Table 1
Comparison of the Fourth and Fifth Universal Definitions of Myocardial Infarction.
| FOURTH UDMI | FIFTH UDMI—WHAT’S NEW | RATIONALE FOR CHANGE |
|---|---|---|
| Numerical classification of myocardial infarction: types 1, 2, 3, 4a, 4b, 4c, 5. | Clinical classification of myocardial infarction; primary, secondary, or procedure related. | To reflect underlying pathophysiology, align with clinical evaluation, and enable consistent application. |
| Type 1 myocardial infarction Restricted to atherothrombosis. | Primary myocardial infarction Includes all acute coronary pathologies: atherothrombosis; spontaneous coronary artery dissection; coronary embolism; vasospasm; and restenosis, stent thrombosis, or graft failure >30 days from procedure. | Prioritizes sensitivity to avoid missing any primary acute coronary pathology. Promotes coronary angiography and adjunctive testing to confirm diagnosis and identify underlying acute coronary pathology with new diagnostic codes for each mechanism. Reclassifies late stent/graft failure as de novo disease, not a procedure-related complication. |
| Type 2 myocardial infarction Myocardial oxygen supply–demand imbalance due to either:
or
| Secondary myocardial infarction Myocardial oxygen supply–demand imbalance due to an alternative acute condition: and
and/or
| Prioritize specificity to differentiate myocardial infarction from acute myocardial injury in conditions resulting in oxygen supply–demand imbalance. Objective diagnostic criteria to allow consistent application in practice and identify patients in whom the diagnosis has treatment implications. |
| Type 3 myocardial infarction Cardiac death where myocardial infarction is the likely cause, but death occurs before diagnostic testing is performed. | Term removed. Where myocardial infarction is the likely cause of death, clinical classification (primary, secondary, or procedure-related) should be applied, based on setting or post-mortem findings. | Limited use in clinical practice. |
| Type 4 and 5 myocardial infarction Type 4a myocardial infarction: cardiac troponin concentration >5 times the 99th percentile with myocardial ischaemia, imaging evidence of new loss of viable myocardium, or angiographic evidence of a procedural complication within 48 h. Type 4b due to stent thrombosis and type 4c due to stent restenosis, at any time after the procedure. Type 5 myocardial infarction: coronary artery bypass graft-related; cardiac troponin >10 times the 99th percentile, with new pathological Q waves, imaging evidence of new loss of viable myocardium, or angiographic evidence of a graft occlusion within 48 h. | Procedure-related myocardial infarction Coronary complication within 30 days of a cardiac procedure resulting in acute myocardial injury with one or more features. Both features are required when the complication arises during the procedure or in the setting of acute myocardial infarction.
| Prioritizes specificity to ensure the diagnosis is clinically meaningful, with objective cardiac imaging criteria. Diagnostic criteria the same for all cardiac procedures to enable meaningful comparisons. Excludes late stent/graft failure as a procedural complication as it typically reflects de novo disease. |
[i] UDMI, universal definition of myocardial infarction.
Figure 1
Central illustration. Fifth Universal Definition of Myocardial Infarction. Myocardial infarction can occur in three clinical settings: spontaneously due to a primary acute coronary pathology, secondary to an acute condition, or following a cardiac procedure.
Table 2
Mechanisms of acute myocardial injury.
