Ask OpenScientist

Ask a research question about Myocardial Infarction. OpenScientist will conduct autonomous deep research using the Disorder Mechanisms Knowledge Base and PubMed literature (typically 10-30 minutes).

Submitting...

Do not include personal health information in your question. Questions and results are cached in your browser's local storage.

2
Pathophys.
5
Phenotypes
2
Pathograph
2
Medical Actions
C

Comorbidities

Disease B A_BEFORE_B CURATED

Pathophysiology

2
Coronary Atherothrombosis
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.
coronary endothelial cell CL:0000115 platelet CL:0000233
platelet activation GO:0030168 ↑ INCREASED blood coagulation GO:0007596 ↑ INCREASED inflammatory response GO:0006954 ↑ INCREASED
coronary artery UBERON:0001621
Show evidence (2 references)
PMID:24902970 SUPPORT Human Clinical
"such plaques may suddenly cause life-threatening coronary thrombosis presenting as an acute coronary syndrome."
Establishes that rupture of an atherosclerotic plaque precipitates coronary thrombosis presenting as acute coronary syndrome (including MI).
PMID:24902970 SUPPORT Human Clinical
"Most often, the culprit morphology is plaque rupture with exposure of highly thrombogenic, red cell-rich necrotic core material."
Identifies plaque rupture exposing thrombogenic necrotic-core material as the dominant culprit lesion mechanism.
Myocardial Ischemia and Cardiomyocyte Death
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.
cardiac muscle cell CL:0000746
cardiac muscle cell apoptotic process GO:0010659 ↑ INCREASED
myocardium UBERON:0002349 heart UBERON:0000948
Show evidence (2 references)
PMID:26426469 SUPPORT Human Clinical
"Myocardial infarction is defined as sudden ischemic death of myocardial tissue."
Directly evidences that MI is ischemic death of myocardium, the core claim of this node.
PMID:26426469 SUPPORT Human Clinical
"Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart."
Evidences ischemic cardiomyocyte necrosis and apoptosis in the infarcted myocardium described by this node.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Myocardial Infarction Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

5
Cardiovascular 3
Myocardial infarction Myocardial infarction HP:0001658
Arrhythmia Arrhythmia HP:0011675
Reduced left ventricular ejection fraction Reduced left ventricular ejection fraction HP:0012664
Constitutional 1
Chest pain Chest pain HP:0100749
Temporal: ACUTE
Other 1
Elevated cardiac troponin Increased circulating troponin T concentration HP:0410174
💊

Medical Actions

2
Coronary Reperfusion (PCI or Fibrinolysis)
Action: percutaneous coronary intervention Ontology label: Percutaneous Coronary Intervention NCIT:C99521
Emergency restoration of coronary blood flow by primary percutaneous coronary intervention or, where unavailable, fibrinolysis, to salvage ischemic myocardium.
Show evidence (1 reference)
PMID:27502078 SUPPORT Human Clinical
"implementation of care delivery systems prioritising immediate revascularisation through percutaneous coronary intervention (or fibrinolysis)"
Identifies immediate revascularisation by PCI or fibrinolysis as central to modern AMI management.
Antiplatelet and Antithrombotic Therapy
Action: Pharmacotherapy NCIT:C15986
Antiplatelet agents and anticoagulants to limit coronary thrombus propagation, plus secondary-prevention statins.
Show evidence (1 reference)
PMID:27502078 SUPPORT Human Clinical
"advances in antiplatelet agents and anticoagulants, and greater use of secondary prevention strategies such as statins."
Identifies antiplatelet agents, anticoagulants, and statins as pillars of pharmacological AMI management.
{ }

Source YAML

click to show
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.