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
definitions:
- name: >-
High-sensitivity cardiac troponin ascertainment of myocardial infarction in
emergency-department suspected acute coronary syndrome
definition_type: PHENOTYPE_ALGORITHM
derivation_basis: ESTABLISHED_CRITERIA
validation_status:
status: UNVALIDATED
rationale: >-
The underlying threshold rule is consensus criteria (Universal Definition
of MI: hs-cTn above the sex-specific 99th centile with a rise and/or fall
in an ischemic context), and the cohort form of it has been executed at
whole-population scale in a linked EHR registry (117,142 consecutive
patients over a decade). What is NOT validated is its specificity for the
type 1 atherothrombotic mechanism this entry models: in a
cluster-randomised trial of the same threshold, most patients it
reclassified had myocardial injury rather than type 1 MI. Treat this as an
ascertainment cohort for suspected ACS, not as a mechanism-specific case
definition, until a query that separates type 1 MI from type 2 MI and
non-ischemic myocardial injury is evaluated against adjudicated diagnoses.
description: >-
EHR/OMOP-style ascertainment used by linked-registry studies of suspected
acute coronary syndrome: take all adult emergency-department presentations
in which high-sensitivity cardiac troponin was measured within 24 hours as
the denominator, and count as cases those meeting the Universal Definition
threshold (hs-cTn above the 99th centile of a normal reference population).
Recorded here because the boundary it draws is mechanistically load-bearing
for this entry, which models type 1 (atherothrombotic) MI: the threshold
detects cardiomyocyte troponin release from any cause, so the cohort it
returns mixes type 1 MI with type 2 MI and non-ischemic myocardial injury.
scope: >-
Emergency-department suspected-ACS ascertainment in linked primary/secondary
care records; denominator plus troponin-threshold case rule, without
adjudication of MI type.
attaches_to:
- pathophysiology#Myocardial Ischemia and Cardiomyocyte Death
criteria_sets:
- name: Troponin-tested suspected-ACS cohort
description: >-
Adults presenting to a secondary- or tertiary-care emergency department in
whom high-sensitivity cardiac troponin was measured within 24 hours of
presentation; cases are those exceeding the 99th-centile diagnostic
threshold.
inclusion_criteria:
- preferred_term: Adult emergency-department presentation
description: Adult patient presenting to a secondary- or tertiary-care emergency department.
laboratory_requirements:
- preferred_term: High-sensitivity cardiac troponin measured within 24 hours
description: >-
hs-cTnI or hs-cTnT measured within 24 hours of presentation; defines the
denominator of the tested population.
- preferred_term: Troponin above the 99th-centile diagnostic threshold
description: >-
Concentration exceeding the (sex-specific) 99th centile of a normal
reference population, the Universal Definition threshold.
additional_requirements:
- preferred_term: MI type not resolved by the algorithm
description: >-
The threshold does not distinguish type 1 MI from type 2 MI or
non-ischemic myocardial injury; adjudication is required for that.
evidence:
- reference: PMID:30170853
reference_title: "High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: a stepped-wedge, cluster-randomised controlled trial."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "The Universal Definition of Myocardial Infarction1 recommends that an increase in troponin above the 99th centile of a normal reference population should be used as the threshold for diagnosis of myocardial infarction."
explanation: States the consensus threshold rule this ascertainment algorithm implements.
- reference: PMID:30170853
reference_title: "High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: a stepped-wedge, cluster-randomised controlled trial."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "Implementation of a high-sensitivity cardiac troponin assay and use of the 99th centile as the diagnostic threshold identifies more patients with myocardial injury than type 1 myocardial infarction and does not lead to a reduction in subsequent cardiac events."
explanation: >-
Randomised-trial evidence that the threshold is not specific for the type 1
atherothrombotic mechanism modeled in this entry — the basis for the
UNVALIDATED status and the MI-type caveat.
- reference: PPR:PPR1272216
reference_title: "Trends in the Assessment, Treatment and Outcomes of Patients with Suspected Acute Coronary Syndrome"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "We included all adult patients presenting to secondary- or tertiary-care EDs in the region between 2014 and 2024, in whom high-sensitivity cardiac troponin was measured within 24 hours of presentation."
explanation: >-
Specifies the troponin-tested emergency-department denominator this
algorithm encodes, as executed in the DataLoch linked registry.
notes: >-
PPR:PPR1272216 is a non-peer-reviewed preprint and is used here only to
document how the cohort was operationalized at population scale; the
threshold rule and the injury-versus-type-1-MI caveat are both carried by the
peer-reviewed randomised trial PMID:30170853. The primary source of the
threshold rule is the Fourth Universal Definition of Myocardial Infarction
(PMID:30165617, Thygesen et al.), but it is not cited as an evidence item
here because no abstract or full text is retrievable for it (the fetcher
caches it as content unavailable), so no snippet can be verified; the rule is
therefore quoted from PMID:30170853's statement of it.
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: OTHER
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: OTHER
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.
- reference: DOI:10.3390/ijms25137295
reference_title: "From Atherosclerotic Plaque to Myocardial Infarction—The Leading Cause of Coronary Artery Occlusion."
supports: SUPPORT
evidence_source: OTHER
snippet: "Type 1 is associated with atherosclerosis, type 2 results from inadequate oxygen supply to cardiomyocytes, type 3 is defined as sudden cardiac death, while types 4 and 5 are associated with procedures such as percutaneous coronary intervention and coronary artery bypass grafting, respectively."
explanation: Establishes the universal MI classification and that type 1 (the mechanism modeled here) is the atherosclerosis-driven form.
- 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
downstream:
- target: Ischemia-Reperfusion Injury
causal_link_type: DIRECT
description: >
Emergency restoration of coronary flow to salvage ischemic myocardium
paradoxically inflicts additional reperfusion injury on the jeopardized
tissue.
- target: Post-Infarction Inflammation and Cardiac Repair
causal_link_type: DIRECT
description: >
Massive cardiomyocyte death releases damage-associated molecular patterns
that ignite the post-infarction inflammatory and reparative cascade.
evidence:
- reference: PMID:26426469
reference_title: "Pathophysiology of Myocardial Infarction."
supports: SUPPORT
evidence_source: OTHER
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: OTHER
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.
- name: Ischemia-Reperfusion Injury
description: >
Restoration of coronary blood flow (by primary PCI or fibrinolysis) is
essential to salvage ischemic myocardium but paradoxically inflicts
additional damage — myocardial ischemia-reperfusion injury (MIRI) — that can
account for up to half of the final infarct size. Reperfusion drives a burst
of reactive oxygen species, cytosolic and mitochondrial calcium overload,
and sustained opening of the mitochondrial permeability transition pore
(MPTP) with collapse of the mitochondrial membrane potential and cessation
of ATP production, together with endothelial dysfunction, NLRP3 inflammasome
activation, and multiple regulated cell-death programs (apoptosis,
necroptosis, pyroptosis, ferroptosis) and dysregulated autophagy.
cell_types:
- preferred_term: cardiac muscle cell
term:
id: CL:0000746
label: cardiac muscle cell
- preferred_term: coronary endothelial cell
term:
id: CL:0000115
label: endothelial cell
biological_processes:
- preferred_term: response to oxidative stress
term:
id: GO:0006979
label: response to oxidative stress
modifier: INCREASED
- preferred_term: intracellular calcium ion homeostasis
term:
id: GO:0006874
label: intracellular calcium ion homeostasis
modifier: DYSREGULATED
locations:
- preferred_term: myocardium
term:
id: UBERON:0002349
label: myocardium
downstream:
- target: Post-Infarction Inflammation and Cardiac Repair
causal_link_type: DIRECT
description: >
Reperfusion-driven necrosis and DAMP release amplify the sterile
inflammatory response in the infarcted myocardium.
evidence:
- reference: DOI:10.1097/crd.0000000000000440
reference_title: "Pathobiology of Myocardial Ischemia and Reperfusion Injury: Models, Modes, Molecular Mechanisms, Modulation, and Clinical Applications"
supports: SUPPORT
evidence_source: OTHER
snippet: "reperfusion salvages a significant amount of ischemic myocardium in the subepicardium while reperfusion injury contributes up to 50% of the final subendocardial infarct."
explanation: Establishes that reperfusion, while salvaging myocardium, contributes up to half of the final infarct size — the defining claim of MIRI.
- reference: DOI:10.1097/crd.0000000000000440
reference_title: "Pathobiology of Myocardial Ischemia and Reperfusion Injury: Models, Modes, Molecular Mechanisms, Modulation, and Clinical Applications"
supports: SUPPORT
evidence_source: OTHER
snippet: "Reperfusion of severely ischemic myocardium leads to sustained opening of the mitochondrial permeability transition pore (MPTP)."
explanation: Evidences the central mitochondrial mechanism (sustained MPTP opening) of lethal reperfusion injury described in this node.