| MECHANISM | CONDITION |
|---|---|
| Ischaemia | Myocardial infarction |
| Inflammation | Myocarditis (autoimmune, infectious, toxic) |
| Heart transplant rejection | |
| Cytokine mediated in sepsis | |
| Haemodynamic stress | Supply–demand imbalancea |
| Tachy- or brady-arrhythmia | |
| Acute heart failure | |
| Acute pulmonary embolism | |
| Malignant hypertension | |
| Physiological stress | Strenuous exercise |
| Catecholamine stress | Takotsubo syndrome |
| Subarachnoid haemorrhage | |
| Stroke | |
| Epileptic seizures | |
| Phaeochromocytoma | |
| Toxicity | Anthracyclines |
| ErbB (erythroblastic oncogene B)-targeted therapies | |
| Tyrosine kinase inhibitors | |
| Immune checkpoint inhibitors | |
| Radiation induced | |
| Trauma | Electrical cardioversion |
| Percutaneous coronary or structural intervention | |
| Catheter ablation or device implantation | |
| Cardiac surgery | |
| Cardiac contusion |
[i] aAny acute condition that results in a myocardial oxygen imbalance with reduced supply (hypoxia, anaemia, hypotension) and/or increased demand (tachycardia, hypertension).
Table 3
Mechanisms of chronic myocardial injury.
| AETIOLOGY | CONDITION |
|---|---|
| Ischaemia | Chronic coronary syndrome |
| Ischaemic cardiomyopathy | |
| Other cardiomyopathies | Hypertrophic cardiomyopathy |
| Hypertensive cardiomyopathy | |
| Dilated cardiomyopathy | |
| Chronic inflammatory cardiomyopathy | |
| Restrictive cardiomyopathy | |
| Infiltrative cardiomyopathy | |
| Uraemic cardiomyopathy in chronic kidney disease | |
| Haemodynamic stress | Chronic heart failure |
| Systemic hypertension | |
| Pulmonary hypertension | |
| Structural | Valvular heart disease |
| Congenital heart disease | |
| Cardiac tumour |
Figure 2
Diagnostic pathway for possible primary myocardial infarction. NSTEMI, non-ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction. aOr other electrocardiographic changes indicative of possible acute coronary occlusion (Figure 9). bFor patients with a working diagnosis of STEMI, acute myocardial injury is necessary to confirm the final diagnosis. cRise and/or fall of cardiac troponin I or T values and with at least one value above the sex-specific 99th percentile upper reference limit on serial testing. dWhere coronary angiography and cardiac imaging are not available or are not considered appropriate, a final diagnosis of primary myocardial infarction can be assigned based on an evaluation that considers biomarkers, electrocardiography, and clinical criteria alone without additional confirmatory features and the codes BA41.09 or BA41.19 applied as the aetiology is unknown. eThis includes patients with a working diagnosis of myocardial injury with non-obstructive coronary arteries (MINOCA).
Figure 3
Primary myocardial infarction due to acute coronary pathology.
Table 4
ICD-11 codes for the classification of myocardial infarction.
| FINAL DIAGNOSIS | ICD-11 | SIXTH DIGIT STEM CODE/EXTENSION CODE |
|---|---|---|
| Acute ST-segment elevation myocardial infarction (STEMI)a | BA41.0 | Primary myocardial infarction BA41._1 atherothrombosis BA41._2 spontaneous coronary artery dissection BA41._3 coronary embolism BA41._4 coronary vasospasm BA41._5 restenosis >30 days from procedure BA41._6 stent thrombosis >30 days from procedure BA41._7 graft failure >30 days from procedure BA41._8 undetermined aetiology BA41._9 unknown aetiology (no coronary imaging) Secondary myocardial infarction BA41._A/ICD-11 code for alternative acute condition Procedure-related myocardial infarction BA41._B due to a complication of any percutaneous cardiac procedure within 30 days BA41._C due to a complication of any open cardiac surgical procedure within 30 days |
| Acute non-ST-segment elevation myocardial infarction (NSTEMI) | BA41.1 | |
| Other diagnoses | ||
| Unstable angina | BA40 | |
| Unspecified myocardial infarction | BA41.Z | Sudden death without evaluationb |
| Unrecognized myocardial infarction | BA50 | |
Figure 4
Diagnostic pathway for possible secondary myocardial infarction. aMyocardial oxygen supply–demand imbalance can occur as a result of increased demand (e.g. tachycardia or severe hypertension) and/or reduced supply (e.g. hypotension, hypoxia, or anaemia). bRise and/or fall of cardiac troponin values and with at least one value above the sex-specific 99th percentile upper reference limit on serial testing. cIf primary myocardial infarction is an unlikely differential diagnosis, then non-invasive computed tomography (CT) coronary angiography following recovery from acute illness may be considered. dObstructive coronary artery disease is defined as ≥70% stenosis in an epicardial vessel by angiography or ≥50% stenosis that is flow-limiting on physiological assessment.
