Myocardial infarction (acute myocardial infarction, AMI; "heart attack") is ischemic death of cardiomyocytes caused by an acute, sustained reduction in coronary blood flow. The most common (type 1) mechanism is atherothrombosis: rupture or erosion of a coronary atherosclerotic plaque exposes thrombogenic material, precipitating an occlusive or near-occlusive coronary thrombus that interrupts perfusion of the downstream myocardium. The resulting ischemia causes cardiomyocyte necrosis with release of cardiac troponin, and clinically presents as an acute coronary syndrome (ST-elevation or non-ST-elevation MI). Acute respiratory infections, including influenza and respiratory syncytial virus, are recognized short-term triggers of type 1 MI. AMI remains a leading cause of morbidity and mortality worldwide.
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name: Myocardial Infarction
creation_date: "2026-06-25T12:00:00Z"
description: >
Myocardial infarction (acute myocardial infarction, AMI; "heart attack") is
ischemic death of cardiomyocytes caused by an acute, sustained reduction in
coronary blood flow. The most common (type 1) mechanism is atherothrombosis:
rupture or erosion of a coronary atherosclerotic plaque exposes thrombogenic
material, precipitating an occlusive or near-occlusive coronary thrombus that
interrupts perfusion of the downstream myocardium. The resulting ischemia
causes cardiomyocyte necrosis with release of cardiac troponin, and clinically
presents as an acute coronary syndrome (ST-elevation or non-ST-elevation MI).
Acute respiratory infections, including influenza and respiratory syncytial
virus, are recognized short-term triggers of type 1 MI. AMI remains a leading
cause of morbidity and mortality worldwide.
category: Complex
parents:
- Cardiovascular Disease
- Atherosclerotic Disease
- Cardiac disorder
synonyms:
- Acute myocardial infarction
- Heart attack
- AMI
disease_term:
preferred_term: myocardial infarction
term:
id: MONDO:0005068
label: myocardial infarction
pathophysiology:
- name: Coronary Atherothrombosis
description: >
A coronary atherosclerotic plaque with a thin fibrous cap and a large
necrotic core ruptures (or, less often, erodes), exposing highly
thrombogenic necrotic-core material and subendothelial collagen to flowing
blood. Platelet adhesion and activation with activation of the coagulation
cascade form an occlusive or near-occlusive coronary thrombus that abruptly
interrupts blood flow to the downstream myocardium. Systemic inflammation,
including that accompanying acute respiratory infection, can destabilize
vulnerable plaque and promote a procoagulant state.
cell_types:
- preferred_term: coronary endothelial cell
term:
id: CL:0000115
label: endothelial cell
- preferred_term: platelet
term:
id: CL:0000233
label: platelet
biological_processes:
- preferred_term: platelet activation
term:
id: GO:0030168
label: platelet activation
modifier: INCREASED
- preferred_term: blood coagulation
term:
id: GO:0007596
label: blood coagulation
modifier: INCREASED
- preferred_term: inflammatory response
term:
id: GO:0006954
label: inflammatory response
modifier: INCREASED
locations:
- preferred_term: coronary artery
term:
id: UBERON:0001621
label: coronary artery
downstream:
- target: Myocardial Ischemia and Cardiomyocyte Death
causal_link_type: DIRECT
description: >
Occlusive coronary thrombosis abruptly interrupts perfusion of the
downstream myocardium, producing ischemia.
evidence:
- reference: PMID:24902970
reference_title: "Mechanisms of plaque formation and rupture."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "such plaques may suddenly cause life-threatening coronary thrombosis presenting as an acute coronary syndrome."
explanation: Establishes that rupture of an atherosclerotic plaque precipitates coronary thrombosis presenting as acute coronary syndrome (including MI).
- reference: PMID:24902970
reference_title: "Mechanisms of plaque formation and rupture."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "Most often, the culprit morphology is plaque rupture with exposure of highly thrombogenic, red cell-rich necrotic core material."
explanation: Identifies plaque rupture exposing thrombogenic necrotic-core material as the dominant culprit lesion mechanism.