- reference: DOI:10.3390/cells14191509
reference_title: "Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons."
supports: SUPPORT
evidence_source: OTHER
snippet: "MIRI refers to paradoxical myocardial damage that occurs upon restoration of coronary blood flow and is driven by complex inflammatory, oxidative, and metabolic mechanisms, which can exacerbate infarct size"
explanation: Defines MIRI as paradoxical reperfusion damage driven by inflammatory, oxidative, and metabolic mechanisms that enlarge the infarct.
- reference: DOI:10.3390/cells14191509
reference_title: "Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons."
supports: SUPPORT
evidence_source: OTHER
snippet: "The principal mechanisms discussed include oxidative stress and mitochondrial dysfunction, calcium overload and ion homeostasis imbalance, inflammatory responses, with particular focus on the NLRP3 inflammasome and cytokine pathways, and multiple forms of cell death (apoptosis, necroptosis, pyroptosis, and autophagy)."
explanation: Enumerates the oxidative-stress, calcium-overload, NLRP3-inflammasome, and multi-modal cell-death mechanisms attributed to MIRI in this node.
- reference: DOI:10.3390/biomedicines12040802
reference_title: "Myocardial Ischemia–Reperfusion Injury: Unraveling Pathophysiology, Clinical Manifestations, and Emerging Prevention Strategies."
supports: SUPPORT
evidence_source: OTHER
snippet: "underscoring its potential to contribute substantially to the final infarct size, up to 50%."
explanation: Independent review corroborating that MIRI can contribute up to 50% of the final infarct size.
- name: Post-Infarction Inflammation and Cardiac Repair
description: >
Massive cardiomyocyte death releases damage-associated molecular patterns
(DAMPs/alarmins) that engage pattern-recognition receptors (TLRs, NLRs),
driving cytokine (IL-1, TNF-alpha, IL-6) and chemokine (CCL2) production and
recruitment of neutrophils and monocytes. Expansion and diversification of
cardiac macrophages clears dead cells; efferocytosis then triggers
anti-inflammatory mediators (IL-10, TGF-beta) that restrain inflammation and
activate reparative fibroblasts and vascular cells. This tightly regulated
inflammatory-to-reparative transition is essential for healing, but an
excessive or unresolved response promotes adverse outcomes.
cell_types:
- preferred_term: cardiac muscle cell
term:
id: CL:0000746
label: cardiac muscle cell
- preferred_term: macrophage
term:
id: CL:0000235
label: macrophage
- preferred_term: neutrophil
term:
id: CL:0000775
label: neutrophil
biological_processes:
- preferred_term: inflammatory response
term:
id: GO:0006954
label: inflammatory response
modifier: INCREASED
- preferred_term: wound healing
term:
id: GO:0042060
label: wound healing
modifier: INCREASED
locations:
- preferred_term: myocardium
term:
id: UBERON:0002349
label: myocardium
downstream:
- target: Cardiac Fibrosis and Ventricular Remodeling
causal_link_type: DIRECT
description: >
Efferocytosis-driven release of TGF-beta and other reparative mediators
activates fibroblasts and myofibroblasts, initiating fibrotic scar
formation and structural remodeling.
evidence:
- reference: DOI:10.1161/circresaha.124.323658
reference_title: "Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities."
supports: SUPPORT
evidence_source: OTHER
snippet: "After infarction, massive cardiomyocyte death releases a broad range of damage-associated molecular patterns that initiate both myocardial and systemic inflammatory responses."
explanation: Evidences DAMP release from dying cardiomyocytes as the trigger of the post-infarction inflammatory response.
- reference: DOI:10.1161/circresaha.124.323658
reference_title: "Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities."
supports: SUPPORT
evidence_source: OTHER
snippet: "Expansion and diversification of cardiac macrophages in the infarcted heart play a major role in the clearance of the infarct from dead cells and the subsequent stimulation of reparative pathways."
explanation: Supports the role of cardiac macrophage expansion in clearing the infarct and initiating repair.
- reference: DOI:10.1161/circresaha.124.323658
reference_title: "Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities."
supports: SUPPORT
evidence_source: OTHER
snippet: "Efferocytosis triggers the induction and release of anti-inflammatory mediators that restrain the inflammatory reaction and set the stage for the activation of reparative fibroblasts and vascular cells."
explanation: Evidences the efferocytosis-driven switch from inflammation to fibroblast-mediated repair that this node describes.
- reference: DOI:10.3390/cells13131125
reference_title: "The Influence of Metabolic Risk Factors on the Inflammatory Response Triggered by Myocardial Infarction: Bridging Pathophysiology to Treatment"
supports: SUPPORT
evidence_source: OTHER
snippet: "Myocardial infarction (MI) sets off a complex inflammatory cascade that is crucial for effective cardiac healing and scar formation."
explanation: Corroborates that the post-MI inflammatory cascade is essential for cardiac healing and scar formation.
- reference: DOI:10.3390/cells13131125
reference_title: "The Influence of Metabolic Risk Factors on the Inflammatory Response Triggered by Myocardial Infarction: Bridging Pathophysiology to Treatment"
supports: SUPPORT
evidence_source: OTHER
snippet: "Yet, if this response becomes excessive or uncontrolled, it can lead to cardiovascular complications."
explanation: Supports that a dysregulated post-MI inflammatory response drives adverse cardiovascular outcomes.
- name: Cardiac Fibrosis and Ventricular Remodeling
conforms_to: "cardiomyopathy_maladaptive_remodeling#Ventricular Remodeling"
description: >
Loss of contractile myocardium and sustained inflammatory/neurohormonal
drive produce adverse structural remodeling of the ventricle. Cardiac
fibroblasts differentiate into myofibroblasts that deposit a collagen-based
extracellular matrix; a well-organized scar protects against rupture and
limits acute dilation, but excessive, prolonged, or dysregulated fibrogenic
signaling drives interstitial fibrosis, chamber dilation, and contractile
dysfunction, progressing to heart failure. This node conforms to the
conserved ventricular-remodeling step of the maladaptive-cardiomyopathy
module, substituting the ischemic infarct scar as the disorder-specific
insult.
cell_types:
- preferred_term: cardiac fibroblast
term:
id: CL:0002548
label: fibroblast of cardiac tissue
- preferred_term: cardiac muscle cell
term:
id: CL:0000746
label: cardiac muscle cell
biological_processes:
- preferred_term: extracellular matrix organization
term:
id: GO:0030198
label: extracellular matrix organization
modifier: INCREASED
- 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
evidence:
- reference: DOI:10.3389/fphar.2023.1070973
reference_title: "Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention."
supports: SUPPORT
evidence_source: OTHER
snippet: "The cardiac fibroblast-to-myofibroblast differentiation and extracellular matrix collagen deposition are the hallmarks of cardiac fibrosis, which are modulated by multiple signaling pathways"
explanation: Evidences fibroblast-to-myofibroblast conversion and ECM collagen deposition as the hallmarks of post-MI cardiac fibrosis.
- reference: DOI:10.3389/fphar.2023.1070973
reference_title: "Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention."
supports: SUPPORT
evidence_source: OTHER
snippet: "Cardiac fibrosis plays an indispensable role in cardiac tissue homeostasis and repair after myocardial infarction (MI)."
explanation: Supports that fibrosis is central to tissue repair and remodeling after MI.
- reference: DOI:10.1161/circresaha.124.323658
reference_title: "Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities."
supports: SUPPORT
evidence_source: OTHER
snippet: "Deposition of a well-organized collagen-based extracellular matrix network protects the heart from catastrophic rupture and attenuates ventricular dilation."
explanation: Evidences the protective role of organized collagen scar in limiting rupture and dilation.
- reference: DOI:10.1161/circresaha.124.323658
reference_title: "Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities."
supports: SUPPORT
evidence_source: OTHER
snippet: "Excessive, prolonged, or dysregulated inflammatory or fibrogenic cascades accentuate adverse remodeling and dysfunction."
explanation: Supports that dysregulated fibrogenic signaling drives adverse ventricular remodeling and dysfunction.
phenotypes:
- category: Cardiovascular
name: Chest pain
description: >-
Chest pain is the cardinal presenting symptom of MI. This entry captures the
broad symptom, including atypical or non-anginal chest pain and painless
("silent") presentations that are common in women, older adults, and people
with diabetes; the classic ischemic substernal pain is captured separately as
Angina pectoris.