Figure 5
Secondary myocardial infarction due to supply–demand imbalance.
Figure 6
Diagnostic pathway for possible procedure-related myocardial infarction. aRising cardiac troponin values with at least one value above the sex-specific 99th percentile AND pre-procedural value (if known) on serial testing. bImmediately following a procedure, the diagnosis is more likely with higher cardiac biomarker levels that have increased from pre-procedural levels and continue to rise at 6 h (e.g. >5 times upper reference limit [URL] for intervention) and 24 h (e.g. >35 times URL for surgery).
Figure 7
Procedure-related myocardial infarction due to a complication of cardiac surgery or intervention.
Figure 8
Diagnostic pathway for possible primary myocardial infarction following sudden death. VF, ventricular fibrillation. Following a sudden death in the community without clinical evaluation, the diagnosis of primary myocardial infarction can be considered. Clinical features such as a history of coronary artery disease, chest pain prior to death, or documented VF in the absence of known cardiomyopathy or channelopathies make the diagnosis more likely, but in the absence of an electrocardiogram or post-mortem investigations the diagnosis is uncertain, and the ICD-11 code of unspecified myocardial infarction (BA41.Z) should be applied to recognize this. Where investigations are incomplete with no biomarker testing or coronary imaging, the diagnosis of myocardial infarction of uncertain aetiology is applied, but where there is uncertainty post-mortem imaging or an autopsy is required to confirm the diagnosis and identify the underlying acute coronary pathology.
Figure 9
Electrocardiographic features of acute coronary occlusion. The electrocardiographic changes associated with primary myocardial infarction due to acute coronary occlusion depend on the time of presentation from the onset of persistent symptoms. The diagnosis of ST-segment elevation myocardial infarction can be made in patients with alternative electrocardiographic changes that are suggestive of acute coronary occlusion or in those who present late where the ST-segment changes have evolved.
Table 5
Electrocardiographic findings of myocardial ischaemia or infarction.
| FEATURE | DESCRIPTION OF ELECTROCARDIOGRAPHIC FINDINGS OF MYOCARDIAL ISCHAEMIA OR INFARCTION |
|---|---|
| ST-segment elevation | New ST-segment elevation at the J-point in two contiguous leads: ≥1 mm in all leads other than leads V2–V3 where the following apply: ≥2.5 mm in males >40 years, ≥2 mm in males ≥40 years, or ≥1.5 mm in females regardless of age, in the absence of bundle branch block and/or left ventricular hypertrophy |
| ST-segment depression | New horizontal or down sloping ST-segment depression ≥0.5 mm at the J-point in two or more contiguous leads |
| Hyperacute T waves | Symmetrical, broad T waves disproportionately large to the preceding QRS complex in two contiguous leads |
| de Winter T waves | Tall, prominent, symmetrical T waves with upsloping ST segment depression in the precordial leads |
| Biphasic T waves | Initial positive deflection followed by a negative deflection |
| T-wave inversion | New or dynamic T-wave inversion ≥1 mm in two contiguous leads |
| Wellens syndrome | Biphasic or deeply inverted T waves in leads V2 and V3 |
| Pathologic Q waves | Q-wave duration ≥40 ms and/or a depth of ≥25% of the R wave in two contiguous leads |
| Sgarbossa criteria | In the presence of left bundle branch block or ventricular pacing; ST-segment elevation ≥1 mm concordant (in the same direction) with the QRS complex; ST-segment depression ≥1 mm in lead V1, V2, or V3; ST-segment elevation ≥5 mm not concordant with the QRS complex |
| Ventricular arrhythmia | Ventricular fibrillation or ventricular tachycardia |
Figure 10
Rise and fall in cardiac troponin over time from symptom onset. Following the onset of acute myocardial infarction, changes in cardiac troponin vary over time: (A) Small absolute changes in cardiac troponin occur early after symptom onset (<3 h). (B) Larger absolute changes in cardiac troponin occur later after symptom onset. (C) Minimal rise and fall in cardiac troponin may occur around 12 to 24 h from symptom onset. (D) Larger fall in cardiac troponin may occur after it has peaked (12 to 24 h from symptom onset). (E) Pattern may mimic chronic myocardial injury if presentation days after symptom onset. (F) Cardiac troponin may take weeks to return to normal after myocardial infarction and some patients may develop chronic myocardial injury following myocardial infarction.
