Case of the Week #573

Frantisek Grochal, Cerine Jeanty
Femicare, Center of prenatal ultrasonographic diagnostics, Martin, Slovakia; St Mary's Medical Center, San Francisco, CA, USA

Posting Dates: Jan 1, 2023 - Jan 14, 2023

A 31-year-old G2P1 presented to our office at 28 weeks, 5 days due to fetal cardiac enlargement.  Her 8-year-old son was monitored due to a “large heart” after delivery, but the finding resolved and he is doing well. During the pregnancy, serologic testing for Toxoplasmosis was negative. Additionally, the mother was infected with COVID at 10 weeks gestation without any complications.

Ultrasonographic examination at 20 weeks was reported to be normal without any cardiac anomalies. However, due to the family history of transient cardiac enlargement in her first child, the patient was sent to the National Institute for Cardiovascular Diseases in the Slovak Republic at 25 weeks gestation where fetal cardiomegaly and possible ventricular septal defect were found.

At 28 weeks, 5 days the patient visited our office, and our examination revealed following findings:

Drawing - Four-chamber view of the heart
Image 1 Drawing - Four-chamber view of the heart © 2022 Frantisek Grochal
Four-chamber view of the heart (RV-right ventricle; LV-left ventricle; RA-right atrium; LA-left atrium)
Image 2 Four-chamber view of the heart (RV-right ventricle; LV-left ventricle; RA-right atrium; LA-left atrium) © 2022 Frantisek Grochal
Color flow mapping demonstrating blood flow entering the ventricles in diastole
Image 3 Color flow mapping demonstrating blood flow entering the ventricles in diastole © 2022 Frantisek Grochal
Color flow mapping demonstrating blood flow entering the ventricles in diastole (RV-right ventricle; LV-left ventricle)
Image 4 Color flow mapping demonstrating blood flow entering the ventricles in diastole (RV-right ventricle; LV-left ventricle) © 2022 Frantisek Grochal
Four-chamber view of the heart (RV-right ventricle; LV-left ventricle)
Image 5 Four-chamber view of the heart (RV-right ventricle; LV-left ventricle) © 2022 Frantisek Grochal
Four-chamber view of the heart (RV-right ventricle; LV-left ventricle; R-right; L-left)
Image 6 Four-chamber view of the heart (RV-right ventricle; LV-left ventricle; R-right; L-left) © 2022 Frantisek Grochal
Four-chamber view of the heart
Image 7 Four-chamber view of the heart © 2022 Frantisek Grochal
Four-chamber view of the heart (RV-right ventricle; LV-left ventricle)
Image 8 Four-chamber view of the heart (RV-right ventricle; LV-left ventricle) © 2022 Frantisek Grochal
Video 1 Four-chamber view of the heart (R-right; L-left) © 2022 Frantisek Grochal
Video 2 Four-chamber view of the heart © 2022 Frantisek Grochal
Video 3 Four-chamber view of the heart © 2022 Frantisek Grochal

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Answer

We present a case of dissecting aneurysm of the interventricular septum.

The baby was born at 34 weeks, 6 days by cesarean section due to polyhydramnios and worsening flow parameters in the umbilical arteries and middle cerebral artery. While there was suspicion of fetal anemia, this was not confirmed after delivery. A female infant (birth weight 2390g, length 45 cm, Apgar 4/7) was born hypotonic, apneic, bradycardic, and required nasal continuous positive airway pressure ventilation.  The baby was admitted to the cardiac neonatal intensive care unit due to cardiomegaly and hemodynamic decompensation.

Postnatal sonography revealed dilated cardiomyopathy with abnormal septum and defective septal myocardium. The septum was not contracting and bulged to both the right and left sides during the cardiac cycle, with predominant compression of the left ventricle. ECG showed first degree atrioventricular block, and right bundle branch block.

