Premature closure of the foramen ovale and hypoplasia of the left heart

Schall, Stewart A.; Dalldorf, Frederic G.

doi:10.1016/0167-5273(84)90068-8

Cited by 20 publications

(7 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A case report of an infant with late FO closure due to a aneurysmatic changes of the intra-atrial septum and mild LV hypoplasia (despite a small VSD) seems to further support this notion 24 . Schall et al speculated that his observed phenotype 8 , which is mimicked by our experiments here, represents the "missing link" between the majority of reported cases with early FO closure and significant deformities of the left heart, and the few cases with late antenatal FO closure as reported by Naeye et al…”

Section: Discussionsupporting

confidence: 78%

“…The findings imply a combination of LV hypoplasia and RV hypertrophy. This phenotype bears a striking resemblance to a report in human babies born with closed FO, hypoplasia of LV, reduced mitral and aortic valve area as well as RV hypertrophy and dilatation 8 . At the cellular level, the significantly lower LV-to-RV ratio of cardiomyocytes and reduced LV cardiomyocytes per biventricular weight in the fetuses with occluded FO also suggested LV hypoplasia with reduced cardiomyocyte proliferation.…”

Section: Discussionsupporting

confidence: 78%

“…Premature closure or restriction of the FO, eliminating or restricting the fetal right to left atrial shunt, has been described to have variable consequences, probably depending on the timing and the presence or absence of accompanying cardiac malformations. Several authors have reported RV to LV growth discrepancy and mild to moderate hypoplasia of the mitral and aortic valves as well as the aortic arch 7,8 , others described LV dilatation and fibro-elastosis 9 . While RV dilation, tricuspid regurgitation, pericardial effusion, pleural effusion, in-utero heart failure and hydrops fetalis as well as early and late pulmonary hypertension have also been reported [10][11][12][13][14] , there is substantial evidence that early (primary) closure of the FO results in hypoplasia of left heart structures and that normal fetal left heart development is dependent on a normal volume of flow though the FO 9,15 .…”

mentioning

confidence: 99%

See 2 more Smart Citations

Induction of left ventricular hypoplasia by occluding the foramen ovale in the fetal lamb

Wong

Veldman

Sasi

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Disturbed fetal haemodynamics often affects cardiac development and leads to congenital cardiac defects. Reduced left ventricular (LV) preload in the fetus may result in hypoplastic LV, mitral and aortic valve, mimicking a moderate form of hypoplastic left heart complex. We aimed to induce LV hypoplasia by occluding the foramen ovale (FO) to reduce LV preload in the fetal sheep heart, using percutaneous trans-hepatic catheterisation. Under maternal anaesthesia and ultrasound guidance, hepatic venous puncture was performed in six fetal lambs (0.7-0.75 gestation). A coronary guidewire was advanced into the fetal inferior vena cava, right and left atrium. A self-expandable stent was positioned across the FO. An Amplatzer Duct Occluder was anchored within the stent for FO occlusion. Euthanasia and postmortem examination was performed after 3 weeks. Nine fetuses were used as age-matched controls. Morphometric measurements and cardiac histopathology were performed. Compared with controls, fetal hearts with occluded FO had smaller LV chamber, smaller mitral and aortic valves, lower LV-to-RV ratio in ventricular weight and wall volume, and lower number of LV cardiomyocyte nuclei. We conclude that fetal fo occlusion leads to a phenotype simulating LV hypoplasia. this large animal model may be useful for understanding and devising therapies for LV hypoplasia.

show abstract

Section: Discussionsupporting

confidence: 78%

Section: Discussionsupporting

confidence: 78%

mentioning

confidence: 99%

See 1 more Smart Citation

Induction of left ventricular hypoplasia by occluding the foramen ovale in the fetal lamb

Wong

Veldman

Sasi

et al. 2020

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Gene targeting of dHAND abolished right ventricular development. On the other hand, premature closure of the foramen ovale is thought to reduce the inflow to the left ventricle causing hypoplastic left heart syndrome (Harh et al, 1973;Schall and Dalldorf, 1984).…”

Section: Av Cushion and Ventricular Chamber Developmentmentioning

confidence: 99%

Anomalous looping, atrioventricular cushion dysplasia, and unilateral ventricular hypoplasia in the mouse embryos with right isomerism induced by retinoic acid

Yasui¹,

Morishima

Nakazawa

et al. 1998

Anat. Rec.

View full text Add to dashboard Cite

An anomalous relation between the atrioventricular cushions and the interventricular septum appeared to have caused a restrictive inflow to the unilateral ventricle, leading to ventricular chamber hypoplasia on the ipsilateral side. Thus, we clarified that retinoic-acid treatment at the primitive streak stage disturbed cardiac looping and formation of atrioventricular cushion development, which secondarily influenced ventricular chamber development.

show abstract

“…This congenital heart disease can result in a wide spectrum of hemodynamic findings. If FO closes during early gestation, hypoplasia of the left ventricle (LV) occurs, and if it closes during late gestation, right heart failure may occur [2][3][4]. 6q duplication syndrome is a rare chromosomal abnormality that is associated with congenital heart disease [5], but no reports on patients with this chromosomal abnormality and premature closure of FO are available.…”

Section: Introductionmentioning

confidence: 99%

Unique Hemodynamics in a Case of Premature Closure of Foramen Ovale with 6q Duplication Syndrome

Yokoo¹,

Marumo²,

Nishida³

et al. 2017

Health Edu Care

View full text Add to dashboard Cite

Premature closure of the foramen ovale (FO) is a rare congenital anomaly that results in a wide spectrum of hemodynamic findings. We experienced the case of a male neonate with this condition who, at birth, showed unique hemodynamics that was similar to that in hypoplastic left heart syndrome, despite having a normal sized left ventricle (LV). His systemic blood flow was dependent on patent ductus arteriosus (DA). Echocardiography on day 0 revealed retrograde flow in the ascending aorta. We could not detect flow across the interatrial septum, and diagnosed premature closure of FO. Because his LV was not hypoplastic, we considered that the systemic blood flow would be maintained by LV output after lung circulation was established. We infused prostaglandin E1 incorporated in lipid microspheres (lipo-PGE 1 ), which confirmed the retrograde flow in the ascending aorta. We stopped the lipo-PGE 1 infusion after the flow in the ascending aorta became antegrade on day 2. After DA closed, systemic blood flow was maintained by LV output, and normal circulation was established. In addition to the congenital heart anomaly, several other anomalies were noted, including a downslanting of the palpebral fissure, micrognathia, and cryptorchidism. A cytogenetic analysis revealed der(20)t(6;20) (q25.2;p13), and 6q duplication syndrome was diagnosed. The patient was discharged without any medications on day 54 despite the presence of mild pulmonary hypertension. This is probably the first report of premature closure of FO in a patient with such hemodynamics and the first one of premature closure of FO associated with 6q duplication syndrome.

show abstract

Premature closure of the foramen ovale and hypoplasia of the left heart

Cited by 20 publications

References 3 publications

Induction of left ventricular hypoplasia by occluding the foramen ovale in the fetal lamb

Induction of left ventricular hypoplasia by occluding the foramen ovale in the fetal lamb

Anomalous looping, atrioventricular cushion dysplasia, and unilateral ventricular hypoplasia in the mouse embryos with right isomerism induced by retinoic acid

Unique Hemodynamics in a Case of Premature Closure of Foramen Ovale with 6q Duplication Syndrome

Contact Info

Product

Resources

About