o_1977r8vv9vk1ts2ms0kd8pksa.pdf

532 W. J. Ott
walls in fetuses of diabetic mothers even in infants of
mothers who were under good glucose control [117].
The hemodynamic effects of these morphological
changes may lead to impairment of cardiac diastolic
function and eventual heart failure. Infants of diabetic
mothers, even in those situations where tight
glucose control has been obtained, have a significantly
higher incidence of sudden fetal death [117±
122]. An increased thickness in the ventricular walls,
particularly in the interventricular septum, has been
noted in these infants. Hypertrophy and disorganization
of the myofibrils of the fetal heart have also been
found at time of autopsy.
Doppler studies have shown evidence that the disproportional
thickening of the intraventricular septum
results in functional left ventricular outflow tract
obstruction which may lead to cardiac failure. Increased
A/E ratios at the level of both atrioventricular
valves and higher peak velocity values at the outflow
tracts were found in such fetuses. Weiner et al. felt
that this was due to an increasing A wave during the
later part of gestation suggesting increased cardiac
contractility and output in fetuses of diabetic women
[121]. Polycythemia, which is frequently present at
birth in infants of diabetic mothers, results in increased
blood viscosity which may alter preload and
affect ventricular filling. The high peak velocity values
in the aorta and pulmonary artery may be due to
increased contractility, or secondary to an increased
intra-cardiac flow volume, due to the fetal macrosomia
frequently seen in infants of diabetic mothers.
Other Causes of Fetal Heart Failure
A wide variety of other known, and probably unknown,
conditions can lead to fetal heart failure
[122±129]. Primary myocarditis of viral etiology has
been reported in the fetus. Blood-borne transplacental
infection or ascending chorioamnionitis may
cause significant systemic fetal infection which, in
turn, may cause fetal cardiac failure. High output failure
in the fetus has been reported in association with
rare fetal tumors, such as fetal teratoma, goitrous hypothyroidism,
hemangiomas, or rhabdomyosarcomas
[122±129]. In most of these cases the high output
failure is due to arterial±venous shunts within the tumor
itself or secondary to vascular compression by
an expanding mass.
Morine et al. described a case of high-output failure
in a fetus (cardiomegaly, pleural effusion, and increased
velocity in the carotid artery) diagnosed with
goitrous hypothyroidism [127]. The symptoms reversed
after intrauterine treatment with levothyroxine.
Arterial±venous malformations in the fetus, such
as an aneurysm of the vein of Galen, have also been
reported to cause fetal hydrops [128]. Chorioangiomas
of the placenta are benign hemangiomas that
can be seen in 1% of all placentas. Usually they cause
no problems, but when large (> 5 cm), they can cause
polyhydramnios and, occasionally, high-output failure
in the fetus secondary to arterial±venous shunts
[129]. Cardiomegaly and abnormal venous flow in the
fetus are typical signs of developing heart failure
[130].
Iatrogenic causes of fetal heart failure may be associated
with maternal drug use, especially indomethacin,
which has been reported to cause premature
closure of the fetal ductus arteriosus resulting in
fetal heart failure. Indomethacin has been shown to
cause transient constriction of the ductus arteriosus,
resulting in an increase in both systolic and diastolic
velocity in the ductus. As a consequence, tricuspid
regurgitation and heart failure may occur. Beta-agonists
have an inotropic effect on the fetal heart which
may lead to an increase of both peak velocity in the
aorta and pulmonary artery and an increase of the
stroke volume. Levy et al. have reported that the combined
use of indomethacin and corticosteroids may
have additive effects on ductal constriction [131]. The
long-term effects of these drugs is still unknown.
Fisher has reviewed many of the causes of cardiomyopathies
that may affect the fetus [132]. Hypoxia
and acidemia, metabolic abnormalities, such as hypocalcemia,
or congenital metabolic diseases, such as
Pompe's disease or endocardial fibroelastosis, have all
been reported to cause fetal cardiac failure.
Summary and Conclusion
A large number of clinical conditions have been
found that may lead to intrauterine cardiac failure.
Pulsed and color Doppler techniques have improved
our knowledge of fetal cardiovascular response to
structural and functional heart diseases. Key features
of developing fetal heart failure that may be seen include:
1. Valvular regurgitation
2. Altered velocities
3. Chamber dilatation
4. Fluid collections: ascites, edema, pericardial
5. Reverse flow: vena cava, umbilical pulsations.
Doppler blood flow studies have enabled investigators
and clinicians to better understand the pathological
processes involved in developing fetal heart failure
and to plan appropriate treatments or interventions.
We can expect that further study and experience with
the use of Doppler blood flow studies will lead to
increased improvement in perinatal morbidity and
mortality.