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
- category: Cardiovascular
name: Angina pectoris
description: Prolonged substernal ischemic chest pressure/pain is the classic (typical) presenting symptom of acute MI, distinct from the atypical/non-anginal presentations captured under Chest pain.
phenotype_term:
preferred_term: Angina pectoris
term:
id: HP:0001681
label: Angina pectoris
temporality: ACUTE
- category: Cardiovascular
name: Dyspnea
description: Shortness of breath, a common presenting symptom and a feature of MI-related heart failure.
phenotype_term:
preferred_term: Dyspnea
term:
id: HP:0002094
label: Dyspnea
- category: Cardiovascular
name: Ventricular fibrillation
description: Malignant ventricular arrhythmia that can complicate acute ischemia/reperfusion and cause sudden cardiac death.
phenotype_term:
preferred_term: Ventricular fibrillation
term:
id: HP:0001663
label: Ventricular fibrillation
- category: Cardiovascular
name: Congestive heart failure
description: Adverse ventricular remodeling after infarction can progress to heart failure.
phenotype_term:
preferred_term: Congestive heart failure
term:
id: HP:0001635
label: Congestive heart failure
- category: Cardiovascular
name: Syncope
description: Transient loss of consciousness may occur, e.g., from arrhythmia or hemodynamic compromise.
phenotype_term:
preferred_term: Syncope
term:
id: HP:0001279
label: Syncope
biochemical:
- name: Elevated cardiac troponin
presence: Elevated
context: >
A rise and/or fall of high-sensitivity cardiac troponin (cTnI or cTnT) above
the 99th-percentile upper reference limit, in a clinical context of
ischemia, is the biomarker cornerstone of the Fourth Universal Definition of
MI; troponin is the most sensitive/specific marker for acute myocardial
injury.
evidence:
- reference: DOI:10.3390/biomedicines13071532
reference_title: "Network Pharmacology Approaches to Myocardial Infarction Reperfusion Injury: Exploring Mechanisms, Pathophysiology, and Novel Therapies"
supports: SUPPORT
evidence_source: OTHER
snippet: "distinguishing reperfusion injury from ischemic damage is challenging and often requires the use of sensitive biomarkers, such as cardiac troponins, alongside advanced imaging modalities."
explanation: Supports cardiac troponin as the sensitive biomarker used to detect myocardial injury in MI.
- reference: PMID:30170853
reference_title: "High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: a stepped-wedge, cluster-randomised controlled trial."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "use of the high-sensitivity assay reclassified one in six patients with myocardial injury, but only a third of these patients had a diagnosis of type 1 myocardial infarction, and the incidence of subsequent myocardial infarction or cardiovascular death at 1 year was unchanged."
explanation: >-
Qualifies the marker: a troponin rise above the 99th centile is sensitive
for cardiomyocyte injury but not specific for the type 1 atherothrombotic
mechanism this entry models, so a positive result is not itself evidence of
plaque rupture.
notes: >-
Sensitivity and mechanistic specificity diverge here. The 99th-centile
threshold detects troponin release from any cause of cardiomyocyte injury,
so widening hs-cTn testing enlarges the myocardial-injury pool faster than
the type 1 MI pool: in a whole-population registry the diagnostic yield among
tested emergency-department patients fell from 73 to 47 per 1000 between 2014
and 2024 as testing extended to lower-risk patients (PPR:PPR1272216, a
preprint), while a cluster-randomised trial found only about a third of
patients reclassified by the assay had type 1 MI (PMID:30170853). See the
`definitions` entry for the ascertainment consequences. The 73-to-47 figures
are deliberately NOT curated as `prevalence:` records: they are a
test-positivity yield inside a clinician-selected denominator, so encoding
them as `rate_per_100000` / `prevalence_class` would present roughly 25-30x
the true adult population MI incidence to any consumer reading those slots,
and the caveat would survive only in prose.
- name: Elevated CK-MB
presence: Elevated
context: >
Creatine kinase-MB isoenzyme and LDH rise more slowly (LDH at roughly 24-48
hours) than troponin; historically used for MI diagnosis and for gauging
infarct timing, now largely superseded by high-sensitivity troponin.
- name: Total lipids in very small VLDL (XS-VLDL-L)
specificity: >
Research NMR lipoprotein measure, not a clinical MI test. Ranked as the
metabolite with the strongest risk-increasing Mendelian randomization
estimate for myocardial infarction across 313 plasma measures in a
274,241-participant UK Biobank atlas.
context: >
XS-VLDL-L quantifies the total lipid carried in the very small VLDL
subclass, the remnant-lipoprotein end of the triglyceride-rich spectrum, on
the Nightingale Health NMR platform used in UK Biobank. No presence value is
recorded because the reported quantity is a genetically instrumented effect
estimate over a general-population cohort rather than an observed level in
patients with infarction. The finding is consistent with the wider
remnant-cholesterol literature and supports curating atherogenic
apoB-lipoprotein burden, not LDL-C alone, as the lipid input to coronary
atherothrombosis. It is a risk-stratification signal and does not displace
troponin, which remains the diagnostic biomarker for an acute event.
readouts:
- target: Coronary Atherothrombosis
relationship: PREDICTS
direction: POSITIVE
endpoint_context: PROGNOSTIC
interpretation: >
Higher very-small-VLDL lipid content marks a more atherogenic
remnant-lipoprotein burden and tracks with a higher risk of the
atherothrombotic event that initiates infarction.
evidence:
- reference: PMID:40973818
reference_title: "Mapping the plasma metabolome to human health and disease in 274,241 adults."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "total lipids in very small VLDL (XS-VLDL-L) exhibited the strongest association with increased risk of myocardial infarction (OR = 1.55 (1.48-1.63)"
explanation: >
Bidirectional Mendelian randomization over 313 NMR metabolites ranks
XS-VLDL-L as the metabolite with the strongest risk-increasing estimate
for myocardial infarction (OR 1.55, 95% CI 1.48-1.63).
- name: Phospholipids to total lipids in small HDL, percent (S-HDL-PL%)
specificity: >
Research NMR lipoprotein-composition ratio, not a clinical MI test. Ranked
as the most protective metabolite for myocardial infarction in the same
Mendelian randomization analysis that ranked XS-VLDL-L most harmful.
context: >
Recorded as the counterpart to the XS-VLDL-L entry so the lipoprotein axis
is not curated one-sidedly. Note that this is a compositional ratio within
small HDL rather than HDL cholesterol concentration, so it should not be
read as reviving HDL-C as a causal protective target, a claim that
randomized HDL-raising trials did not support.
evidence:
- reference: PMID:40973818
reference_title: "Mapping the plasma metabolome to human health and disease in 274,241 adults."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "the ratio of phospholipids to total lipids in the small HDL percentage (S-HDL-PL%; OR = 0.63 (0.59-0.67)"
explanation: >
Names S-HDL-PL% and quotes its Mendelian randomization effect estimate
for myocardial infarction directly, rather than leaving the number in
curator prose.
- reference: PMID:40973818
reference_title: "Mapping the plasma metabolome to human health and disease in 274,241 adults."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "exhibited the most notable protective effect (Fig. 7e)"
explanation: >
The predicate of the same sentence, quoted so the protective claim
itself is carried by source text rather than by the explanation.
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: OTHER
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: OTHER
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.
- name: Anti-Inflammatory / Immunomodulatory Therapy
description: >
Emerging cytokine-directed therapy targeting the post-infarction
inflammatory response, notably IL-1 (canakinumab) and IL-6 (tocilizumab)
pathway inhibitors, to reduce cardiovascular events and mitigate
ischemia-reperfusion injury.
treatment_term:
preferred_term: Pharmacotherapy
term:
id: NCIT:C15986
label: Pharmacotherapy
therapeutic_agent:
- preferred_term: canakinumab
term:
id: NCIT:C80971
label: Canakinumab
- preferred_term: tocilizumab
term:
id: NCIT:C84217
label: Tocilizumab
therapeutic_modality: MONOCLONAL_ANTIBODY
evidence:
- reference: DOI:10.3390/cells14191509
reference_title: "Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons."
supports: SUPPORT
evidence_source: OTHER
snippet: "including IL-1 and IL-6 inhibitors such as Canakinumab and Tocilizumab"
explanation: Identifies IL-1 (canakinumab) and IL-6 (tocilizumab) inhibitors as immunotherapeutic strategies in MI/MIRI.
clinical_trials:
- name: NCT06118281
phase: PHASE_III
status: RECRUITING
description: >
ARTEMIS — randomized trial of the anti-IL-6 monoclonal antibody
ziltivekimab versus placebo for prevention of recurrent cardiovascular
events in patients with acute myocardial infarction.
target_phenotypes:
- preferred_term: Myocardial infarction
term:
id: HP:0001658
label: Myocardial infarction
evidence:
- reference: clinicaltrials:NCT06118281
reference_title: "ARTEMIS - Effects of Ziltivekimab Versus Placebo on Cardiovascular Outcomes in Patients With Acute Myocardial Infarction"
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "The research study is being done to see if ziltivekimab can be used to treat people who were admitted to hospital because of a heart attack."
explanation: ClinicalTrials.gov summary confirms ARTEMIS tests ziltivekimab in post-MI patients, evidencing the anti-inflammatory therapeutic strategy.
