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NÃO RARA NA EUROPA: Defeito do septo ventricular
ORPHA:1480CID-10 · Q21.0DOENÇA RARA

Presença de defeito (abertura) no septo que separa os dois ventrículos do coração. Pode ser congênito ou adquirido.

Mantido por Agente Raras·Colaborar como especialista →

Introdução

O que você precisa saber de cara

📋

Presença de defeito (abertura) no septo que separa os dois ventrículos do coração. Pode ser congênito ou adquirido.

Publicações científicas
1 artigos
Último publicado: 2014 Jan-Feb
Medicamentos
3 registrados
KETAMINE, PROPRANOLOL HYDROCHLORIDE, PROPRANOLOL

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3 medicamentos registrados
Ver detalhes, fases e interações →
KETAMINEPROPRANOLOL HYDROCHLORIDEPROPRANOLOL
🏥
SUS: Cobertura mínimaScore: 15%
CID-10: Q21.0
🇧🇷Dados SUS / DATASUS
PROCEDIMENTOS SIGTAP (5)
0202010503
Cariótipo — bandas G, Q ou Rgenetic_test
0202010600
Pesquisa de microdeleções/microduplicações por FISHlab_test
0202010694
Sequenciamento completo do exoma (WES)rehabilitation
0202010260
Dosagem de alfa-fetoproteína
0301070040
Atendimento em reabilitação — doenças raras
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Entender a doença

Do básico ao detalhe, leia no seu ritmo

Preparando trilha educativa...

Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

❤️
Coração
10 sintomas
😀
Face
4 sintomas
📏
Crescimento
3 sintomas
👂
Ouvidos
1 sintomas
🦴
Ossos e articulações
1 sintomas
🧠
Neurológico
1 sintomas

+ 12 sintomas em outras categorias

Características mais comuns

Fenda submucosa do palato duro
Ponte nasal deprimida
Fissura palpebral estreita
Anormalidade da cartilagem da orelha externa
Hipocalcemia
Aplasia/Hipoplasia do timo
33sintomas
Sem dados (33)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 33 características clínicas mais associadas, ordenadas por frequência.

Fenda submucosa do palato duroSubmucous cleft hard palate
Ponte nasal deprimidaDepressed nasal bridge
Fissura palpebral estreitaNarrow palpebral fissure
Anormalidade da cartilagem da orelha externaAbnormality of cartilage of external ear
HipocalcemiaHypocalcemia

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa10
Total histórico1PubMed
Últimos 10 anos4publicações
Pico20161 papers
Linha do tempo
20202016Hoje · 2026
Publicações por ano (últimos 10 anos)

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Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

3 genes identificados com associação a esta condição.

NKX2-5Homeobox protein Nkx-2.5Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Transcription factor required for the development of the heart and the spleen (PubMed:22560297). During heart development, acts as a transcriptional activator of NPPA/ANF in cooperation with GATA4 (By similarity). May cooperate with TBX2 to negatively modulate expression of NPPA/ANF in the atrioventricular canal (By similarity). Binds to the core DNA motif of NPPA promoter (PubMed:22849347, PubMed:26926761). Together with PBX1, required for spleen development through a mechanism that involves CD

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (3)
Physiological factorsYAP1- and WWTR1 (TAZ)-stimulated gene expressionCardiogenesis
MECANISMO DE DOENÇA

Atrial septal defect 7, with or without atrioventricular conduction defects

A congenital heart malformation characterized by incomplete closure of the wall between the atria resulting in blood flow from the left to the right atria, and atrioventricular conduction defects in some cases.

EXPRESSÃO TECIDUAL(Tecido-específico)
Coração - Átrio
113.8 TPM
Coração - Ventrículo esquerdo
108.3 TPM
Baço
44.1 TPM
Adipose Visceral Omentum
0.5 TPM
Testículo
0.3 TPM
OUTRAS DOENÇAS (15)
hypoplastic left heart syndrome 2tetralogy of fallotventricular septal defect 3hypothyroidism, congenital, nongoitrous, 5
HGNC:2488UniProt:P52952
GATA4Transcription factor GATA-4Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Transcriptional activator that binds to the consensus sequence 5'-AGATAG-3' and plays a key role in cardiac development and function (PubMed:24000169, PubMed:27984724, PubMed:35182466). In cooperation with TBX5, it binds to cardiac super-enhancers and promotes cardiomyocyte gene expression, while it down-regulates endocardial and endothelial gene expression (PubMed:27984724). Involved in bone morphogenetic protein (BMP)-mediated induction of cardiac-specific gene expression. Binds to BMP respons

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (10)
Developmental Lineage of Pancreatic Acinar CellsDevelopmental Lineage of Multipotent Pancreatic Progenitor CellsDevelopmental Lineage of Pancreatic Ductal CellsSynthesis, secretion, and inactivation of Glucose-dependent Insulinotropic Polypeptide (GIP)Cardiogenesis
MECANISMO DE DOENÇA

Atrial septal defect 2

A congenital heart malformation characterized by incomplete closure of the wall between the atria resulting in blood flow from the left to the right atria. Patients show other heart abnormalities including ventricular and atrioventricular septal defects, pulmonary valve thickening or insufficiency of the cardiac valves. The disease is not associated with defects in the cardiac conduction system or non-cardiac abnormalities.

