Mobitz type I atrioventricular block

Summary

Mobitz type I atrioventricular block (MONDO:0020744) is a disease. A subtype of second-degree atrioventricular block — 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	Mobitz type I atrioventricular block
Mondo ID	MONDO:0020744
NCIT	C62017
UMLS	C0264907
MedGen	82687
Is cancer (heuristic)	no

Also known as: AV block second degree Mobitz type I · AV block second degree Möbitz type I · Mobitz I · Mobitz type I · Mobitz type I second degree AV block · Möbitz I · Möbitz type I second degree AV block · second degree atrioventricular block Mobitz type I · second degree atrioventricular block Möbitz type I · type 1 2nd degree AV block · type 1 second degree atrioventricular block · type 1 second degree AV block · Wenckebach block

Disease family

This is a subtype of second-degree atrioventricular block. 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 conduction disease › atrioventricular block › second-degree atrioventricular block › Mobitz type I atrioventricular block

Related subtypes (1): Mobitz type II atrioventricular block

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.