A couple of days later, the echocardiographic appearance of the heart had changed, and was described as concentric hypertrophic cardiomyopathy affecting both ventricles without left outflow tract obstruction. There was systolic dysfunction of the right ventricle and mild systolic dysfunction of the left ventricle (Image 1). Metabolic tests were normal. A genetic study evaluating 128 genes relevant to cardiomyopathies did not find any anomalies.

Ten months later, ultrasonographic examinations showed normal function of both ventricles (Image 2). At the time of this publication, the baby is 14 months old and is doing well. The cardiac finding has improved, and the heart has nearly a normal appearance.

Postnatal image of the heart obtained a couple of days after delivery showing concentric cardiomyopathy.
Image 1 Postnatal image of the heart obtained a couple of days after delivery showing concentric cardiomyopathy. © 2022 Monika Kaldararova, The National Institute for Cardiovascular Diseases, Slovak Republic
Postnatal image of the heart obtained 10 months after delivery showing enlarged heart but with normal appearance of the ventricular and septal musculature.
Image 2 Postnatal image of the heart obtained 10 months after delivery showing enlarged heart but with normal appearance of the ventricular and septal musculature. © 2022 Monika Kaldararova, The National Institute for Cardiovascular Diseases, Slovak Republic

The ultrasound findings are demonstrated in the following images, videos and figures.

Images 3-5 and Video 1, 2 show a four-chamber view of the heart. The heart is enlarged with dilated ventricles, predominantly affecting the right side. The interventricular septum (IVS) of the heart has an abnormal appearance with a central cavity and separation of the left and right walls. A defect can be seen in the right wall close to the apex. During the cardiac cycle, blood flows in and out of the abnormal interventricular septal cavity through the defect in the right wall (depicted by white curved arrows in Images 3-5). Blood flowing into the septum dissects its walls, and the left wall of the septum bulges into the left ventricle, obstructing the outflow tract. These structural changes are responsible for worsening cardiac function with diminished ejection fraction and dilated cardiomyopathy.

Color Doppler four-chamber view of the heart showing blood flow (red) out of the dissected cavity within the interventricular septum (curved arrow). (RV–right ventricle; LV–left ventricle)
Image 3 Color Doppler four-chamber view of the heart showing blood flow (red) out of the dissected cavity within the interventricular septum (curved arrow). (RV–right ventricle; LV–left ventricle) © 2022 Frantisek Grochal
Color Doppler four-chamber view of the heart showing blood flow (blue) entering the cavity within the interventricular septum (curved arrow). (RV–right ventricle; LV–left ventricle)
Image 4 Color Doppler four-chamber view of the heart showing blood flow (blue) entering the cavity within the interventricular septum (curved arrow). (RV–right ventricle; LV–left ventricle) © 2022 Frantisek Grochal
Four-chamber view showing an abnormal interventricular septum with separated left and right walls and central cavitation. A defect can be seen in its right wall (curved arrow) which enables the blood to enter and dissect the interventricular septum.
Image 5 Four-chamber view showing an abnormal interventricular septum with separated left and right walls and central cavitation. A defect can be seen in its right wall (curved arrow) which enables the blood to enter and dissect the interventricular septum. © 2022 Frantisek Grochal
Video 1 Color Doppler four-chamber view of the heart demonstrating blood flow in and out of the dissected cavity within the interventricular septum. (R-right; L–left) © 2022 Frantisek Grochal
Video 2 Color Doppler four-chamber view of the heart demonstrating blood flow in and out of the dissected cavity within the interventricular septum. (R-right; L–left) © 2022 Frantisek Grochal

