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\begin{document}

\title{Transient Fetal Atrioventricular Block: A Series of Four Cases and
Approach to Management}



\author[1]{Sandra D. Kikano}%
\author[1]{Stacy A. S. Killen}%
\affil[1]{Monroe Carell Junior Children's Hospital at Vanderbilt}%


\vspace{-1em}



  
  \date{May 22, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Fetal atrioventricular block (AVB) is a failure of conduction from atria
to ventricles. Immune- and non-immune-mediated forms occur, especially
in association with congenital heart disease. Second-degree (2\selectlanguage{ngerman}°) AVB may
be reversible with dexamethasone and IVIG in immune-mediated disease.
However, once third-degree AVB develops, it is deemed irreversible with
need for a pacemaker and risk for cardiomyopathy. Rarely, 2° AVB is a
transient, benign phenomenon in the immature conduction system. Few case
series of transient AVB have been reported, but a management approach
has not been defined. We report four patients with self-resolving,
non-immune fetal AVB and outline a management strategy.%
\end{abstract}\selectlanguage{ngerman}%



\sloppy


\textbf{Transient Fetal Atrioventricular Block: A Series of Four Cases
and Approach to Management}

Sandra D. Kikano, MD and Stacy A. S. Killen, MD, MSCI

Thomas P. Graham Division of Pediatric Cardiology Monroe Carell Jr
Children's Hospital at Vanderbilt University, Nashville, TN, USA.

Funding: none

Disclosures: none

Correspondence:

Stacy A. S. Killen, MD, MSCI

2220 Children's Way, Suite 5230

Nashville, TN 37232-9119

Phone (615) 322-7447

Fax (615) 322-2210

E-mail: stacy.statemann@vumc.org

\textbf{Abstract} :

Fetal atrioventricular block (AVB) is a failure of conduction from atria
to ventricles. Immune- and non-immune-mediated forms occur, especially
in association with congenital heart disease. Second-degree (2\selectlanguage{ngerman}°) AVB may
be reversible with dexamethasone and IVIG in immune-mediated disease.
However, once third-degree AVB develops, it is deemed irreversible with
need for a pacemaker and risk for cardiomyopathy. Rarely, 2° AVB is a
transient, benign phenomenon in the immature conduction system. Few case
series of transient AVB have been reported, but a management approach
has not been defined. We report four patients with self-resolving,
non-immune fetal AVB and outline a management strategy.

Key Words: Fetal atrioventricular block, Fetal heart block, Fetal
second-degree atrioventricular block, Long QT syndrome

\textbf{Introduction} :

Fetal atrioventricular block (AVB) is estimated to occur in
\textasciitilde{} 1: 20,000 live births\textsuperscript{{[}1{]}}. It
occurs in immune- and non-immune-mediated
forms\textsuperscript{{[}1-6{]}}. Immune-mediated block develops from
transplacental passage of maternal anti-Ro/SSA autoantibodies that,
beginning in the second trimester, damage the fetal AV
node\textsuperscript{{[}1{]}}. Complete (third-degree) immune-mediated
AVB is considered irreversible and has significant associated mortality
(15-30\%) and morbidity, with about two-thirds of infants requiring
permanent pacing postnatally\textsuperscript{{[}2-4{]}}. Non-immune AVB
most often occurs in the setting of complex structural heart disease,
such as left atrial isomerism (LAI) and congenitally-corrected
transposition of the great arteries (ccTGA), in which discontinuity of
the AV node and ventricular tissue causes complete heart
block\textsuperscript{{[}5, 6{]}}.

There are a few case reports of non-immune-mediated fetal AVB without
structural heart disease, with variable outcomes. Some reports describe
hydrops or permanent pacing in most patients\textsuperscript{{[}7{]}}.
Other reports describe transient AVB without significant long-term
complications\textsuperscript{{[}8-11{]}}. We describe four patients,
evaluated in the Vanderbilt University Medical Center fetal cardiology
clinic from 2016-2020, with benign, self-resolving, non-immune-mediated,
second-degree (2°) fetal AVB and outline a management approach.

