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\begin{document}

\title{Critical Coarctation of the Aorta in the Donor twin in Twin-Twin
Transfusion Syndrome and successful treatment with Balloon Angioplasty
after Birth: A Case Report}



\author[1]{alireza golbabaei}%
\author[2]{farshad jafari}%
\author[1]{Maasoumeh Saleh}%
\author[3]{kamran hessami}%
\author[4]{mohammadhassan darabi}%
\author[1]{mahsa naemi}%
\author[1]{azadeh rastgar}%
\affil[1]{Tehran University of Medical Sciences}%
\affil[2]{Iran University of Medical Sciences}%
\affil[3]{Baylor College of Medicine}%
\affil[4]{Shiraz University of Medical Sciences}%


\vspace{-1em}



  
  \date{May 25, 2024}


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\selectlanguage{english}
\begin{abstract}
Monochorionic twins (MC) are at increased risk of CHDs, especially
acquired CHDs in twin-twin transfusion syndrome (TTTS). Multiple cardiac
abnormalities in MC twins with TTTS are to be expected due to cardiac
hemodynamic changes. Therefore, more attention to this group of patients
should be given regarding heart abnormalities.%
\end{abstract}%



\sloppy


\textbf{Introduction}

Twin to twin transfusion syndrome (TTTS) is a rare and serious condition
that occurs in monochorionic (MC) pregnancies. It has a high perinatal
morbidity and mortality if left untreated(1). In the recipient fetus
biventricular hypertrophy, atrio-ventricular valves regurgitation,
cardiomegaly, cardiac dysfunction and finally fetal hydrops may occur
all of them mainly due to hypervolemic status. Moreover, right
ventricular outflow obstruction (RVOTO), valvar pulmonary stenosis (PS)
and atresia and left ventricular hypertrophic cardiomyopathy may also be
presented. Donor twin on the other hand, usually shows little cardiac
pathologies on echocardiography(2-5). Different types of cardiac
abnormalities in TTTS can be explained by the altered fetal
hemodynamics(6). Fetoscopic laser photocoagulation (FLP) at 16-26 weeks
of gestation is the treatment of choice for TTTS. There are evidences of
normalization of cardiac function in fetuses with severe TTTS after FLP
Acquired structural cardiac anomalies are detected in a proportion of
treated pregnancies, as a consequence of the altered hemodynamics(7).
Due to increased rate of CHDs in TTTS, especially PS in recipient twin,
prenatal and postnatal echocardiographic assessment is needed (8).

\textbf{Case presentation}

A 27-year-old pregnant woman, primigravida, MC twin pregnancy, with a
gestational age of 21 weeks was referred to our center due to stage 3
TTTS. Her pregnancy was a product of in vitro fertilization (IVF). She
had no significant past medical history and she did not use any drugs.
Fetal echocardiography showed severe coarctation of aorta (CoA) in the
descending aorta with retrograde flow in the donor twin (Figure 1). No
other major anomalies were detected in the fetuses. FLP was performed at
our center for treating TTTS. Accordingly, further development of TTTS
was stopped and at 33 weeks of gestation, the pregnancy was terminated
by cesarean section due to the onset of labor pains. Both babies were
born with good APGAR score and appropriate weight. Postnatal
echocardiography of donor twin in the supra-sternal view showed severe
narrowing of proximal part of aorta with flow acceleration (Figure 2).
In Doppler assessment, we detected a typical saw tooth appearance in the
location of coarctation (Figure 3) and apical four chamber view showed
left ventricular hypertrophy (LVH), significant left ventricular
enlargement (LVE) and left atrial enlargement (LAE) (Figure 4). With a
diagnosis of persistent aortic coarctation (figure 5), donor twin
underwent balloon inflation of aorta in the stenotic portion at the age
of one month. Balloon inflation of aorta in the stenotic location caused
the narrowing to completely resolve (Figure 6, 7, 8) and transthoracic
echocardiography after balloon angioplasty in suprasternal view showed
significant reduction in aortic stenosis (Figure 9).

\textbf{Discussion}

CoA is a common congenital heart defect that is characterized by a
narrowing distal to the aortic arch and the prenatal diagnosis is
challenging and difficult.(9) Its coincidence with TTTS is rare and
there have been only a few cases in the literature. (6) Assessment of
ventricular size is helpful in prenatal diagnosis and the left ventricle
is usually smaller than the right ventricle. Also, comparison of the
width of the aorta, ductus arteriosus and coarctation shelf in color
doppler studies may suggest that the defect will require an intervention
after birth (10). TTTS is associated with an increased prevalence of
congenital heart diseases (CHDs). In MC pregnancies with TTTS, the risk
of at least one of the infants with CHD is threefold compared to
uncomplicated MC twin pregnancies (11). The development of acquired CHDs
in MC twins is associated with TTTS, indicating an influence of
hemodynamic alterations on cardiac development. MC twins with TTTS are
associated with increased risk of ventricular septal defect (VSD),
RVOTO, atrial septal defect (ASD), CoA, and aortic stenosis (AS). Some
of them are uncommon, such as CoA and AS (8). There are reports of a
small number of CoA in recipient and donor twins in TTTS. After birth,
due to ductal closure, a variety of hemodynamic changes may occur
according to the severity of obstruction and critical coarctation
increases the risk of heart failure and death in infants when the ductus
arteriosus closes. So, prenatal diagnosis is important to reduce
postnatal complications. After birth, prostaglandins type 1 is necessary
to avoid closure of ductus arteriosus and definite treatment is
end-to-end anastomosis, but transcatheter treatment is also an accepted
alternative with comparable results (9). Balloon angioplasty is an
acceptable technique, similar to what was done in our case. It is a safe
procedure in infants between one and six months of age and also in
critically ill patients regardless of age (12). The best time for CoA
correction is in infancy or childhood in order to prevent persistence or
late recurrence of systemic hypertension (13).