EXPRESSÃO TECIDUAL(Tecido-específico)
Ovário
144.1 TPM
Coração - Átrio
53.7 TPM
Testículo
51.1 TPM
Coração - Ventrículo esquerdo
45.2 TPM
Artéria coronária
40.7 TPM
OUTRAS DOENÇAS (12)
tetralogy of fallotventricular septal defect 1testicular anomalies with or without congenital heart diseaseatrial septal defect 2
HGNC:4173UniProt:P43694
CITED2Cbp/p300-interacting transactivator 2Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Transcriptional coactivator of the p300/CBP-mediated transcription complex. Acts as a bridge, linking TFAP2 transcription factors and the p300/CBP transcriptional coactivator complex in order to stimulate TFAP2-mediated transcriptional activation. Positively regulates TGF-beta signaling through its association with the SMAD/p300/CBP-mediated transcriptional coactivator complex. Stimulates the peroxisome proliferator-activated receptors PPARA transcriptional activity. Enhances estrogen-dependent

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (4)
Regulation of gene expression by Hypoxia-inducible FactorActivation of the TFAP2 (AP-2) family of transcription factorsTFAP2 (AP-2) family regulates transcription of other transcription factorsFOXO-mediated transcription of cell death genes
MECANISMO DE DOENÇA

Ventricular septal defect 2

A common form of congenital cardiovascular anomaly that may occur alone or in combination with other cardiac malformations. It can affect any portion of the ventricular septum, resulting in abnormal communications between the two lower chambers of the heart. Classification is based on location of the communication, such as perimembranous, inlet, outlet (infundibular), central muscular, marginal muscular, or apical muscular defect. Large defects that go unrepaired may give rise to cardiac enlargement, congestive heart failure, pulmonary hypertension, Eisenmenger's syndrome, delayed fetal brain development, arrhythmias, and even sudden cardiac death.

OUTRAS DOENÇAS (6)
ventricular septal defect 2atrial septal defect 8atrial septal defect, ostium secundum typeatrial septal defect, sinus venosus type
HGNC:1987UniProt:Q99967

Medicamentos e terapias

KETAMINEPhase 2

Mecanismo: Glutamate [NMDA] receptor negative allosteric modulator

PROPRANOLOL HYDROCHLORIDEPhase 1

Mecanismo: Beta-2 adrenergic receptor antagonist

PROPRANOLOLPhase 1

Mecanismo: Beta-1 adrenergic receptor antagonist

Ver mais no OpenTargets

Variantes genéticas (ClinVar)

607 variantes patogênicas registradas no ClinVar.

🧬 CITED2: NM_006079.5(CITED2):c.541AGC[3] (p.Ser183_Gly184insSer) ()
🧬 CITED2: NM_006079.5(CITED2):c.-8-11T>C ()
🧬 CITED2: NM_006079.5(CITED2):c.-8G>T ()
🧬 CITED2: NM_006079.5(CITED2):c.389C>G (p.Pro130Arg) ()
🧬 CITED2: NM_006079.5(CITED2):c.76C>G (p.His26Asp) ()
Ver todas no ClinVar

Diagnóstico

Os sinais que médicos procuram e os exames que confirmam

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Tratamento e manejo

Remédios, cuidados de apoio e o que precisa acompanhar

Pipeline de tratamentos
Pipeline regulatório — de medicamentos já aprovados a drogas em pesquisa exploratória.
2Fase 21
1Fase 12
Medicamentos catalogadosEnsaios clínicos· 3 medicamentos · 0 ensaios
Carregando informações de tratamento...

Onde tratar no SUS

Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)

🇧🇷 Atendimento SUS — NÃO RARA NA EUROPA: Defeito do septo ventricular

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Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.

Pesquisa ativa

Ensaios clínicos abertos e novidades científicas recentes

Pesquisa e ensaios clínicos

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Publicações mais relevantes

Timeline de publicações
0 papers (10 anos)
#1

Arrhythmias including atrial fibrillation and congenital heart disease in Kleefstra syndrome: a possible epigenetic link.

Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology2023 Dec 28

Kleefstra syndrome (KS), often diagnosed in early childhood, is a rare genetic disorder due to haploinsufficiency of EHMT1 and is characterized by neuromuscular and intellectual developmental abnormalities. Although congenital heart disease (CHD) is common, the prevalence of arrhythmias and CHD subtypes in KS is unknown. Inspired by a novel case series of KS patients with atrial tachyarrhythmias in the USA, we evaluate the two largest known KS registries for arrhythmias and CHD: Radboudumc (50 patients) based on health record review at Radboud University Medical Center in the Netherlands and GenIDA (163 patients) based on worldwide surveys of patient families. Three KS patients (aged 17-25 years) presented with atrial tachyarrhythmias without manifest CHD. In the international KS registries, the median [interquartile range (IQR)] age was considerably younger: GenIDA/Radboudumc at 10/13.5 (12/13) years, respectively. Both registries had a 40% prevalence of cardiovascular abnormalities, the majority being CHD, including septal defects, vascular malformations, and valvular disease. Interestingly, 4 (8%) patients in the Radboudumc registry reported arrhythmias without CHD, including one atrial fibrillation (AF), two with supraventricular tachycardias, and one with non-sustained ventricular tachycardia. The GenIDA registry reported one patient with AF and another with chronic ectopic atrial tachycardia (AT). In total, atrial tachyarrhythmias were noted in six young KS patients (6/213 or 3%) with at least four (three AF and one AT) without structural heart disease. In addition to a high prevalence of CHD, evolving data reveal early-onset atrial tachyarrhythmias in young KS patients, including AF, even in the absence of structural heart disease.

#2

Congenital Heart Defects and the Risk of Spontaneous Preterm Birth.

The Journal of pediatrics2021 Feb

To estimate the association between major types of congenital heart defects (CHD) and spontaneous preterm birth, and to assess the potential underlying mechanisms. This nationwide, registry-based study included a cohort of all singleton pregnancies in Denmark from 1997 to 2013. The association between CHD and spontaneous preterm birth was estimated by multivariable Cox regression, adjusted for potential confounders. The following potential mechanisms were examined: maternal genetics (sibling analyses), polyhydramnios, preterm prelabor rupture of membranes, preeclampsia, and indicators of fetal and placental growth. The study included 1 040 474 births. Compared with the general population, CHD was associated with an increased risk of spontaneous preterm birth, adjusted hazard ratio 2.1 (95% CI, 1.9-2.4). Several subtypes were associated with increased risks, including pulmonary stenosis combined with a septal defect, 5.2 (95% CI, 3.7-7.5); pulmonary stenosis or atresia, 3.1 (95% CI, 2.4-4.1); tetralogy of Fallot 2.5 (95% CI, 1.6-3.8); coarctation or interrupted aortic arch 2.2 (95% CI, 1.5-3.2); and hypoplastic left heart syndrome, 2.0 (95% CI, 1.0-4.1). Overall, preterm prelabor rupture of membranes mediated more than one-half of the association. Maternal genetics, polyhydramnios, or indicators of fetal or placental growth did not explain the reported associations. CHD, especially right ventricular outflow tract obstructions, were associated with an increased risk of spontaneous preterm birth. The risk was carried by the CHD and not by maternal genetics. Moreover, preterm prelabor rupture of membranes was identified as a potential underlying mechanism.

#3

Prenatal diagnosis, associated findings and postnatal outcome of fetuses with double outlet right ventricle (DORV) in a single center.