\textbf{Case Presentations (Table 1):}

Patient A was initially evaluated by pediatric cardiology at 20 1/7
weeks gestational age (wga) for fetal bradycardia noted that same day on
20-wga anatomy scan, with persistent heart rates of 72-78 beats per
minute (bpm). The fetal heart rate was 163 bpm on a 12 wga ultrasound.
Fetal echocardiogram (echo) demonstrated regular atrial rates of 146-152
bpm and ventricular rates of 75-80 bpm in a pattern consistent with 2:1
2° AVB. The echo was otherwise normal. Due to concerns for
immune-mediated heart block, we initiated dexamethasone but discontinued
this therapy when maternal anti-Ro/SSA and anti-La/SSB antibodies were
negative; of note, this treatment strategy was used for all the cases
reported in this series. Follow-up ultrasound at 21 6/7 wga demonstrated
a normal heart rate and rhythm of 163 bpm. Weekly ultrasounds until 25
wga and then every few weeks through the remainder of pregnancy
confirmed normal rate and rhythm. A female infant was delivered at 39
2/7 wga via emergency c-section for prolonged heart rate deceleration
and maternal chorioamnionitis; Apgar scores were 2, 4, 8. Postnatal EKG
demonstrated sinus rhythm with a normal QTc interval; telemetry
monitoring demonstrated intact AV conduction. Postnatal echo confirmed a
structurally normal heart.

Patient B was initially seen at 19 1/7 wga for bradycardia noted on
routine obstetrical evaluation at 19 wga. Fetal echo confirmed a
structurally normal heart and 2:1 2° AVB with atrial rates of 145-162
bpm and ventricular rates of 72-75 bpm. The pregnancy was also notable
for selective reduction of a twin with trisomy 21. Follow-up echo at 21
1/7 wga demonstrated atrial and ventricular rates of 146-155 bpm with a
normal mechanical PR interval. Weekly obstetrical fetal heart rate
assessments were normal through 25 4/7 wga, at which time a follow-up
echo also confirmed normal rate and rhythm. The mother was returned to
routine obstetrical monitoring. A female infant was delivered at term
(37 5/7wga) at another hospital; a postnatal EKG was recommended.

Patient C (\textbf{Figure 2)} was diagnosed with multiple fetal
anomalies (open neural tube defect with hydrocephalus, horseshoe kidney,
echogenic bowel, anorectal malformation, 2-vessel umbilical cord) at 25
1/7 wga and referred to pediatric cardiology for right \textgreater{}
left ventricular size discrepancy and ventricular septal defect. The
initial fetal echo demonstrated a left superior vena cava to coronary
sinus and suspected coarctation of the aorta; the fetal heart rate was
138 bpm with a normal mechanical PR interval. However, during an
ultrasound in the Maternal Fetal Medicine Center 2 hours later, fetal
AVB was suspected. An urgent, repeat fetal echo confirmed 2° AVB with
atrial rates of 130-140 bpm and ventricular rates of 65-70 bpm. There
was also a brief period of sinus bradycardia (92 bpm) with first-degree
AVB (mechanical PR interval 160-180 msec). A follow-up fetal heart
rate/rhythm check the next day was normal (137 bpm). A repeat echo at 25
4/7 wga confirmed atrial and ventricular rates of 129-141 bpm with a
normal mechanical PR interval. Weekly fetal heart rate checks for 4-6
weeks and follow-up echos at 31 1/7 wga and 35 1/7 wga demonstrated
normal rate and rhythm. A male infant was born at 37 wga via c-section
for spontaneous rupture of membranes with an open neural tube defect; he
was confirmed to have a large lumbar meningomyelocele and CHARGE
syndrome. Postnatal echo confirmed bilateral superior vena cavae,
bicuspid aortic valve, and long-segment coarctation of the aorta, for
which he underwent aortic arch augmentation at 1 month of age. Although
his post-operative course was complicated by an accelerated junctional
rhythm, his EKGs and telemetry monitoring otherwise demonstrated sinus
rhythm and normal QTc intervals.

Patient D was found to have bradycardia on obstetrical anatomy
ultrasound at 18 6/7 wga. Fetal echo the following day (19 wga)
confirmed 2° AVB with atrial rates of 150-158 bpm and ventricular rates
of 73-77 bpm. Follow-up obstetrical ultrasound at 21 wga demonstrated
atrial and ventricular rates of 144 bpm; fetal rate and rhythm remained
normal for the duration of pregnancy. A female infant was born at term
(40 1/7wga) via an uncomplicated vaginal delivery. Postnatal EKGs
demonstrated sinus rhythm with normal QTc intervals.

\textbf{Discussion} :

Fetal immune-mediated AVB is well understood and is known to be
associated with maternal anti-Ro/SSA antibodies that can irreversibly
damage the developing AV node and injure the
myocardium\textsuperscript{{[}1-4{]}}. However, AVB is often diagnosed
in women who do not know they have anti-Ro/SSA
antibodies\textsuperscript{{[}12{]}}. Disease onset mostly commonly
occurs between 16 and 26 wga; diagnosis after 28 wga is
rare\textsuperscript{{[}1{]}}. The transition between sinus rhythm and
complete AVB may be as short as 12 hours\textsuperscript{{[}13{]}}.
Children with third-degree AVB require lifelong cardiac pacing; there is
also risk for developing cardiomyopathy with need for heart
transplantation\textsuperscript{{[}1-4{]}}. However,
anti-Ro/SSA-mediated 2° AVB treated rapidly with dexamethasone and
intravenous immunoglobulin (IVIG) has been shown to be
reversible\textsuperscript{{[}13{]}}.