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.
datasets:
- accession: geo:GSE306012
title: Temporal inhibition of ADAM17 in fibroblasts reduces stiffness and promotes vascularization following myocardial infarction
description: Myocardial infarction (MI) triggers a complex remodelling process that leads to heat failure if uncontrolled. A Disintegrin and metalloproteinase-17 (ADAM17), a transmembrane sheddase, is upregulated in patients with ischemic cardiomyopathy, colocalized to myofibroblasts (myoFB) in the infarct tissues. Fibroblasts are key players in post-MI scar formation and exist in different states with diverse functions. Using mice with inducible Adam17 deletion in homeostatic FBs (Adam17 FB-KD ), or activated FBs (Adam17 myoFB-KD ), we found that ADAM17 loss in homeostatic FBs impaired infarct formation post-MI and increased mortality due to left ventricular (LV) rupture.
organism:
preferred_term: mouse
term:
id: NCBITaxon:10090
label: Mus musculus
data_type: BULK_RNA_SEQ
sample_count: 28
publication: PMID:41524432
notes: Identified by GEO DataSets index search for Myocardial Infarction (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-07-31. Title, sample count, and organism are GEO's own values.
- accession: geo:GSE304168
title: mRNA Therapeutics Encoding Multiple Reparative Factors using Polyplex Nanomicelle Attenuating Myocardial Infarction
description: 'Background: Gene therapy for heart failure has been explored using single factors such as angiogenic agents; however, clinical success remains limited. In this study, we investigated an alternative approach by directly administering mRNA encoding multiple genes that are transiently upregulated during cardiac recovery. Using a model in which heart function is restored through the administration of extracellular vesicles secreted by human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM-derived EVs), we aimed to evaluate the potential of multi-gene mRNA therapy for heart failure, being delivered using polyplex nanomicelles, which serve as an effective delivery system with superio...'
organism:
preferred_term: mouse
term:
id: NCBITaxon:10090
label: Mus musculus
data_type: BULK_RNA_SEQ
sample_count: 6
publication: PMID:42272746
notes: Identified by GEO DataSets index search for Myocardial Infarction (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-07-31. Title, sample count, and organism are GEO's own values.
- accession: geo:GSE291962
title: CCR8 expression on regulatory T cells reveals trajectories of tissue adaptation and protects against myocardial infarction [bulk RNA-seq]
description: We employed single-cell RNA sequencing (scRNA-seq) in a mouse model of MI to gain a detailed analysis of heart and lymphoid Tregs, focusing on their developmental trajectories. Bulk RNA sequencing was used to further characterize the phenotype of CC motif chemokine receptor 8 positive (CCR8+) Tregs in the heart and lymph nodes. scRNA-seq of murine Tregs from the mediastinal lymph node (mLN) and heart after MI identified three Treg populations, one of which was mainly derived from the heart.
organism:
preferred_term: mouse
term:
id: NCBITaxon:10090
label: Mus musculus
data_type: BULK_RNA_SEQ
sample_count: 16
publication: PMID:41685444
notes: Identified by GEO DataSets index search for Myocardial Infarction (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-07-31. Title, sample count, and organism are GEO's own values.
- accession: ega:EGAS00001006330
title: Spatial multi-omic map of human myocardial infarction
description: Myocardial infarction is a leading cause of mortality worldwide 1 . While advances have been made in acute treatment, an incomplete understanding of remodelling processes has limited the effectiveness of therapies to reduce late-stage mortality 2 . Here, we generate an integrative high- resolution map of human cardiac remodelling after myocardial infarction using single-cell gene expression, chromatin accessibility, and spatial transcriptomic profiling of multiple physiological zones at distinct time points in myocardium from myocardial infarction and control patients.
organism:
preferred_term: human
term:
id: NCBITaxon:9606
label: Homo sapiens
notes: 'European Genome-phenome Archive study, matched because the disease is named in the study''s own title ("Myocardial Infarction"); description-level mentions were not accepted. EGA study_type: Other. Controlled access -- data require a Data Access Agreement. EGA metadata retrieved 2026-08-01.'
- accession: ega:EGAS00001007021
title: Single-cell dissection of the immune response after a myocardial infarction
organism:
preferred_term: human
term:
id: NCBITaxon:9606
label: Homo sapiens
data_type: SINGLE_CELL_RNA_SEQ
notes: 'European Genome-phenome Archive study, matched because the disease is named in the study''s own title ("Myocardial Infarction"); description-level mentions were not accepted. EGA study_type: Transcriptome Analysis. Controlled access -- data require a Data Access Agreement. EGA metadata retrieved 2026-08-01.'
- accession: metabolomics_workbench:ST001908
title: Post Acute Myocardial Infarction Left Ventricular Remodeling Bio marker Analysis (PAMILA)
notes: Located via OmicsDI, which aggregates across omics repositories; this record comes from metabolomics_workbench. Only repositories with no other discovery route in this project and with a working accession resolver are curated from OmicsDI -- GEO, ArrayExpress, PRIDE, MetaboLights and EGA hits are excluded as duplicates of dedicated passes. Matched because the disease is named in the dataset's own title ("Myocardial Infarction"). Retrieved 2026-08-02.
- accession: massive:MSV000085040
title: Effect of senolytics (Navitoclax, ABT263) on recovery following Myocardial Infarction
description: Ischemia reperfusion injury (IRI) following intervention for myocardial infarction remains an unmet clinical problem. Using an established mouse model, we demonstrated that IRI induces multiple cardiac cell linages to senescence. Senescence is is detrimental to recovery, as treatment with the senolytic navitoclax improves functional recovery.Here we are using SWATH-MS to investigate the molecular mechanisms responsible for the effect of navitoclax treatment.
notes: Located via OmicsDI, which aggregates across omics repositories; this record comes from massive. Only repositories with no other discovery route in this project and with a working accession resolver are curated from OmicsDI -- GEO, ArrayExpress, PRIDE, MetaboLights and EGA hits are excluded as duplicates of dedicated passes. Matched because the disease is named in the dataset's own title ("Myocardial Infarction"). Retrieved 2026-08-02.
Myocardial infarction (MI) is defined as cardiomyocyte necrosis in a clinical setting consistent with acute myocardial ischemia, identified through clinical symptoms (prolonged chest pain), biochemical markers (elevated cardiac troponin), and instrumental findings (ECG changes and/or regional wall motion abnormalities) (fede2025myocardialischemiareperfusioninjury pages 1-2). MI is the leading component of cardiovascular disease (CVD) contributing to mortality, with approximately 4 million CVD-related deaths annually in Europe alone (młynarska2024fromatheroscleroticplaque pages 17-19). MI is classified into five types: Type 1 (atherosclerosis-related, most common), Type 2 (oxygen supply-demand mismatch), Type 3 (sudden cardiac death), Type 4 (PCI-related), and Type 5 (CABG-related) (młynarska2024fromatheroscleroticplaque pages 17-19).
Heart attack, acute myocardial infarction (AMI), STEMI (ST-elevation myocardial infarction), NSTEMI (non-ST-elevation myocardial infarction), coronary thrombosis, acute coronary syndrome (broader term)
Type 1 MI results from atherosclerotic plaque destabilization—either rupture or erosion—in coronary arteries, leading to thrombus formation that interrupts myocardial blood flow (das2025networkpharmacologyapproaches pages 1-2, młynarska2024fromatheroscleroticplaque pages 17-19). The pathogenesis involves chronic inflammation, lipid accumulation, endothelial dysfunction, and ultimately acute coronary artery occlusion.
Genetic Risk Factors: GWAS analyses have identified numerous susceptibility loci for MI. Meta-analyses combining Saudi Arabian cohorts with the CardioGRAMplusC4D and UK BioBank GWAS revealed 66 loci with genome-wide significance (p < 5 × 10⁻⁸). Key genes implicated include PCSK9, CETP, CDKN2B-AS1 (involved in lipid metabolism, inflammation, and endothelial function), STOX1, VPS26A, and LDLR (zhou2024associationofmetabolic pages 1-2, zhou2024associationofmetabolic pages 10-13). Polygenic risk scores (PRS) demonstrate that a high genetic risk is associated with a threefold increase in MI risk (OR: 3.074, 95% CI: 2.354–4.014) (zhou2024associationofmetabolic pages 1-2). Elevated lipoprotein(a) levels are independently associated with an increased risk of coronary artery disease, with risk increasing threefold in young patients (zhou2024associationofmetabolic pages 13-15).