Drawing - four-chamber view of the heart with dissecting aneurysm of the interventricular septum. RV – right ventricle, LV – left ventricle, IVS – interventricular septum, RA – right atrium, LA – left atrium, Ao – aorta.
Image 6 Drawing - four-chamber view of the heart with dissecting aneurysm of the interventricular septum. RV – right ventricle, LV – left ventricle, IVS – interventricular septum, RA – right atrium, LA – left atrium, Ao – aorta. © 2022 Frantisek Grochal
 As blood accumulates in the interventricular septum, the left septal wall bulges into the left ventricular cavity. (RV–right ventricle; LV–left ventricle; IVS–interventricular septum; RA–right atrium; LA–left atrium; Ao–aorta)
Image 7 As blood accumulates in the interventricular septum, the left septal wall bulges into the left ventricular cavity. (RV–right ventricle; LV–left ventricle; IVS–interventricular septum; RA–right atrium; LA–left atrium; Ao–aorta) © 2022 Frantisek Grochal

Image 6 caption: Diagram demonstrating the dissecting aneurysm of the interventricular septum seen in our case. There is a defect in the right wall of the septum which allows blood flow into the interventricular septum. (RV–right ventricle; LV–left ventricle; IVS–interventricular septum; RA–right atrium; LA–left atrium; Ao–aorta)

Discussion

Congenital ventricular aneurysms are broad-based bulges in the ventricular wall with noncontractile, or dyskinetic myocardium [1]. While in the postnatal period, a ventricular aneurysm can be acquired as a complication of surgical procedures [2], trauma [3], Kawasaki disease [4], infection [4], or following a myocardial infarction [6], congenital aneurysms have no clear causative factor.  In contrast, a congenital ventricular diverticulum is a fingerlike pouch with a narrow connection to the ventricle that contains epicardium, myocardium, and endocardium on histology, and contracts either normally or near normally [1]. On prenatal imaging, it can be difficult to distinguish between ventricular aneurysms and diverticula [1]. Given their rarity, the prevalence of ventricular diverticula and aneurysms is difficult to estimate. A study reviewing 12,924 consecutive autopsies in children found 750 cases with congenital cardiac defects and only 3 cases of ventricular diverticula (23 in 100,000 cases) [7]. A more recent publication in 12,271 consecutive adult patients undergoing coronary angiography demonstrated a prevalence of 76 in 10,000 cases of congenital left ventricular aneurysm and diverticula [8]. The etiology of congenital ventricular aneurysms is not known, though may be related to prenatal ischemia leading to aneurysm formation [9], connective tissue disorders in patients with Ehlers-Danlos syndrome [10], or a genetic defect in mesenchymal cell migration in patients with familial occurrence [11,12].

Congenital ventricular aneurysms are more commonly located in the apex and anterolateral wall of the ventricle [8], and are rarely found in the interventricular septum. In ventricular septal aneurysms, the abnormal tissue can involve the membranous or muscular portion of the septum [13]. In cases involving the membranous portion of the ventricular septum, aneurysms may represent a mechanism for spontaneous closure of ventricular septal defects [14].

Congenital aneurysms of the muscular intraventricular septum are extremely rare. There have been 22 cases reported in the literature (Table 1) [11,13,15-29], 10 of which were diagnosed prenatally. Approximately 75% (16) of cases had associated cardiac anomalies, most commonly ventricular septal defect (7) located either in the perimembranous septum or in the aneurysm, atrial septal defect (5), and right heart lesions (5) such as pulmonary atresia with tricuspid valve stenosis and right ventricular aneurysm. Patients rarely presented with extracardiac anomalies. While 55% (12) of patients were asymptomatic, rhythm disturbances such as first-degree atrioventricular block, right bundle branch block, and Wolf-Parkinson-White occurred in 18% (4), and symptoms of congestive heart failure occurred in another 18% (4). Seven cases were treated surgically, though only 3 cases required plication or resection of the aneurysm, and the remainder underwent surgical treatment of concomitant cardiac structural defects. Survival was approximately 90% with one termination of pregnancy and one death. Follow up extended anywhere between 3 months and 12 years.

