Stenosis or atrophy of the coronary ostium

Summary

Stenosis or atrophy of the coronary ostium (MONDO:0020423) is a disease. A subtype of coronary artery congenital malformation — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	stenosis or atrophy of the coronary ostium
Mondo ID	MONDO:0020423
Orphanet	99087
UMLS	C5575847
MedGen	1842382
GARD	0019643
Is cancer (heuristic)	no

Also known as: coronary ostial stenosis or atresia

Disease family

This is a subtype of coronary artery congenital malformation. 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 › vascular disorder › arterial disorder › coronary artery disorder › coronary artery congenital malformation › stenosis or atrophy of the coronary ostium

Related subtypes (8): anomalous left coronary artery from the pulmonary artery, coronary arterial fistulas, congenital coronary artery aneurysm, coronary artery intramyocardial course, aortopulmonary coronary arterial course, intramural coronary arterial course, abnormal number of coronary ostia, malposition of the coronary ostium

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.