Figure 11
Stages of primary myocardial infarction by cardiac magnetic resonance imaging. LGE, late gadolinium enhancement. Each stage of myocardial injury is progressive and is discernible from aggregate evidence derived from T2 maps (colour bar provided), LGE, and T2*-weighted (T2*w) short-axis cardiac magnetic resonance images along each row. Stage 1 is marked by oedema only (high signal on T2 map), absence of myocardial necrosis (lack of signal enhancement on LGE image), or myocardial haemorrhage (absence of low signal on T2*w images). Stage 2 demonstrates both myocardial necrosis (high signal on LGE image) and oedema (high signal on T2 map) but absence of persistent microvascular obstruction (absence of low signal within the zone of LGE image) or myocardial haemorrhage. Stage 3 highlights the presence of microvascular obstruction (presence of low signal within the zone of high signal on LGE image) along with myocardial necrosis and oedema. Note that myocardial haemorrhage is also absent at Stage 3 as evidenced by lack of low signal within the zone of infarction on T2*w image. Stage 4 is characterized by myocardial haemorrhage (low signal within the zone of high signal in the T2*w image), along with microvascular obstruction, myocardial necrosis, and oedema. High signal (brighter than surrounding tissue) and low signal (darker than surrounding tissue). Black arrowheads point to high signal on T2 maps, white arrow heads point to high signal on LGE, and blue arrow heads point to low signal on T2*-w image. Note that low signal zones on Stage 3 and Stage 4 within LGE are demarcated by contoured zones within high signal zones in LGE. Red and green contours on LGE and T2w images are endocardial and epicardial contours segmenting the left ventricular myocardium. Adapted from Kumar et al. with permission (232).
Figure 12
Role of cardiac magnetic resonance imaging in possible or confirmed primary myocardial infarction. Illustration of common cardiac magnetic resonance imaging findings in patients with possible or confirmed primary myocardial infarction. (Top, left) Acute myocarditis with myocardial oedema of the basal inferior and inferolateral wall (white arrow, left panel) with corresponding epicardial late enhancement (white arrow, right panel). (Top, middle) Focal myocardial infarction with transmural oedema of the mid anterolateral wall (white arrow, left panel) and corresponding transmural late enhancement (white arrow, right panel). (Top, right) Takotsubo syndrome with transmural oedema of the apical segments (white arrows, left panel), corresponding to the area of akinesia and in the absence of any late myocardial enhancement (right panel). (Bottom, left) Transmural myocardial infarction in the left circumflex territory with myocardial oedema of the lateral wall (white arrow, left panel) and corresponding transmural late enhancement with a large dark or low signal core representing microvascular obstruction (white arrow, right panel). (Bottom, middle) Transmural myocardial infarction in the left anterior descending artery territory with left ventricular thrombus (white arrow, both panels). (Bottom, right) Transmural myocardial infarction with contained rupture of the basal inferoseptal wall with myocardial oedema of the acutely injured wall (white arrow, left panel) and corresponding transmural late myocardial enhancement (white arrow, right panel).