In patients with congenital muscular interventricular septal defect, there have been several familial cases, suggesting an autosomal dominant inheritance with variable expressivity [11,27,28]. Of the 22 cases reported in the literature, 32% (7) mentioned a family history of heart disease. Development of a muscular interventricular septal defect may be a result of a genetic mutation in mesenchymal cell migration from the atrioventricular and conotruncal regions to the cephalic portion of the developing interventricular septum [11,12]. Alternatively, a muscular septal aneurysm may be a result of ischemia or embolism [22]. In our literature review, 13 cases documented the coronary artery anatomy, 9 of which were normal, 3 showed right ventricular sinusoids associated with pulmonary atresia, and one showed abnormal circumflex artery distribution.

Table 1Literature review of pediatric cases with muscular interventricular septal aneurysm.
Study
Prenatal DX
Age
Symptoms
Cardiac findings
Cardiac rhythm
Coronary circulation
Associated anomalies
treatment
Family history
Survived
Abbreviations: ASD: atrial septal defect;  AV: atrioventricular;  Dx: diagnosis;  LCA: left coronary artery;  LBBB: left bundle branch block;  NA: not available;  NSR: normal sinus rhythm;  m: months;  PA: pulmonary atresia; PDA: patient ductus arteriosus;  RBBB: right bundle branch block;  RV: right ventricle;  SOB: shortness of breath;  TOP: termination of pregnancy;  VSD: ventricular septal defect;  VT: ventricular tachycardia;  w GA: weeks gestational age;  y: years
Baspinar 2005
no
5m
none
ASD
Wolf-Parkinson-White
normal
no
none
no
yes
Chen 1991
no
4y
none
none
NSR
NA
no
none
yes
yes
Edelstein 1965
no
8y
none
VSD
incomplete RBBB
NA
no
none
NA
yes
Eriksson 1998
no
7y
none
ASD
NSR
normal
no
none
yes
yes
Eriksson 1998
no
5y
none
none
NSR
normal
no
none
yes
yes
Fasoli 1988
no
15y
exertional dyspnea
ASD, mitral valve cleft
VT
normal
no
surgery- ASD
NA
yes
Magherini 1988
no
10y
none
VSD
abnormal R wave progression, ST-T changes consistent with septal MI
normal
no
none
NA
yes
Mohan 1992
no
18y
none
VSD
NSR
NA
no
none
NA
yes
Nguyen 2008
no
neonate
NA
pulmonary atresia,  tricuspid stenosis,  VSD
NA
single LCA, multiple RV sinusoids
NA
surgery-PA, aneurysm plication
NA
yes
Nguyen 2022
no
18m
none
none
1st degree AV block, RBBB
normal
no
none
no
yes
Prabhakar 1993
no
1y
SOB with feeding
VSD
NSR
normal
no
surgery-aneurysm resection
NA
yes
Wong 2007
no
neonate
poor feeding
PDA
LBBB, RBBB
NA
chromosome 20
none
NA
yes
Carr 2008
yes
19w GA
diaphoresis with feeding
none
NSR
normal
no
cardiac transplant
no
yes
Donofrio 2002
yes
26w GA
none
ASD
nonspecific ST segment and T wave abnormality
abnormal circumflex artery distribution
no
medical
yes
yes
Fujiwara 2001
yes
26w GA
none
none
NSR
NA
no
none
yes
yes
Fujiwara 2001
yes
28w GA
none
ASD, VSD
NSR
NA
no
none
yes
yes
Ivanitskaya 2017
yes
22w GA
NA
hypoplastic aortic arch, VSD
NA
NA
hydrocephaly
NA
no
TOP
Nguyen 2008
yes
28w GA
NA
pulmonary atresia,  tricuspid stenosis, cleft mitral valve
NA
multiple RV sinusoids
NA
surgery-PA
NA
yes
Nguyen 2008
yes
23w GA
NA
pulmonary atresia,  tricuspid stenosis,
NA
multiple RV sinusoids
NA
surgery-PA
NA
yes
Nguyen 2008
yes
28w GA
NA
absent pulmonary valve,  tricuspid stenosis, PDA
NA
NA
NA
none
NA
no
Nicholae 2007
yes
NA
cyanosis
none
NA
normal
no
surgery-aneurysm resection
yes
yes
Ozkavukcu 2018
yes
22w GA
none
RV aneurysm
no arrythmias
NA
no
none
NA
yes

