Congenital tricuspid regurgitation: review and a proposed new classification

Gupta, Anubhav; Grover, Vijay; Gupta, Vijay

doi:10.1017/s104795111000168x

Cited by 12 publications

(9 citation statements)

References 39 publications

(143 reference statements)

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“…Severe AV valve regurgitation, cardiac dysfunction and increases in atrial size were observed in NOS3 −/− mice. These phenotypes highly resemble congenital AV valve insufficiency, a clinical condition with infants born with shortened or a complete lack of AV valves [26], [27]. Mitral valve insufficiency is often associated with other cardiac defects such as atrial septal defects (ASD), ventricular septal defects (VSD), aortic valve insufficiency and tricuspid valve insufficiency [28].…”

Section: Discussionmentioning

confidence: 99%

“…Mitral valve insufficiency is often associated with other cardiac defects such as atrial septal defects (ASD), ventricular septal defects (VSD), aortic valve insufficiency and tricuspid valve insufficiency [28]. Tricuspid valve insufficiency, also known as tricuspid valve regurgitation, is also associated with congenital cardiac defects such as VSD and mitral valve regurgitation [26]. These accompanying cardiac defects are very similar to phenotypes seen in the NOS3 −/− mice providing an excellent animal model to study AV insufficiency [18], [19].…”

Section: Discussionmentioning

confidence: 99%

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Nitric Oxide Synthase-3 Promotes Embryonic Development of Atrioventricular Valves

Yin

Xiang

et al. 2013

PLoS ONE

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Nitric oxide synthase-3 (NOS3) has recently been shown to promote endothelial-to-mesenchymal transition (EndMT) in the developing atrioventricular (AV) canal. The present study was aimed to investigate the role of NOS3 in embryonic development of AV valves. We hypothesized that NOS3 promotes embryonic development of AV valves via EndMT. To test this hypothesis, morphological and functional analysis of AV valves were performed in wild-type (WT) and NOS3−/− mice at postnatal day 0. Our data show that the overall size and length of mitral and tricuspid valves were decreased in NOS3−/− compared with WT mice. Echocardiographic assessment showed significant regurgitation of mitral and tricuspid valves during systole in NOS3−/− mice. These phenotypes were all rescued by cardiac specific NOS3 overexpression. To assess EndMT, immunostaining of Snail1 was performed in the embryonic heart. Both total mesenchymal and Snail1+ cells in the AV cushion were decreased in NOS3−/− compared with WT mice at E10.5 and E12.5, which was completely restored by cardiac specific NOS3 overexpression. In cultured embryonic hearts, NOS3 promoted transforming growth factor (TGFβ), bone morphogenetic protein (BMP2) and Snail1expression through cGMP. Furthermore, mesenchymal cell formation and migration from cultured AV cushion explants were decreased in the NOS3−/− compared with WT mice. We conclude that NOS3 promotes AV valve formation during embryonic heart development and deficiency in NOS3 results in AV valve insufficiency.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Synthase-3 Promotes Embryonic Development of Atrioventricular Valves

Yin

Xiang

et al. 2013

PLoS ONE

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“…Congenital tricuspid regurgitation, except in Ebstein's anomaly, is uncommon and may be classified as being due to cuspal anomaly, chordal anomaly, commissural deficiency or annular dilatation, a combination of the above or double orifice valve [8]. Among these morphological abnormalities of the tricuspid valve, there are two reported cases of the absent anterior tricuspid leaflet [9,10] and one case of the absent posterior tricuspid leaflet [1].…”

Section: Discussionmentioning

confidence: 99%

Absence of posterior tricuspid valve leaflet and valve reconstruction

Komoda¹,

Stamm²,

Fleck³

et al. 2012

Interactive CardioVascular and Thoracic Surgery

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We report a rare case of the absence of a posterior tricuspid valve leaflet. A male patient, aged 46, suffering from severe tricuspid valve regurgitation (TR) of unknown aetiology and atrial septal aneurysm was referred to our hospital for surgery. On surgical inspection, the posterior tricuspid valve leaflet and its subvalvular apparatus were completely absent and only the valve annulus was seen in the corresponding position. The anterior and septal leaflets were normal. We successfully reconstructed the tricuspid valve as follows: the head of an anterior papillary muscle was approximated to the ventricular septum (Sebening stitch). After the approximation of the centre of the tricuspid annulus of the anterior leaflet to the tricuspid annulus on the opposite side, a sizer of 29 mm in diameter was easily passed through the anterior orifice. The posterior orifice was closed with running sutures (posterior annulorrhaphy after Hetzer). Before these procedures, we attempted to reconstruct the tricuspid valve with a posterior annulorrhaphy alone; however, valve competence was insufficient. A Sebening stitch was necessary to improve the valve competence. Echocardiography showed TR grade 1 at the patient's discharge from hospital and TR grade 1 to 2 at the follow-up, 10 months after the operation.

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“…Grade I represents myxoid changes of the leaflets and chordae tendineae; grade II represents thickened and often retracted leaflets, and grade III represents extreme dysplasia of the leaflets (Formigari et al, 1993). More recently, a novel grading system that could guide surgical management, has been published (Gupta et al, 2011).…”

Section: Pathophysiology Of Tricuspid Valve Dysplasiamentioning

confidence: 99%

Tricuspidalisdysplasie bij de hond

Favril¹,

Broeckx²,

Rooster³

et al. 2018

Vlaams Diergeneeskundig Tijdschrift

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A general overview of tricuspid valve dysplasia in dogs is presented in this review. This congenital disease has been described in numerous large dog breeds but especially the Labrador retriever is predisposed. The condition is relatively uncommon, with a prevalence of approximately seven percent of all congenital heart diseases in dogs. The asymptomatic phase may last for several years and depends on the severity of the valve malformation. In the clinical phase, exercise intolerance, fatigue, anorexia, cardiac cachexia, dyspnea and signs of right-sided congestive heart failure can be present. Echocardiography including Doppler imaging is warranted to confirm the diagnosis. Curative treatment involves surgical valve replacement but is technically challenging and still in its experimental phase in dogs. As such, treatment in dogs involves the administration of supportive medication once the dogs develop symptoms of congestive heart failure and consists of diuretics, ace-inhibitors and positive inotropic drugs.

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Congenital tricuspid regurgitation: review and a proposed new classification

Cited by 12 publications

References 39 publications

Nitric Oxide Synthase-3 Promotes Embryonic Development of Atrioventricular Valves

Nitric Oxide Synthase-3 Promotes Embryonic Development of Atrioventricular Valves

Absence of posterior tricuspid valve leaflet and valve reconstruction

Tricuspidalisdysplasie bij de hond

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