Environmental and Lifestyle Risk Factors: Traditional risk factors include hypercholesterolemia (high LDL-C), cigarette smoking, chronic kidney disease, diabetes mellitus, hypertension, obesity, sedentary lifestyle, and poor dietary habits (młynarska2024fromatheroscleroticplaque pages 17-19, zhou2024associationofmetabolic pages 13-15). Air pollution, even below regulatory thresholds, promotes atherosclerosis, vascular dysfunction, and cardiac events.
Moderate fat intake (>15 energy percent), moderate alcohol consumption (<30 g/day), and non-smoking reduce MI risk even in individuals with high genetic predisposition (zhou2024associationofmetabolic pages 1-2, zhou2024associationofmetabolic pages 13-15). MI risk is negatively correlated with the consumption of olive oil, sesame oil, and perilla oil (rg = −0.364), which have anti-inflammatory and vasodilatory effects (zhou2024associationofmetabolic pages 13-15).
PRS interacts significantly with dietary fat intake, alcohol consumption, and smoking status to modulate MI risk, demonstrating that healthy lifestyle habits can substantially mitigate genetic susceptibility (zhou2024associationofmetabolic pages 1-2, zhou2024associationofmetabolic pages 13-15).
Suggested HPO terms for risk factors: HP:0003119 (Abnormality of lipid metabolism); HP:0000822 (Hypertension); HP:0001513 (Obesity); HP:0005978 (Type II diabetes mellitus)
Atypical presentations: Over one-third of NSTE-ACS patients may present with normal ECG findings (młynarska2024fromatheroscleroticplaque pages 7-8). Older patients often exhibit atypical symptoms with diminished sensitivity of traditional symptoms with age.
Post-MI patients experience significant reductions in quality of life, with long-term impacts on functional capacity, psychological well-being (anxiety, depression), and return-to-work rates, particularly in younger patients.
OpenTargets analysis identifies the following high-priority targets for MI (MONDO:0005068) (OpenTargets Search: myocardial infarction):
| Target Gene Symbol | Full Target Name | Target Category | Association Score | Drug Class/Examples | Clinical Stage | Evidence |
|---|---|---|---|---|---|---|
| GUCY1A1 | Guanylate cyclase 1 soluble subunit alpha 1 | Enzyme / nitric oxide receptor subunit | 0.695 | Soluble guanylate cyclase stimulators/activators; nitrates act upstream via NO-sGC-cGMP signaling | Approved-linked evidence in OpenTargets | (OpenTargets Search: myocardial infarction) |
| LDLR | Low density lipoprotein receptor | Receptor | 0.689 | LDL-lowering strategies acting through LDLR pathway: statins, PCSK9 inhibitors, inclisiran | Literature + clinical/approved-linked evidence | (OpenTargets Search: myocardial infarction, ramosregalado2024theinfluenceof pages 10-11) |
| PCSK9 | Proprotein convertase subtilisin/kexin type 9 | Secreted protease | 0.670 | PCSK9 inhibitors: evolocumab, alirocumab; siRNA inclisiran | Approved | (OpenTargets Search: myocardial infarction, ramosregalado2024theinfluenceof pages 10-11) |
| ADRB1 | Adrenoceptor beta 1 | G protein-coupled receptor | 0.624 | Beta-blockers: metoprolol, bisoprolol, atenolol | Approved | (OpenTargets Search: myocardial infarction, młynarska2024fromatheroscleroticplaque pages 11-12) |
| P2RY12 | Purinergic receptor P2Y12 | G protein-coupled receptor | 0.620 | P2Y12 inhibitors: clopidogrel, prasugrel, ticagrelor, cangrelor | Approved / Phase 4 evidence | (OpenTargets Search: myocardial infarction, młynarska2024fromatheroscleroticplaque pages 11-12, nicolau2025molecularmechanismsof pages 8-10) |
| AGTR1 | Angiotensin II receptor type 1 | G protein-coupled receptor | 0.617 | ARBs: losartan, valsartan, candesartan | Approved | (OpenTargets Search: myocardial infarction, ramosregalado2024theinfluenceof pages 10-11) |
| HMGCR | 3-hydroxy-3-methylglutaryl-CoA reductase | Enzyme | 0.616 | Statins: atorvastatin, rosuvastatin, simvastatin | Approved | (OpenTargets Search: myocardial infarction, alradwan2024emergingtrendsand pages 4-7, ramosregalado2024theinfluenceof pages 10-11) |
| ACE | Angiotensin I converting enzyme | Enzyme | 0.612 | ACE inhibitors: ramipril, lisinopril, enalapril | Approved | (OpenTargets Search: myocardial infarction, ramosregalado2024theinfluenceof pages 10-11) |
| PLAT | Plasminogen activator, tissue type | Serine protease | 0.566* | Thrombolytics/fibrinolytics: alteplase, tenecteplase | Approved | (OpenTargets Search: myocardial infarction, occhipinti2025pharmacologicalandinterventional pages 6-8) |
| LPA | Lipoprotein(a) | Lipoprotein / secreted risk factor | 0.435* | Emerging Lp(a)-lowering agents: olpasiran, pelacarsen; indirect lowering with PCSK9 inhibitors | Clinical development / emerging | (OpenTargets Search: myocardial infarction) |
| APOE | Apolipoprotein E | Lipid transport protein | 0.428* | No direct MI-targeted approved therapy; informs lipid biology/risk stratification | Literature-associated | (OpenTargets Search: myocardial infarction) |
| PTGS2 | Prostaglandin-endoperoxide synthase 2 (COX-2) | Enzyme | 0.606 | NSAID/COX pathway modulators; aspirin acts primarily on PTGS1 rather than PTGS2 | Approved-linked / Phase 4 evidence | (OpenTargets Search: myocardial infarction) |
| TCF21 | Transcription factor 21 | Transcription factor | 0.373* | No approved direct therapy; biomarker/mechanistic target in vascular remodeling | Literature-associated | (OpenTargets Search: myocardial infarction) |
| SORT1 | Sortilin 1 | Sorting receptor | 0.365* | No approved direct MI therapy; implicated in lipoprotein trafficking and residual risk biology | Literature-associated | (OpenTargets Search: myocardial infarction) |
| ITGA2B | Integrin subunit alpha 2b | Platelet integrin receptor subunit | 0.360* | GPIIb/IIIa inhibitors: abciximab, eptifibatide, tirofiban | Approved / Phase 3 evidence | (OpenTargets Search: myocardial infarction, sagris2024myocardialischemia–reperfusioninjury pages 8-10, occhipinti2025pharmacologicalandinterventional pages 6-8) |
| ITGB3 | Integrin subunit beta 3 | Platelet integrin receptor subunit | 0.360* | GPIIb/IIIa inhibitors: abciximab, eptifibatide, tirofiban | Approved / Phase 3 evidence | (OpenTargets Search: myocardial infarction, sagris2024myocardialischemia–reperfusioninjury pages 8-10, occhipinti2025pharmacologicalandinterventional pages 6-8) |
Table: This table summarizes key myocardial infarction drug targets prioritized from OpenTargets together with clinically relevant drug classes and development stage. It is useful for linking disease biology to established and emerging therapeutic mechanisms.
GWAS meta-analyses have identified over 66 loci associated with MI at genome-wide significance. The SHISA5 locus (rs11707229) was notably enriched at >12% minor allele frequency in Saudi MI populations. Genes including PCSK9, LDLR, APOE, LPA, TCF21, and SORT1 are consistently implicated (OpenTargets Search: myocardial infarction, zhou2024associationofmetabolic pages 10-13). Genetic variants rs3864814 and rs2081208 are associated with MI through colocalization analysis with genes STOX1, VPS26A, and RP11-744D14.2 (zhou2024associationofmetabolic pages 10-13).
DNA methylation, histone modifications (particularly via HDAC inhibitors), and non-coding RNAs (miR-144, miR-22) are key regulators of gene expression associated with atherosclerosis, MI, and cardiac remodeling. HDAC inhibitors reduce cardiomyocyte apoptosis, while specific microRNAs modulate oxidative stress pathways during ischemia-reperfusion injury (das2025networkpharmacologyapproaches pages 9-10).
