Acute myocardial infarction

# Overview
AMI (Acute myocardial infarction) can refer to:
- ST elevation myocardial infarction
- Non ST elevation myocardial infarction

# Types of AMI
This page outlines the terminology and types of myocardial infarction according to the Fourth Universal Definition of Myocardial Infarction endorsed by the ESC/ACC/AHA/WHF (Eur Heart J. 2019 Jan 14;40(3):237-269. doi: 10.1093/eurheartj/ehy462).
- Type 1
Caused by atherothrombotic coronary artery disease and usually precipitated by atherosclerotic plaque disruption (plaque rupture or plaque erosion).
- Caused by atherothrombotic coronary artery disease and usually precipitated by atherosclerotic plaque disruption (plaque rupture or plaque erosion).
- Type 2
Caused by an imbalance between myocardial oxygen supply and demand.
Unrelated to acute coronary atherothrombosis.
Attributable to:
Reduced myocardial perfusion:
Fixed coronary atherosclerosis without plaque rupture.
Coronary artery spasm.
Coronary microvascular dysfunction (including endothelial dysfunction, smooth muscle cell dysfunction, and dysregulation of sympathetic innervation).
Coronary embolism.
Coronary artery dissection with or without intramural hematoma.
Reduced oxygen supply:
Severe bradyarrhythmia.
Respiratory failure with severe hypoxemia.
Severe anemia.
Hypotension/shock.
Increased myocardial oxygen demand:
Sustained tachyarrhythmia.
Severe hypertension with or without left ventricular hypertrophy.
- Caused by an imbalance between myocardial oxygen supply and demand.
- Unrelated to acute coronary atherothrombosis.
- Attributable to:
Reduced myocardial perfusion:
Fixed coronary atherosclerosis without plaque rupture.
Coronary artery spasm.
Coronary microvascular dysfunction (including endothelial dysfunction, smooth muscle cell dysfunction, and dysregulation of sympathetic innervation).
Coronary embolism.
Coronary artery dissection with or without intramural hematoma.
Reduced oxygen supply:
Severe bradyarrhythmia.
Respiratory failure with severe hypoxemia.
Severe anemia.
Hypotension/shock.
Increased myocardial oxygen demand:
Sustained tachyarrhythmia.
Severe hypertension with or without left ventricular hypertrophy.
- Reduced myocardial perfusion:
Fixed coronary atherosclerosis without plaque rupture.
Coronary artery spasm.
Coronary microvascular dysfunction (including endothelial dysfunction, smooth muscle cell dysfunction, and dysregulation of sympathetic innervation).
Coronary embolism.
Coronary artery dissection with or without intramural hematoma.
- Fixed coronary atherosclerosis without plaque rupture.
- Coronary artery spasm.
- Coronary microvascular dysfunction (including endothelial dysfunction, smooth muscle cell dysfunction, and dysregulation of sympathetic innervation).
- Coronary embolism.
- Coronary artery dissection with or without intramural hematoma.
- Reduced oxygen supply:
Severe bradyarrhythmia.
Respiratory failure with severe hypoxemia.
Severe anemia.
Hypotension/shock.
- Severe bradyarrhythmia.
- Respiratory failure with severe hypoxemia.
- Severe anemia.
- Hypotension/shock.
- Increased myocardial oxygen demand:
Sustained tachyarrhythmia.
Severe hypertension with or without left ventricular hypertrophy.
- Sustained tachyarrhythmia.
- Severe hypertension with or without left ventricular hypertrophy.
- Type 3
Patients who suffer cardiac death, with symptoms suggestive of myocardial ischemia accompanied by presumed new ischemic ECG changes or ventricular fibrillation, but die before blood samples for biomarkers can be obtained, or before increases in cardiac biomarkers can be identified, or MI is detected by autopsy examination.
- Patients who suffer cardiac death, with symptoms suggestive of myocardial ischemia accompanied by presumed new ischemic ECG changes or ventricular fibrillation, but die before blood samples for biomarkers can be obtained, or before increases in cardiac biomarkers can be identified, or MI is detected by autopsy examination.
- Type 4a
Related to percutaneous coronary intervention (PCI), with increased cTn values >5 times the 99th percentile URL and new myocardial ischemia evidenced by ECG, imaging or complications leading to reduced coronary blood flow.
- Related to percutaneous coronary intervention (PCI), with increased cTn values >5 times the 99th percentile URL and new myocardial ischemia evidenced by ECG, imaging or complications leading to reduced coronary blood flow.
- Type 4b
Stent/scaffold thrombosis.
Classified by elapsed time since stent/scaffold implantation:
Acute: 024 hours.
Subacute: >24 hours to 30 days.
Late: > 30 days to 1 year.
Very late: >1 year.
- Stent/scaffold thrombosis.
- Classified by elapsed time since stent/scaffold implantation:
Acute: 024 hours.
Subacute: >24 hours to 30 days.
Late: > 30 days to 1 year.
Very late: >1 year.
- Acute: 024 hours.
- Subacute: >24 hours to 30 days.
- Late: > 30 days to 1 year.
- Very late: >1 year.
- Type 4c
In-stent restenosis or restenosis following balloon angioplasty in the infarct territory.
No other culprit lesion or thrombus can be identified.
- In-stent restenosis or restenosis following balloon angioplasty in the infarct territory.
- No other culprit lesion or thrombus can be identified.
- Type 5
Related to coronary artery bypass grafting (CABG), with increased cTn values >10 times 99th percentile URL and new myocardial ischemia or new loss of myocardial viability.
- Related to coronary artery bypass grafting (CABG), with increased cTn values >10 times 99th percentile URL and new myocardial ischemia or new loss of myocardial viability.