Inflammation of heart layer

Summary

Inflammation of heart layer (MONDO:0024636) is a disease with 1 GWAS associations across 6 studies. A subtype of heart disorder — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

• GWAS associations: 1

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	inflammation of heart layer
Mondo ID	MONDO:0024636
SNOMED CT	399617002
UMLS	C0869523
MedGen	163689
Is cancer (heuristic)	no

Also known as: carditis · heart layer inflammation

Data availability: 1 GWAS association (6 studies).

Disease family

This is a subtype of heart 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 › inflammation of heart layer

Related subtypes (33): endocardium disorder, pericardium disorder, cardiac tuberculosis, heart conduction disease, hypertensive heart disease, heart valve disorder, cardiomyopathy, coronary artery disorder, heart failure, congenital heart disease, heart aneurysm, rheumatic heart disease, cardiac rhythm disease, white forelock with malformations, atrioventricular defect-blepharophimosis-radial and anal defect syndrome, microcephaly-cardiac defect-lung malsegmentation syndrome, PHACE syndrome, microcephaly-facio-cardio-skeletal syndrome, Hadziselimovic type, cardiac anomalies-heterotaxy syndrome, polyvalvular heart disease syndrome, Thomas syndrome, 22q11.2 deletion syndrome, myocardial rupture, heart neoplasm, aortopulmonary window, cor biloculare, myocardial disorder, carcinoid heart disease, omphalocele-diaphragmatic hernia-cardiovascular anomalies-radial ray defect syndrome, coronary microvascular disorder, cardiac ventricle disorder, cardiogenetic disease, cardiogenic shock

Subtypes (2): myocarditis, endocarditis

Genetics & variants

GWAS landscape

1 GWAS associations across 6 studies. Top hits map to 0 distinct genes (as reported by GWAS).

Top associations by p-value

rsID	p-value	Gene	Risk allele	Odds ratio
rs77093617	5e-07	TLN2 - TPM1-AS	?

Top studies (by case count)

Study	Lead author	Year	Cases	Controls	Title
GCST90477891	Verma A	2024	7,247	435,038	Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
GCST90477890	Verma A	2024	2,074	117,335	Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
GCST90480798	Verma A	2024	2,074	117,335	Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
GCST90436089	Zhou W	2018	2,020	405,779	Efficiently controlling for case-control imbalance and sample relatedness in large-scale genetic association studies.
GCST90652144	Liu TY	2025	785	235,604	Diversity and longitudinal records: Genetic architecture of disease associations and polygenic risk in the Taiwanese Han population.
GCST90477889	Verma A	2024	723	58,136	Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.

Variant details and genetic-evidence tiers

Tier distribution (top 50 variants)

Tier	Variants
Tier 1: coding	0
Tier 2: splice/UTR	0
Tier 3: regulatory	0
Tier 4: intronic/intergenic	1

MAF distribution

Bucket	Variants
common (>=0.05)	1
low_freq (0.01-0.05)	0
rare (<0.01)	0
unknown	0

Functional consequences

Consequence	Count
intergenic_variant	1

Top variants

rsID	Chr	Pos	Alleles	MAF	Consequence	Gene	p-value	Tier
rs77093617	15	62937348	T>G	0.05	intergenic_variant	TLN2 - TPM1-AS	5e-07	Tier 4: intronic/intergenic

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.