Air pollution promotes atherosclerosis, vascular dysfunction, and cardiac events even below current regulatory thresholds. Occupational exposures, noise pollution, and extreme temperatures are additional contributors.
Smoking, sedentary lifestyle, high-fat and high-sugar diets, and excessive alcohol consumption are established modifiable risk factors (młynarska2024fromatheroscleroticplaque pages 17-19). Physical activity reduces cardiovascular risk through improved cardiac output, vascular efficiency, and metabolic health.
The pathophysiology of MI begins with atherosclerotic plaque rupture or erosion, leading to thrombus formation and coronary artery occlusion. Prolonged ischemia causes irreversible cardiomyocyte death, beginning in the subendocardium and progressing as a necrotic wavefront toward the subepicardium (buja2023pathobiologyofmyocardial pages 2-4, buja2023pathobiologyofmyocardial pages 1-2). Reversible injury lasts approximately 15 minutes, with irreversible injury developing between 20–60 minutes after coronary occlusion (buja2023pathobiologyofmyocardial pages 2-4).
The following table summarizes the major signaling pathways involved:
| Pathway Name | Key Components/Mediators | Role in MI Pathophysiology | Cellular Process Affected | Therapeutic Implications |
|---|---|---|---|---|
| MAPK (p38, JNK, ERK1/2) | p38 MAPK, JNK, ERK1/2, ADAM17, ACE2, Bim | Activated during ischemia/reperfusion and post-MI remodeling; promotes inflammatory signaling, apoptosis, mitochondrial dysfunction, ferroptosis, and adverse remodeling/fibrosis. p38/JNK are generally injury-amplifying; ERK can be context-dependent with survival and remodeling effects. (wang2025theroleof pages 16-17, wang2025theroleof pages 4-6) | Apoptosis, mitochondrial fission, oxidative stress response, ferroptosis, remodeling | Experimental inhibition of p38/JNK/ERK-axis components can reduce myocardial injury; pathway is a candidate for cardioprotection and anti-remodeling therapies, though translation remains challenging. (wang2025theroleof pages 16-17, wang2025theroleof pages 4-6) |
| PI3K/AKT/mTOR | PI3K, AKT, mTOR, BAD, Mdm2, PKD1, GLUT4 | Core pro-survival pathway in MI and reperfusion injury; suppresses apoptosis, modulates autophagy, supports metabolic adaptation, and can limit inflammatory injury. Reduced signaling is associated with greater injury. (fede2025myocardialischemiareperfusioninjury pages 26-28, das2025networkpharmacologyapproaches pages 7-9, fede2025myocardialischemiareperfusioninjury pages 10-12) | Cell survival, glucose uptake, metabolism, autophagy control, anti-apoptotic signaling | Therapies that enhance PI3K/AKT signaling or fine-tune mTOR/autophagy may reduce infarct size and improve reperfusion outcomes; a major cardioprotective target in preclinical studies. (das2025networkpharmacologyapproaches pages 7-9, fede2025myocardialischemiareperfusioninjury pages 10-12) |
| NF-κB | NF-κB, TLR4, MyD88, IL-1β, TNF-α, IL-6, Beclin-1 | Central inflammatory transcriptional program activated by DAMPs and innate immune receptors after cardiomyocyte necrosis; drives cytokine/chemokine expression, leukocyte recruitment, and can suppress protective autophagy in some contexts. (fede2025myocardialischemiareperfusioninjury pages 26-28, das2025networkpharmacologyapproaches pages 7-9, fede2025myocardialischemiareperfusioninjury pages 10-12, hilgendorf2024repairofthe pages 3-4) | Inflammation, cytokine production, leukocyte recruitment, autophagy regulation | Anti-inflammatory strategies targeting upstream TLR4/MyD88/NF-κB signaling may attenuate reperfusion injury and maladaptive remodeling; promising but requires timing-specific modulation. (fede2025myocardialischemiareperfusioninjury pages 26-28, das2025networkpharmacologyapproaches pages 7-9) |
| Wnt/β-catenin | Canonical Wnt/β-catenin, non-canonical Wnt/PCP, Wnt/Ca2+, JNK, CaMKII, PKC, calcineurin | Wnt signaling shows pathway-specific effects in MI/I/R injury: canonical Wnt/β-catenin tends to support recovery and survival, whereas non-canonical Wnt signaling can worsen apoptosis, calcium overload, inflammation, fibrosis, and hypertrophy. (zhang2024ischemiareperfusioninjurymolecular pages 3-4) | Apoptosis, macrophage polarization, oxidative stress, ECM remodeling, angiogenesis, fibrosis | Selective activation of canonical Wnt or inhibition of damaging non-canonical Wnt branches is a potential precision strategy for limiting reperfusion injury and fibrosis. (zhang2024ischemiareperfusioninjurymolecular pages 3-4) |
| TGF-β/Smad | TGF-β, TGF-β receptors, Smad proteins, MMP-2, MMP-9 | Master profibrotic pathway after MI; activated during repair/remodeling and drives fibroblast activation, myofibroblast conversion, collagen synthesis, EndoMT, and scar formation. Essential for structural repair but excessive activation promotes pathological fibrosis. (yin2023postmyocardialinfarctionfibrosis pages 6-8, hilgendorf2024repairofthe pages 3-4) | Fibroblast activation, collagen deposition, scar formation, fibrosis, EndoMT | Targeted modulation may preserve necessary scar formation while reducing adverse remodeling; attractive for anti-fibrotic therapy after MI. (yin2023postmyocardialinfarctionfibrosis pages 6-8, hilgendorf2024repairofthe pages 3-4) |
| NLRP3 inflammasome | NLRP3, ASC, caspase-1, IL-1β, ROS, DAMPs | Activated in macrophages, fibroblasts, and injured myocardium after ischemia/reperfusion; links mitochondrial damage and oxidative stress to IL-1β release and inflammatory amplification, and contributes to pyroptotic cell death. (fede2025myocardialischemiareperfusioninjury pages 26-28, das2025networkpharmacologyapproaches pages 7-9, fede2025myocardialischemiareperfusioninjury pages 1-2, hilgendorf2024repairofthe pages 15-17) | Inflammasome activation, pyroptosis, sterile inflammation | NLRP3/caspase-1/IL-1 axis inhibitors are promising candidates to reduce infarct inflammation, reperfusion injury, and downstream remodeling. (sagris2024myocardialischemia–reperfusioninjury pages 8-10, fede2025myocardialischemiareperfusioninjury pages 26-28) |
| TLR4/MyD88 | TLR4, MyD88, DAMPs/alarmins, HMGB1, NF-κB | One of the earliest innate immune sensing systems after MI; recognizes DAMPs released from necrotic cardiomyocytes and triggers downstream inflammatory cascades, endothelial activation, and leukocyte recruitment. (fede2025myocardialischemiareperfusioninjury pages 26-28, hilgendorf2024repairofthe pages 3-4, hilgendorf2024repairofthe pages 1-3) | Innate immune activation, cytokine induction, leukocyte trafficking | TLR4/MyD88 blockade is a mechanistically strong anti-inflammatory strategy for limiting sterile injury and reperfusion damage, but may risk impairing necessary repair if over-suppressed. (fede2025myocardialischemiareperfusioninjury pages 26-28, hilgendorf2024repairofthe pages 3-4) |
| JAK-STAT | JAKs, STATs, IL-6, STAT3 | Implicated in vascular inflammation, smooth muscle cell proliferation/differentiation, and post-MI inflammatory signaling; also participates in reparative cytokine signaling such as IL-10/STAT3-mediated suppression of excessive inflammation. (młynarska2024fromatheroscleroticplaque pages 17-19, hilgendorf2024repairofthe pages 19-20) | Cytokine signaling, inflammation resolution, vascular remodeling, cell proliferation | JAK inhibition has been proposed as a strategy in atherosclerosis/MI biology, while preserving beneficial STAT3-mediated repair signaling may be important; pathway likely needs selective modulation. (młynarska2024fromatheroscleroticplaque pages 17-19, hilgendorf2024repairofthe pages 19-20) |
| Apoptosis | Fas, TNF receptors, cytochrome c, caspase-8, caspase-9, executioner caspases, BAX/BAK, Bcl-2 | Major programmed cell-death pathway in ischemia/reperfusion injury; initiated during ischemia and executed during reperfusion via intrinsic mitochondrial and extrinsic death-receptor mechanisms. (fede2025myocardialischemiareperfusioninjury pages 26-28, das2025networkpharmacologyapproaches pages 7-9, fede2025myocardialischemiareperfusioninjury pages 1-2) | Programmed cell death, cardiomyocyte loss | Anti-apoptotic therapies, mitochondrial stabilizers, and survival-pathway activators may reduce infarct expansion and preserve viable myocardium. (das2025networkpharmacologyapproaches pages 15-16, fede2025myocardialischemiareperfusioninjury pages 26-28) |
