by the time in gestation when left
ventricular outflow or inflow obstruction occurs and the
severity of obstruction as eluded to earlier.
The antenatal development of left heart hypoplasia in the presence of severe aortic outflow tract obstruction has been shown in case reports8 13 15 and in 1 fetus of the present study. We have recently encountered another, very similar case (currently in utero). At 18 weeks, in a twin gestation, one fetus was found to have a dilated, poorly contractile left ventricle associated with severe aortic outflow tract obstruction. Despite these findings, the fetus continued to thrive and grow, as did his twin. At 31 weeks, on repeat fetal echocardiogram there was a moderate-to-severe hypoplastic, hypertrophied, and dysfunctional left ventricle with evidence of endocardial fibroelastosis and left-to-right atrial shunting through a restrictive foramen ovale. The aortic valve was thickened and hypoplastic, and antegrade flow could not be demonstrated through the ascending aorta or mitral valve. We would propose that these cases do not represent an "unusual" form of hypoplastic left heart syndrome as previously described4 but rather are a part of the antenatal natural history and spectrum of severe aortic outflow obstruction.
Progression in the severity of obstruction as evidenced by an increase in Doppler gradient with a concomitant change in the morphology of the aortic valve was only observed in 1 fetus of this study. To our knowledge, this is the first report of the development of severe aortic stenosis in utero.
Clinical Implications
Although in general fetal
echocardiographic
features of congenital heart disease are similar to findings at
birth,28 recent longitudinal studies have revealed the
potential for progression of certain cardiac lesions. For example,
fetal tetralogy of Fallot may be associated with progression in the
severity of pulmonary hypoplasia and development of valvar
pulmonary atresia.29 Coarctation of the aorta may
be associated with progressive distal arch hypoplasia.8
Prenatal counseling of affected families should take into account
knowledge of both the known prenatal and postnatal prognosis of a
particular cardiac lesion and its potential for evolution through the
latter half of gestation.
We have shown that left heart obstructive lesions in utero can be associated with the development or progression of left heart hypoplasia, which may influence postnatal outcome. The potential for reduced left heart growth should be suspected, especially when more severe left heart obstruction is identified earlier in gestation and when there is reversed foramen ovale flow or retrograde distal arch flow, even in the presence of normal left heart dimensions in the second trimester. The z scores of the mitral valve and ascending aortic diameter in the midtrimester may serve ultimately as predictors of postnatal left heart size given their strong correlation with postnatal left ventricular end-diastolic volume in our retrospective analysis. Observations of the rate of growth of left heart dimensions may be even more sensitive indicators of postnatal left heart size, although depending on the timing of diagnosis, this may not be consistently useful in early second-trimester counseling. The limited number of cases in our series necessitates prospective verification of the clinical usefulness of growth rates and the developed regression equations.
The ability to recognize fetuses at risk for the development or progression of left heart obstruction or hypoplasia early in utero might facilitate the development of effective and appropriate intrauterine therapy. Balloon dilation of the aortic valve has been performed in late-gestation human fetuses with failing left ventricles.30 If antegrade flow were established earlier in gestation, perhaps normal or near-normal left heart growth and function would ensue.
In conclusion, left heart obstructive lesions in the fetus can evolve through pregnancy. During the second half of gestation, cardiovascular growth and fetal growth in general continue at a very rapid pace, and abnormalities of left heart growth that are initiated in or before the midtrimester may significantly influence the relative size of the left heart by term. The potential for progression in the degree of left heart obstruction, and, more important, left heart hypoplasia necessitates serial study of affected fetuses carried to term.
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Acknowledgments |
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Supported in part by National Institutes of Health training grant HL-07574-11 and an American Heart Association, Massachusetts Affiliate, Physician-Investigator Fellowship (Dr Hornberger).
Received January 24, 1995; accepted March 27, 1995.
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