\textbf{Conclusion}

It is necessary to pay attention to cardiac abnormalities in MC twins,
especially in cases with TTTS, and follow up even if they are treated
with FLP during pregnancy and after birth to best treatment.

\textbf{Author Contributions}

Author 1: Responsible for patient treatment

Author 2: Responsible for patient treatment

Author 3: Coordinating various stage of manuscript preparation between
authors

Author 4: Writing the manuscript and draft review

Author 5: Writing the manuscript and draft review

Author 6: Writing the manuscript and draft review

Author 7: Writing the manuscript and draft review

Author 8: Writing the manuscript and draft review

\textbf{References:}

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Australian and New Zealand twin-twin transfusion syndrome registry.
American journal of obstetrics and gynecology. 2000;182(3):706-12.

2. Gembruch U, Bald R, Fahnenstich H, Arabin B, Hansmann M.
Echocardiographic function in cases of twin-twin transfusion syndrome.
Ultrasound Obstet Gynecol. 1994;4:S183.

3. Simpson LL, Marx GR, Elkadry EA, D'alton ME. Cardiac dysfunction in
twin--twin transfusion syndrome: a prospective, longitudinal study.
Obstetrics \& Gynecology. 1998;92(4):557-62.

4. Villa L, Nava S, Mosca F, Nicolini U. Fetal and neonatal
echocardiographic findings in twin-twin transfusion syndrome. American
journal of obstetrics and gynecology. 1998;179(4):1056-62.

5. Zosmer N, Bajoria R, Weiner E, Rigby M, Vaughan J, Fisk NM. Clinical
and echographic features of in utero cardiac dysfunction in the
recipient twin in twin-twin transfusion syndrome. Heart.
1994;72(1):74-9.

6. Van Den Boom J, Battin M, Hornung T. Twin--twin transfusion syndrome,
coarctation of the aorta and hypoplastic aortic arch: a case series
report. Journal of Paediatrics and Child Health. 2010;46(3):76-9.

7. Herberg U, Gross W, Bartmann P, Banek CS, Hecher K, Breuer J. Long
term cardiac follow up of severe twin to twin transfusion syndrome after
intrauterine laser coagulation. Heart. 2006;92(1):95-100.

8. Michelfelder E, Tan X, Cnota J, Divanovic A, Statile C, Lim FY, et
al. Prevalence, spectrum, and outcome of right ventricular outflow tract
abnormalities in twin--twin transfusion syndrome: a large, single-center
experience. Congenital Heart Disease. 2015;10(3):209-18.

9. Buyens A, Gyselaers W, Coumans A, Al Nasiry S, Willekes C, Boshoff D,
et al. Difficult prenatal diagnosis: fetal coarctation. Facts, views \&
vision in ObGyn. 2012;4(4):230.

10. Ropacka-Lesiak M, Kowalska-Jasiecka J, Kowalska K, Lech J, Malewski
W, Br\selectlanguage{polish}ę\selectlanguage{english}borowicz GH. Aortic coarctation in the recipient in
TTTS--diagnostic problems--a case report. Ginekologia Polska.
2012;83(7).

11. Pettit K, Merchant M, Machin G, Tacy T, Norton M. Congenital heart
defects in a large, unselected cohort of monochorionic twins. Journal of
Perinatology. 2013;33(6):457-61.

12. Feltes TF, Bacha E, Beekman III RH, Cheatham JP, Feinstein JA, Gomes
AS, et al. Indications for cardiac catheterization and intervention in
pediatric cardiac disease: a scientific statement from the American
Heart Association. Circulation. 2011;123(22):2607-52.

13. Seirafi PA, Warner KG, Geggel RL, Payne DD, Cleveland RJ. Repair of
coarctation of the aorta during infancy minimizes the risk of late
hypertension. The Annals of thoracic surgery. 1998;66(4):1378-82.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1.} Sagittal view shows retrograde (reversal) flow in
descending aorta (DAO), indicating severe coarctation of aorta (COA).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

\textbf{Figure 2.} Suprasternal view of transthoracic echocardiography
shows severe narrowing of proximal portion of aorta (coarctation) with
flow acceleration after birth.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

\textbf{Figure 3.} Doppler spectral in the location of coarctation shows
a typical saw tooth appearance.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

\textbf{Figure 4.} Apical four chamber view shows left ventricular
hypertrophy (LVH), significant left ventricular enlargement (LVE), and
left atrial enlargement (LAE).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

\textbf{Figure 5.} Angiographic coronal view of aorta shows significant
narrowing of location of coarctation with post stenotic dilation.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}

\textbf{Figure 6.} Balloon inflation of aorta in stenotic location shows
a full dilation of narrowing.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image7/image7}

\end{center}
\end{figure}

\textbf{Figure 7.} Contrast injection in angiography shows significant
reduction of stenosis in the location of aorta.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image8/image8}

\end{center}
\end{figure}

\textbf{Figure 8.} Comparison of stenotic portion of aorta before and
after balloon angioplasty.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image9/image9}

\end{center}
\end{figure}

\textbf{Figure 9.} Transthoracic echocardiography after balloon
angioplasty in a suprasternal view shows significant reduction of
stenosis in aorta.\selectlanguage{english}
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