| Necroptosis | RIPK1, RIPK3, MLKL | Regulated necrotic death contributes to cardiomyocyte loss during reperfusion and overlaps with inflammatory amplification because cell lysis releases DAMPs. (fede2025myocardialischemiareperfusioninjury pages 10-12, fede2025myocardialischemiareperfusioninjury pages 1-2) | Regulated necrotic cell death, DAMP release | RIPK/MLKL-targeted inhibition is a potential cardioprotective approach in reperfusion injury. (fede2025myocardialischemiareperfusioninjury pages 10-12) |
| Pyroptosis | Caspase-1, caspase-4/5/11, GSDMD, NLRP3, ASC, calpains | Inflammatory cell death pathway activated by inflammasomes in MIRI; causes membrane pore formation, cytokine release, and propagation of sterile inflammation. (fede2025myocardialischemiareperfusioninjury pages 10-12, fede2025myocardialischemiareperfusioninjury pages 12-14, fede2025myocardialischemiareperfusioninjury pages 1-2) | Inflammatory programmed cell death, cytokine release | Caspase-1, GSDMD, or inflammasome inhibition may reduce inflammatory tissue damage and infarct progression. (sagris2024myocardialischemia–reperfusioninjury pages 8-10, fede2025myocardialischemiareperfusioninjury pages 12-14) |
| Ferroptosis | Iron-dependent lipid peroxidation machinery, ROS, MAPK/ERK-associated regulators | Emerging reperfusion-related death mechanism characterized by iron-dependent lipid peroxidation; contributes to myocardial injury and interacts with oxidative stress/MAPK signaling. (wang2025theroleof pages 16-17, wang2025theroleof pages 4-6, das2025networkpharmacologyapproaches pages 4-6) | Lipid peroxidation-driven cell death, oxidative membrane damage | Ferroptosis inhibitors and antioxidant/lipid-peroxidation-targeting strategies are under investigation as adjunct cardioprotective therapies. (wang2025theroleof pages 16-17, das2025networkpharmacologyapproaches pages 4-6) |
| Autophagy | Beclin-1, mTOR, LAMP2, ATF6, IRE1, PERK, ROS | Context-dependent in MI: basal or adaptive autophagy can be protective, but dysregulated or excessive autophagy during reperfusion may worsen injury. Controlled by PI3K/AKT/mTOR, TLR4/NF-κB, ER stress, and ROS signaling. (das2025networkpharmacologyapproaches pages 7-9, fede2025myocardialischemiareperfusioninjury pages 10-12, fede2025myocardialischemiareperfusioninjury pages 12-14) | Organelle quality control, stress adaptation, cell survival vs cell death balance | Therapies that restore balanced autophagic flux rather than simple inhibition/activation may improve myocardial salvage and remodeling. (das2025networkpharmacologyapproaches pages 7-9, fede2025myocardialischemiareperfusioninjury pages 10-12) |
Table: This table summarizes the major molecular signaling pathways implicated in myocardial infarction pathophysiology, emphasizing their mediators, biological roles, affected cellular processes, and therapeutic relevance. It is useful for linking mechanistic disease biology to candidate intervention points.
Reperfusion, while essential for myocardial salvage, paradoxically contributes up to 50% of the final infarct size through ischemia-reperfusion injury (MIRI) (buja2023pathobiologyofmyocardial pages 1-2, das2025networkpharmacologyapproaches pages 1-2). Key mechanisms include:
Post-MI repair involves three overlapping phases: inflammatory, proliferative, and maturation/remodeling (hilgendorf2024repairofthe pages 3-4, hilgendorf2024repairofthe pages 1-3):
Cardiac macrophages are the predominant immune cells, existing in heterogeneous subpopulations with pro-inflammatory CCR2⁺ monocyte-derived macrophages and anti-inflammatory resident populations (Trem2hi, Bhlhe41⁺) (hilgendorf2024repairofthe pages 14-15, yang2025omicsbasedapproachtowards pages 4-5).
Suggested GO terms: GO:0006915 (apoptotic process); GO:0006954 (inflammatory response); GO:0042060 (wound healing); GO:0048661 (positive regulation of smooth muscle cell proliferation) Suggested CL terms: CL:0000746 (cardiac muscle cell); CL:0000235 (macrophage); CL:0000775 (neutrophil); CL:0000057 (fibroblast)
Ischemic injury begins in the papillary muscle and subendocardium, then progresses toward the subepicardium (buja2023pathobiologyofmyocardial pages 2-4). The left anterior descending (LAD) coronary artery territory is the most commonly affected.
Cardiovascular diseases, led by ischemic heart disease (IHD) including MI, are the leading cause of death globally. According to GBD 2021, high systolic blood pressure is the dominant modifiable risk factor, with resource-abundant regions showing notable reductions in age-standardized death rates (EAPC of −3.43, 95% CI: −3.32, −3.53), while resource-limited regions experienced stagnation or increases.
MI is a polygenic/multifactorial disease with complex inheritance. A high PRS is associated with a threefold increase in MI risk (zhou2024associationofmetabolic pages 1-2). Key loci include 9p21 (CDKN2B-AS1), LPA, PCSK9, and LDLR. Penetrance is incomplete and strongly modified by environmental/lifestyle factors.
ECG Criteria: For STEMI diagnosis, new ST-segment elevation is required in ≥2 contiguous leads: ≥2.5 mm in men <40 years, ≥2 mm in men >40 years, or ≥1.5 mm in women in leads V2–V3, and/or ≥1 mm in other leads (młynarska2024fromatheroscleroticplaque pages 7-8).
Biomarkers: High-sensitivity cardiac troponin (hs-cTn I and T) is the preferred biomarker, with a rise-and-fall pattern above the 99th percentile upper reference limit consistent with acute myocardial injury (fede2025myocardialischemiareperfusioninjury pages 1-2, das2025networkpharmacologyapproaches pages 12-13). LDH rises later (24–48 hours) and may help differentiate infarction from reperfusion injury (das2025networkpharmacologyapproaches pages 12-13).
Imaging: Cardiac MRI is the gold standard for assessing myocardial damage, using late gadolinium enhancement (LGE) to distinguish infarcted from viable tissue and T2-weighted imaging for edema assessment (das2025networkpharmacologyapproaches pages 12-13). Echocardiography is widely used for wall motion assessment. Coronary angiography remains the definitive tool for identifying culprit lesions.
The Fourth Universal Definition of Myocardial Infarction (2018), published by ESC/ACC/AHA/WHF, establishes MI diagnosis based on evidence of myocardial injury (troponin rise/fall) in a clinical context of myocardial ischemia (fede2025myocardialischemiareperfusioninjury pages 1-2).
MI remains the leading cause of cardiovascular mortality globally. In-hospital mortality for STEMI has declined substantially with primary PCI implementation. Cardiogenic shock complicates approximately 10% of AMI cases and carries high mortality. Long-term outcomes depend on infarct size, left ventricular function, completeness of revascularization, and comorbidities.
Antiplatelet Therapy (MAXO:0001001): Dual antiplatelet therapy (DAPT) combining aspirin with a P2Y12 receptor inhibitor is standard care. Prasugrel is preferred over ticagrelor for PCI patients, with clopidogrel reserved for high bleeding risk or contraindications (młynarska2024fromatheroscleroticplaque pages 11-12, nicolau2025molecularmechanismsof pages 8-10). Cangrelor provides rapid intravenous platelet inhibition during PCI (nicolau2025molecularmechanismsof pages 8-10, occhipinti2025pharmacologicalandinterventional pages 6-8).
Anticoagulants: Unfractionated heparin (UFH) is recommended for STEMI patients undergoing primary PCI, with enoxaparin and bivalirudin as alternatives (młynarska2024fromatheroscleroticplaque pages 11-12). Fondaparinux is preferred for NSTE-ACS patients not undergoing early invasive angiography (młynarska2024fromatheroscleroticplaque pages 11-12).
Beta-Blockers: Metoprolol is recommended for STEMI patients without acute heart failure, reducing ventricular fibrillation risk and microvascular obstruction (młynarska2024fromatheroscleroticplaque pages 11-12).
Statins: Atorvastatin, rosuvastatin, and simvastatin reduce LDL-cholesterol by up to 50% and exert cardioprotective anti-inflammatory effects (alradwan2024emergingtrendsand pages 4-7, ramosregalado2024theinfluenceof pages 10-11).