Journal of perinatal medicine2019 Apr 24

Objective To assess the spectrum of associated anomalies, the intrauterine course, postnatal outcome and management of fetuses with double outlet right ventricle (DORV). Methods All cases of DORV diagnosed prenatally over a period of 8 years were retrospectively collected in a single tertiary referral center. All additional prenatal findings were assessed and correlated with the outcome. The accuracy of prenatal diagnosis was assessed. Results Forty-six cases of DORV were diagnosed prenatally. The mean gestational age at first diagnosis was 21+4 weeks (range, 13-37). A correct prenatal diagnosis of DORV was made in 96.3% of the cases. If the relation of the great arteries, the position of the ventricular septal defect (VSD) and additional cardiac anomalies are taken into account, the prenatal diagnosis was correct in 92.6% of the cases. One case was postnatally classified as transposition of the great arteries with subpulmonary VSD and was excluded from further analysis. A total of 41 (91.1%) fetuses with DORV had major additional cardiac anomalies, 30 (66.7%) had extracardiac anomalies and 13 (28.9%) had chromosomal or syndromal anomalies. Due to their complex additional anomalies, five (11.1%) of our 45 fetuses had multiple malformations and were highly suspicious for non-chromosomal genetic syndromes, although molecular diagnosis could not be provided. Disorders of laterality occurred in 10 (22.2%) fetuses. There were 17 terminations of pregnancy (37.8%), two (4.4%) intrauterine and seven (15.6%) postnatal deaths. Nineteen of 22 (86.4%) live-born children with an intention to treat were alive at last follow-up. The mean follow-up among survivors was 32 months (range, 2-72). Of 21 children who had already undergone postnatal surgery, eight (38.1%) achieved biventricular repair and 13 (61.9%) received univentricular palliation. One recently born child is still waiting for surgery. All children predicted prenatally to need a single ventricle palliation, and all children predicted to achieve biventricular repair, ultimately received the predicted type of surgery. After surgery, 14 of 18 (77.8%) children were healthy without any impairment. Conclusion DORV is a rare and often complex cardiac anomaly that can be diagnosed prenatally with high precision. DORV is frequently associated with major additional anomalies, leading to a high intrauterine and postnatal loss rate due to terminations or declined postnatal therapy. Without additional anomalies, the prognosis is good, although approximately 60% of children will have single ventricle palliation.

#4

Congenital Heart Defects and Indices of Fetal Cerebral Growth in a Nationwide Cohort of 924 422 Liveborn Infants.

Circulation2016 Feb 09

Neurodevelopmental disorders are the most common and distressful comorbidities associated with congenital heart defects (CHD). Head circumference at birth (HC), a proxy for prenatal cerebral growth, is an established risk factor for neurodevelopmental disorders. In a nationwide cohort, we included all 924 422 liveborn Danish singletons, 1997 to 2011. CHD was present in 5519. The association between CHD and growth indices was analyzed by multivariable linear regression, adjusted for potential confounders. We report mean differences in gestational age-specific z scores in comparison with the general population. CHD was associated with lower HC z scores, -0.10 (95% confidence interval [CI], -0.13 to -0.08). Several CHD subtypes were associated with smaller HC, eg, hypoplastic left heart syndrome, -0.39 (95% CI, -0.58 to -0.21); common arterial trunk, -0.41 (95% CI, -0.74 to -0.09); and major ventricular septal defects, -0.25 (95% CI, -0.35 to -0.15). Other single-ventricle defects, transposition of the great arteries, tetralogy of Fallot, and anomalous pulmonary venous return, were also associated with smaller HC. Transposition of the great arteries was associated with smaller HC relative to birth weight, -0.26 (95% CI, -0.39 to -0.13). Major ventricular septal defects were associated with larger HC relative to birth weight. The results were consistent under various conditions, eg, when siblings of infants with CHD (n=5311) or infants with other major malformations (n=24 974) were used as the reference. Several subtypes of CHD were associated with smaller HC. The associations with major ventricular septal defects, common arterial trunk, and anomalous pulmonary venous return have not previously been described. Only infants with transposition of the great arteries had smaller HC relative to birth weight.

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Associações

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Comunidades

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Doenças relacionadas

Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico

Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. Arrhythmias including atrial fibrillation and congenital heart disease in Kleefstra syndrome: a possible epigenetic link.
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology· 2023· PMID 38195854mais citado
  2. Congenital Heart Defects and the Risk of Spontaneous Preterm Birth.
    The Journal of pediatrics· 2021· PMID 32980375mais citado
  3. Prenatal diagnosis, associated findings and postnatal outcome of fetuses with double outlet right ventricle (DORV) in a single center.
    Journal of perinatal medicine· 2019· PMID 30676006mais citado
  4. Congenital Heart Defects and Indices of Fetal Cerebral Growth in a Nationwide Cohort of 924 422 Liveborn Infants.
    Circulation· 2016· PMID 26769743mais citado
  5. Timing in resolution of left heart dilation according to the degree of mitral regurgitation in children with ventricular septal defect after surgical closure.
    J Pediatr (Rio J)· 2014· PMID 24140379recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:1480(Orphanet)
  2. MONDO:0002070(MONDO)
  3. Variantes catalogadas(ClinVar)
  4. Busca completa no PubMed(PubMed)
  5. Artigo Wikipedia(Wikipedia)
  6. Q838139(Wikidata)

Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.

Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar

NÃO RARA NA EUROPA: Defeito do septo ventricular
Compêndio · Raras BR

NÃO RARA NA EUROPA: Defeito do septo ventricular

ORPHA:1480 · MONDO:0002070
CID-10
Q21.0 · Comunicação interventricular
Medicamentos
3 registrados
MedGen
UMLS
C0018818
Wikidata
Wikipedia
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