Differentiating transient, non-immune mediated AVB from
anti-Ro/SSA-mediated AVB is critical, as the therapeutic window for
anti-Ro/SSA-mediated 2° AVB is short\textsuperscript{{[}13{]}}. The
differential diagnosis also includes AVB from LQTS, myocarditis, ccTGA
or LAI and blocked atrial bigeminy\textsuperscript{{[}14-20{]}}.

Transient, fetal non-immune mediated AVB has rarely been described in
the setting of normal intracardiac anatomy and appears to be benign.
There have been a few prior case reports of fetal AV
block\textsuperscript{{[}8-11{]}} that self-resolved in a similar time
frame to our reported cases. In our cases, there were no structural
cardiac abnormalities that led to malformation of the fetal conduction
system.

The mechanism of transient, non-immune fetal AVB remains poorly
understood; some suggest it may be a vagally-mediated phenomenon in the
immature conduction system, which has a preponderance of parasympathetic
tone\textsuperscript{{[}8{]}}. All reported cases demonstrate complete
and permanent resolution within a couple of
weeks\textsuperscript{{[}8-11{]}}. In the absence of maternal
anti-Ro/SSA antibodies, it is reasonable to monitor fetuses who are
otherwise well without intervention. A management approach is detailed
below (\textbf{Figure 3} ).

Careful analysis with fetal echo includes rhythm evaluation and
screening for structural heart disease. Simultaneous pulse Doppler
assessment of the mitral inflow and aortic outflow, the superior vena
cava and aorta, or the pulmonary artery and pulmonary vein can be used
to determine the atrial and ventricular relationship and to measure the
mechanical PR interval; M-mode and color M-mode can supplement this
assessment\textsuperscript{{[}14{]}}. Hepatic vein Doppler can be used
to determine if there is a regular or irregular atrial rate and to
confirm that the rhythm does not represent blocked atrial bigeminy,
characterized by a ``short-long-short-long'' atrial interval and a
variable atrial rate\textsuperscript{{[}20, 21{]}}. Second-degree AVB is
characterized by a regular atrial interval and
rate\textsuperscript{{[}20{]}}. Structural analysis should exclude ccTGA
or LAI\textsuperscript{{[}5, 6{]}} and evaluate for other echo signs
that may suggest anti-Ro/SSA-mediated disease or
myocarditis\textsuperscript{{[}12, 22-25{]}}. It is also important to
measure the isovolumic relaxation time (IVRT), which is prolonged in
LQTS\textsuperscript{{[}15{]}}, and surveil for other LQTS arrhythmias,
including ventricular tachycardia, torsade de pointes, and persistent
sinus bradycardia, defined by fetal heart rate below the third
percentile for gestational age\textsuperscript{{[}17-19{]}}.

Upon initial diagnosis of fetal AVB, maternal screening for autoimmune
disease includes testing for maternal anti-Ro/SSA antibodies and careful
clinical evaluation for signs/symptoms of autoimmune disease, which is
often unrecognized prior to detection of fetal
AVB\textsuperscript{{[}12{]}}. Dexamethasone should also be considered
pending anti-Ro/SSA results given the risks of rapid progression of
anti-Ro/SSA-mediated 2° AVB. This can be discontinued if anti-Ro/SSA
antibodies are negative. Maternal thyroid studies can also be obtained,
as maternal thyroid disease may also impair fetal cardiac
conduction\textsuperscript{{[}26{]}}. Parental EKGs, as well as
inquiries into a family history of long QT syndrome, seizures, syncope,
cardiac arrest, or sudden unexplained death encompass a complete
screening for LQTS or other inherited
channelopathies\textsuperscript{{[}17{]}}. Maternal avoidance of QT
prolonging medications should also be considered until the fetal
diagnosis is made\textsuperscript{{[}17{]}}.

