o_1977r8vv9vk1ts2ms0kd8pksa.pdf

a Chapter 33 Doppler Echocardiography for Managing Congenital Cardiac Disease 503
Fig. 33.25. Color M-mode echocardiogram
of the atrioventricular flow in supraventricular
tachyarrhythmias. The
cardiac rate was approximately
210 bpm. Note the atrial origin of the
tachycardia. RA right atrium, RV right
ventricle
tural integrity of the fetal heart and recognition of fetal
cardiac failure. Color flow mapping significantly
facilitates this process.
The prognosis of fetal SVT depends on the fetal
cardiac status and the obstetric and maternal medical
conditions. The prognosis is worse in the presence of
(1) any cardiac malformation and its complexity; (2)
hydrops signifying fetal cardiac failure; (3) refractoriness
to therapy; (4) fetal viral infection; (5) prematurity;
or (6) maternal medical complications such as fever
or hyperthyroidism.
Antepartum surveillance consists in serial echocardiography
to assess progression of the disease (e.g.,
development of fetal cardiac failure) and to monitor
the response to therapy. In the presence of SVT, cardiotocography
becomes uninterpretable in terms of
recognizing fetal compromise.
Congenital Complete Heart Block
Congenital complete heart block is characterized by a
complete failure of A-V conduction associated with
structural malformations or immune complex-mediated
injury to the conduction system (Fig. 33.26).
The ventricular rate is sustained below 100 bpm,
usually at 60±80 bpm. The atrial rhythm is discordant
with the ventricular rhythm, and its rate is maintained
within the normal range of fetal sinus rhythm
for the gestational age (120±160 bpm). Although it is
the third most common arrhythmia seen in the fetus,
it is still a relatively rare complication, with the reported
incidence ranging from 1 in 10,000 to 1 in
20,000 births [50, 51].
From an echocardiographic diagnostic perspective,
it is important to note that almost half the cases are
associated with congenital malformations of the fetal
Fig. 33.26. Electrophysiology of congenital complete heart
block. SA sinoatrial, AV atrioventricular
heart. Traditionally, left atrial isomerism and less frequently
right atrial isomerism have been implicated.
Other malformations include AVSD, outflow tract
anomalies such as corrected transposition, or doubleoutlet
right ventricle, many of which cases accompany
situs reversal or ambiguity. In most cases without
cardiac malformations, maternal autoimmune disease
predominates. Specifically, such mothers demonstrate
the presence of antibodies against small ribonucleic
autoantigens Ro/SS-A and La/SS-B [52].
Transplacental passage of these antibodies from the
mother to the fetus and their subsequent cross reaction
with fetal cardiac antigens apparently leads to fetal
myocarditis, fibrosis, and consequent damage to
the cardiac conduction system. It has been demonstrated
that anti-La/SS-B, but not anti-Ro/SS-A, antibodies
cross react with laminin, the major component