Acute anterolateral myocardial infarction

Summary

Acute anterolateral myocardial infarction (MONDO:0001090) is a disease. A subtype of acute myocardial infarction — 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	acute anterolateral myocardial infarction
Mondo ID	MONDO:0001090
DOID	DOID:10651
SNOMED CT	70211005
UMLS	C0155627
MedGen	510040
Is cancer (heuristic)	no

Also known as: acute myocardial infarction of anterolateral wall · anterolateral myocardial infarction, acute

Disease family

This is a subtype of acute myocardial infarction. 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 › myocardial disorder › myocardial infarction › acute myocardial infarction › acute anterolateral myocardial infarction

Related subtypes (5): acute subendocardial myocardial infarction, acute inferoposterior infarction, acute inferolateral myocardial infarction, strictly posterior acute myocardial infarction, ST-elevation myocardial infarction

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.