Our case more specifically represents a dissecting aneurysm of the interventricular septum. There are several reports in adults with a prevalence of 1.6 to 19.5 in 100,000 cases [30, 31]. While acquired lesions are a result of myocardial infarction, cardiac surgery, or endocarditis [30], an aneurysm of the sinus of Valsalva is a common etiology of an interventricular septal dissection [30, 31]. The mechanism is thought to be a result of compression of the coronary artery by the aneurysm of the coronary sinus of Valsalva leading to ventricular septal ischemia [32]. In cases with dissecting interventricular aneurysm, approximately 90% had an aneurysm that originated in the right coronary sinus of Valsalva [33].

This is the first case of dissecting aneurysm of the interventricular septum identified prenatally. Six cases have been reported in children, five of which were in adolescents [33-38]. These all originated from a right sinus of Valsalva aneurysm except for one in which there was no communication found between the dissecting interventricular aneurysm and the sinus of Valsalva (38). Similarly, two cases documented by Wu et al had normal sinuses of Valsalva, suggesting there may be other causes of this condition [31]. In our case, we hypothesize that a partial rupture of the interventricular aneurysm may lead to bleeding into the interventricular septum with dissection of the interstitium. The diagonal course of the defect through the interventricular septum may be a predisposing factor for the dissection (Image 8-9, Video 3-4).

4-chamber-view showing diagonal defect within the interventricular septum which makes kind of “dissection” of its walls. LA - left atrium, LV - left ventricle, RA - right atrium, RV - right ventricle, IVS – interventricular septum.
Image 8 4-chamber-view showing diagonal defect within the interventricular septum which makes kind of “dissection” of its walls. LA - left atrium, LV - left ventricle, RA - right atrium, RV - right ventricle, IVS – interventricular septum. © 2022 Frantisek Grochal
4-chamber-view showing diagonal defect within the interventricular septum which makes kind of “dissection” of its walls. LA - left atrium, LV - left ventricle, RA - right atrium, RV - right ventricle, IVS – interventricular septum.
Image 9 4-chamber-view showing diagonal defect within the interventricular septum which makes kind of “dissection” of its walls. LA - left atrium, LV - left ventricle, RA - right atrium, RV - right ventricle, IVS – interventricular septum. © 2022 Frantisek Grochal
Video 3 4-chamber-view showing diagonal defect within the interventricular septum which makes kind of “dissection” of its walls. LA - left atrium, LV - left ventricle, RA - right atrium, RV - right ventricle, IVS – interventricular septum. © 2022 Frantisek Grochal
Video 4 4-chamber-view showing diagonal defect within the interventricular septum which makes kind of “dissection” of its walls. LA - left atrium, LV - left ventricle, RA - right atrium, RV - right ventricle, IVS – interventricular septum. © 2022 Frantisek Grochal

While adult and adolescent patients with interventricular septal dissection may have significant anatomic and hemodynamic derangements leading to arrhythmias or congestive heart failure and necessitating surgery [30, 31, 33-37], there is no data to understand the natural history in fetal and neonatal life. Aneurysms of the membranous portion of the ventricular septum can be associated with complications such as cerebral infarction secondary to embolism [39], and right ventricular outflow obstruction [40]. In our literature review, muscular aneurysms can lead to conduction abnormalities [15, 17, 22, 24], and congestive heart failure [18, 23, 25, 28], though several cases documented improvement of the interventricular septal findings on serial echocardiography likely due to ventricular remodeling [22, 24, 29]. This was the case in our patient with a favorable outcome of the pregnancy and delivery, and gradual improvement of the cardiac findings. Due to lack of data, counselling patients can be a challenge, though lack of cardiac failure, such as fetal hydrops, or pericardial effusion could be a favorable predictive sign.

References

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