- name: Myocardial Ischemia and Cardiomyocyte Death
description: >
Sustained interruption of coronary perfusion causes regional myocardial
ischemia. If flow is not restored, cardiomyocytes undergo necrosis and
apoptosis, releasing cardiac troponin into the circulation (the biomarker
basis of MI diagnosis). Loss of contractile myocardium reduces left
ventricular systolic function and provides an arrhythmogenic substrate,
and can progress to heart failure.
cell_types:
- preferred_term: cardiac muscle cell
term:
id: CL:0000746
label: cardiac muscle cell
biological_processes:
- preferred_term: cardiac muscle cell apoptotic process
term:
id: GO:0010659
label: cardiac muscle cell apoptotic process
modifier: INCREASED
locations:
- preferred_term: myocardium
term:
id: UBERON:0002349
label: myocardium
- preferred_term: heart
term:
id: UBERON:0000948
label: heart
evidence:
- reference: PMID:26426469
reference_title: "Pathophysiology of Myocardial Infarction."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "Myocardial infarction is defined as sudden ischemic death of myocardial tissue."
explanation: Directly evidences that MI is ischemic death of myocardium, the core claim of this node.
- reference: PMID:26426469
reference_title: "Pathophysiology of Myocardial Infarction."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart."
explanation: Evidences ischemic cardiomyocyte necrosis and apoptosis in the infarcted myocardium described by this node.
phenotypes:
- category: Cardiovascular
name: Chest pain
description: Acute ischemic chest pain (angina) is the cardinal presenting symptom.
phenotype_term:
preferred_term: Chest pain
term:
id: HP:0100749
label: Chest pain
temporality: ACUTE
- category: Cardiovascular
name: Myocardial infarction
description: Ischemic necrosis of myocardium.
phenotype_term:
preferred_term: Myocardial infarction
term:
id: HP:0001658
label: Myocardial infarction
- category: Laboratory
name: Elevated cardiac troponin
description: Release of cardiac troponin from dying cardiomyocytes; the biomarker basis of MI diagnosis.
phenotype_term:
preferred_term: Increased circulating troponin concentration
term:
id: HP:0410174
label: Increased circulating troponin T concentration
- category: Cardiovascular
name: Arrhythmia
description: Ischemia creates an arrhythmogenic substrate (e.g., ventricular arrhythmias).
phenotype_term:
preferred_term: Arrhythmia
term:
id: HP:0011675
label: Arrhythmia
- category: Cardiovascular
name: Reduced left ventricular ejection fraction
description: Loss of contractile myocardium reduces systolic function and can progress to heart failure.
phenotype_term:
preferred_term: Reduced left ventricular ejection fraction
term:
id: HP:0012664
label: Reduced left ventricular ejection fraction
treatments:
- name: Coronary Reperfusion (PCI or Fibrinolysis)
description: >
Emergency restoration of coronary blood flow by primary percutaneous
coronary intervention or, where unavailable, fibrinolysis, to salvage
ischemic myocardium.
treatment_term:
preferred_term: percutaneous coronary intervention
term:
id: NCIT:C99521
label: Percutaneous Coronary Intervention
evidence:
- reference: PMID:27502078
reference_title: "Acute myocardial infarction."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "implementation of care delivery systems prioritising immediate revascularisation through percutaneous coronary intervention (or fibrinolysis)"
explanation: Identifies immediate revascularisation by PCI or fibrinolysis as central to modern AMI management.
- name: Antiplatelet and Antithrombotic Therapy
description: >
Antiplatelet agents and anticoagulants to limit coronary thrombus
propagation, plus secondary-prevention statins.
treatment_term:
preferred_term: Pharmacotherapy
term:
id: NCIT:C15986
label: Pharmacotherapy
evidence:
- reference: PMID:27502078
reference_title: "Acute myocardial infarction."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "advances in antiplatelet agents and anticoagulants, and greater use of secondary prevention strategies such as statins."
explanation: Identifies antiplatelet agents, anticoagulants, and statins as pillars of pharmacological AMI management.
notes: >
Created as an endpoint entry to support directional comorbidity/trajectory
modeling of acute respiratory infection (influenza, RSV) as a short-term
trigger of type 1 myocardial infarction. Type 1 (atherothrombotic) MI is
modeled here; type 2 MI (supply-demand mismatch without acute
atherothrombosis) is a related but distinct mechanism.