Once a diagnosis of fetal AVB is made, home fetal heart rate monitoring
can be an empowering tool for ongoing fetal
assessment\textsuperscript{{[}27, 28{]}}. At least weekly fetal heart
rate assessment, by the obstetrician or the cardiologist, is recommended
until AVB resolves and should be considered for at least four subsequent
weeks to exclude recurrence, which is not typical for transient, benign
AVB\textsuperscript{{[}11{]}}. A follow-up fetal echo in 2-4 weeks can
be used to confirm resolution of AVB, with additional fetal echos during
the remainder of pregnancy as needed to support obstetrical assessment.
In our patients, we chose to repeat a fetal echo at
\textasciitilde{}35-36 wga to confirm normal fetal heart rate and rhythm
prior to delivery. Fetal magnetocardiography can be considered for more
precise determination of fetal cardiac conduction and evaluation for
channelopathies; but this currently has limited
availability\textsuperscript{{[}14-16{]}}. A postnatal EKG completes the
assessment.

\textbf{Conclusion} :

Transient, benign 2° AVB is a rare phenomenon that occurs in the second
trimester of pregnancy and is a diagnosis of exclusion. Key management
approaches include careful screening for anti-Ro/SSA mediated AVB and
LQTS, evaluation for structural heart disease, close in utero monitoring
for self-resolution, and postnatal EKG.

\textbf{Table 1} . Summary of Cases of Transient Second-Degree
Atrioventricular Block\selectlanguage{english}
\begin{longtable}[]{@{}lllll@{}}
\toprule
\begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
\textbf{Patient A}\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
\textbf{Patient B}\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
\textbf{Patient C}\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
\textbf{Patient D}\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
WGA at Diagnosis\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
20 1/7\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
18 5/4\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
25 1/7\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
18 6/7\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
WGA at Resolution\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
21 6/7\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
21 1/7\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
25 2/7\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
21 0/7\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Gravida/ Para\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
G1P0\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
G3P2\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
G5P3\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
G3P2\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Maternal age (years)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
26\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
39\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
37\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
21\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Atrial Rate (bpm)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
146-152\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
145-152\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
130-140\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
150-158\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Ventricular Rate (bpm)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
75-80\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
72-75\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
65-70\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
73-77\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Parental ECG\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Maternal Thyroid studies\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
Maternal Medications\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
Prenatal Vitamin\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
Prenatal Vitamin\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
Prenatal Vitamin\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
Prenatal Vitamin\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Postnatal EKG\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Normal\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Other\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
CHARGE Syndrome\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Figure 2} . Fetal echocardiography images from case 3 with
Doppler and M-mode showing second-degree atrioventricular block with 2:1
AV conduction. (A) On initial consult for fetal right
\textgreater{}~left ventricular size discrepancy and probable
coarctation of the aorta there was sinus~rhythm at 138 bpm with
mechanical PR=130 msec (B-D) On follow up, there was 2:1 AV conduction
with regular atrial rates of 130-140 bpm and ventricular rates 65-70
bpm, as demonstrated by mitral inflow-aortic outflow Doppler {[}B{]},
color M-mode {[}C{]}, and hepatic vein Doppler {[}D{]}, confirming
regular atrial rates. (E) There was also a brief period of sinus
bradycardia (92 bpm) with PR prolongation/first-degree AV block
(mechanical PR interval 160-180 msec) (F-G) At next clinical follow ups,
there was normal fetal heart rate and rhythm of 129-141bpm

(A)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

(B)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

(C)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

(D)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

(E)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

(F)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}

(G)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image7/image7}

\end{center}
\end{figure}

\textbf{Figure 3.} Suggested Management Approach for Fetal Second-Degree
Atrioventricular Block

\textbf{References:}

1. Buyon, J.P., et al.,\emph{Autoimmune-associated congenital heart
block: demographics, mortality, morbidity and recurrence rates obtained
from a national neonatal lupus registry.} J Am Coll Cardiol, 1998.
\textbf{31} (7): p. 1658-66.

2. Brucato, A., F. Franceschini, and J.P. Buyon, \emph{Neonatal lupus:
long-term outcomes of mothers and children and recurrence rate.} Clin
Exp Rheumatol, 1997. \textbf{15} (5): p. 467-73.

3. Julkunen, H., et al.,\emph{Isolated congenital heart block: fetal and
infant outcome and familial incidence of heart block.} Obstet Gynecol,
1993.\textbf{82} (1): p. 11-6.

4. McCune, A.B., W.L. Weston, and L.A. Lee, \emph{Maternal and fetal
outcome in neonatal lupus erythematosus.}Ann Intern Med, 1987.
\textbf{106} (4): p. 518-23.

5. Machado, M.V., et al., \emph{Fetal complete heart block.} Br Heart J,
1988. \textbf{60} (6): p. 512-5.

6. Gembruch, U., et al., \emph{Fetal complete heart block: antenatal
diagnosis, significance and management.}Eur J Obstet Gynecol Reprod
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