Congenital tricuspid malformation

Summary

Congenital tricuspid malformation (MONDO:0020289) is a disease (an umbrella term covering 10 Mondo subtypes). A subtype of tricuspid valve disorder — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

• Umbrella term: 10 Mondo subtypes

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	congenital tricuspid malformation
Mondo ID	MONDO:0020289
Orphanet	98721
UMLS	C5681691
MedGen	1842501
GARD	0019555
Is cancer (heuristic)	no

Data availability: 1 HPO phenotype.

Disease family

This is a subtype of tricuspid valve disorder. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by body system or component › cardiovascular disorder › heart disorder › heart valve disorder › tricuspid valve disorder › congenital tricuspid malformation

Related subtypes (3): tricuspid valve insufficiency, tricuspid valve stenosis, cleft leaflet of tricuspid valve

Subtypes (10): tricuspid valve prolapse, Ebstein anomaly, cardiac valvular dysplasia, X-linked, tricuspid atresia, tricuspid valve agenesis, congenital tricuspid stenosis, straddling or overriding tricuspid valve, accessory tricuspid valve tissue, anomaly of the tricuspid valve chordae, parachute tricuspid valve

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.