ACE Inhibitors/ARBs: ACE inhibitors and ARBs provide cardioprotection by mitigating adverse effects of angiotensin II during and after MI (ramosregalado2024theinfluenceof pages 10-11).
PCSK9 Inhibitors: Evolocumab and alirocumab provide additional LDL-lowering and modulate inflammatory responses via TLR4/NFκB signaling interference (ramosregalado2024theinfluenceof pages 10-11).
Novel Agents: SGLT2 inhibitors (dapagliflozin) show clinical promise in both diabetic and non-diabetic MI patients, reducing inflammatory response and infarct size (ramosregalado2024theinfluenceof pages 10-11). Anti-inflammatory agents including tocilizumab (IL-6 inhibitor), anakinra (IL-1 receptor antagonist), and colchicine show cardioprotective effects by reducing infarct size (sagris2024myocardialischemia–reperfusioninjury pages 8-10).
Primary percutaneous coronary intervention (PCI) is the gold standard for STEMI reperfusion. The 2023 ESC guidelines recommend consideration of intravascular imaging (OCT/IVUS) to guide PCI (Class IIa) (nicolau2025molecularmechanismsof pages 15-17).
Key currently recruiting Phase 3 clinical trials are summarized below:
| NCT Number | Trial Name/Description | Intervention/Drug | Sponsor | Enrollment | Novel Mechanism/Target |
|---|---|---|---|---|---|
| NCT06118281 | ARTEMIS – research study of ziltivekimab vs placebo after heart attack | Ziltivekimab | Novo Nordisk A/S | 10000 | Anti-inflammatory IL-6 pathway inhibition to reduce recurrent events after MI (sagris2024myocardialischemia–reperfusioninjury pages 8-10) |
| NCT07478003 | PULSE-MI 2 – prehospital pulse-dose glucocorticoid in STEMI | Pulse-dose glucocorticoid | Rigshospitalet, Denmark | 5204 | Early anti-inflammatory immunomodulation during acute STEMI/reperfusion |
| NCT06174753 | Dapagliflozin in STEMI | Dapagliflozin | Ottawa Heart Institute Research Corporation | 256 | SGLT2 inhibition; metabolic and anti-inflammatory cardioprotection with infarct-limiting potential (ramosregalado2024theinfluenceof pages 10-11) |
| NCT06364150 | Therapeutic use of angiopoietin-primed autologous peripheral blood stem cell in myocardial infarction | Angiopoietin-primed autologous peripheral blood stem cells | Seoul National Hospital | 30 | Regenerative cell therapy aimed at myocardial repair and neovascularization (das2025networkpharmacologyapproaches pages 32-33, alradwan2024emergingtrendsand pages 4-7) |
| NCT05577988 | Early de-escalation to low-potency single antiplatelet therapy guided by genetics vs systematic high-potency single antiplatelet therapy after ACS | Genotype-guided antiplatelet de-escalation | Assistance Publique - Hôpitaux de Paris | 2468 | Precision antiplatelet therapy using pharmacogenetic guidance for P2Y12-pathway modulation (młynarska2024fromatheroscleroticplaque pages 11-12, nicolau2025molecularmechanismsof pages 8-10) |
| NCT07320625 | Efficacy of montelukast on STEMI patients | Montelukast | Shanghai Zhongshan Hospital | 512 | Leukotriene receptor antagonism to modulate inflammation in STEMI |
| NCT07301034 | Study of ziltivekimab effect on coronary plaque vs placebo after heart attack | Ziltivekimab with plaque imaging endpoint | Novo Nordisk A/S | 332 | IL-6 pathway inhibition with imaging-based assessment of plaque biology/inflammation |
| NCT07467213 | Routine use of potassium competitive acid blocker vs guideline-directed gastrointestinal protection in acute myocardial infarction | Potassium-competitive acid blocker strategy | Samsung Medical Center | 5000 | Supportive strategy to optimize GI protection during intensive antithrombotic therapy after AMI |
| NCT07295223 | GALACTUS – effect of GLP-1 and antidiabetic SGLT2 agents for myocardial infarction and ultrasensitive inflammatory surveillance | GLP-1 agent and SGLT2 agent strategy | Instituto Mexicano del Seguro Social | 44 | Cardiometabolic and anti-inflammatory modulation using incretin/SGLT2 pathways after MI (ramosregalado2024theinfluenceof pages 10-11) |
Table: This table summarizes currently recruiting phase 3 interventional trials in myocardial infarction and related acute coronary syndromes mentioned in the evidence-gathering workflow. It highlights sponsor, scale, and the mechanistic rationale of each study to support translational and therapeutic landscape mapping.
Diet modification (Mediterranean diet, omega-3 fatty acids), regular exercise, stress management, and alcohol moderation are established risk-reducing strategies (zhou2024associationofmetabolic pages 1-2, zhou2024associationofmetabolic pages 13-15).
MI occurs naturally in dogs, cats, horses, and non-human primates, though it is less common than in humans. Companion animals, particularly dogs, can develop MI secondary to coronary atherosclerosis or vasculitis.
Zebrafish have high genetic homology with humans (70% of human genes have identifiable zebrafish orthologs) and offer unique advantages for cardiovascular research due to their remarkable cardiac regenerative capacity (wang2026zebrafishincardiovascular pages 1-3). Unlike mammals, zebrafish scars after cardiac injury are temporary and do not permanently hinder regeneration (wang2026zebrafishincardiovascular pages 14-16).
Mouse and Rat Models: Left anterior descending (LAD) coronary artery ligation is the standard injury model, inducing ischemia followed by reperfusion (alsadder2025cardiacischaemia–reperfusioninjury pages 8-9, das2025networkpharmacologyapproaches pages 10-12). Genetically modified models include Spontaneously Hypertensive Rats (SHR), diabetic rats, and Apoe⁻/⁻ mice for studying cardiovascular disease mechanisms. Limitations include higher heart rates and different electrophysiological properties compared to humans (alsadder2025cardiacischaemia–reperfusioninjury pages 8-9).
Zebrafish Models (Danio rerio; NCBI Taxon: 7955): Zebrafish offer high-throughput screening capability, embryonic transparency for real-time cardiac imaging, and robust cardiac regenerative capacity through cardiomyocyte proliferation (wang2026zebrafishincardiovascular pages 14-16, wang2026zebrafishincardiovascular pages 1-3). Injury models include cryoinjury and genetic ablation. Comparative single-cell profiling has identified distinct cardiac resident macrophage populations (hbaa⁺ Mac and timp4.3⁺ Mac3) essential for zebrafish heart regeneration. Key limitation: two-chambered heart with single-circuit circulation (wang2026zebrafishincardiovascular pages 14-16).
Porcine Models: Offer the greatest translational value due to closest resemblance to human cardiac physiology. Used for PCI-related research and device testing. Limitation: typically healthy animals that don't fully represent pathological comorbidity conditions (alsadder2025cardiacischaemia–reperfusioninjury pages 8-9).
Emerging models include iPSC-derived cardiomyocytes and organ-on-chip systems for studying ischemia-reperfusion injury with improved human relevance (alsadder2025cardiacischaemia–reperfusioninjury pages 14-15).
Translation of preclinical findings to clinical settings remains challenging due to species differences in cardiac physiology, immune responses, and myocardial repair mechanisms. Variability in experimental protocols between in vitro and in vivo models can lead to inconsistent results and reproducibility issues (das2025networkpharmacologyapproaches pages 10-12, alsadder2025cardiacischaemia–reperfusioninjury pages 14-15).
Disease Ontology: MONDO:0005068 (myocardial infarction) Key HPO Terms: HP:0001658 (Myocardial infarction); HP:0001681 (Angina pectoris); HP:0001649 (Tachycardia); HP:0002094 (Dyspnea) Key GO Terms: GO:0006915 (apoptotic process); GO:0006954 (inflammatory response); GO:0042060 (wound healing); GO:0097193 (intrinsic apoptotic signaling pathway); GO:0070059 (intrinsic apoptotic signaling in response to ER stress) Key UBERON Terms: UBERON:0000948 (heart); UBERON:0002349 (myocardium); UBERON:0001621 (coronary artery) Key CL Terms: CL:0000746 (cardiac muscle cell); CL:0000235 (macrophage); CL:0000775 (neutrophil); CL:0000057 (fibroblast); CL:0000115 (endothelial cell) Key CHEBI Terms: CHEBI:39025 (high-density lipoprotein cholesterol); CHEBI:39026 (low-density lipoprotein cholesterol) Key MAXO Terms: MAXO:0001001 (antiplatelet therapy); MAXO:0000474 (surgical intervention); MAXO:0000009 (drug therapy)
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