The following is a summary of the key points in the “Fourth Universal Definition of Myocardial Infarction (2018)” published in the November 2018 issue of Circulation. Full text of the article can be downloaded here (PubMed.) The document represents a collaborative effort by the following organizations:

  • European Society of Cardiology(ESC)
  • American College of Cardiology (ACC)
  • American Heart Association(AHA)
  • World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction

Definitions:

  • Myocardial Infarction : Presence of myocardial injury (elevated troponin) in the setting of evidence of acute myocardial ischemia.
  • Myocardial Injury : Isolated elevated troponin
  • Acute Myocardial Injury : Rising or falling troponin

Causes of Myocardial Injury: (Reasons for troponin elevation- Table 1)

  • Myocardial injury related to acute myocardial ischemia
    • Atherosclerotic plaque disruption with thrombosis
  • Myocardial injury related to acute myocardial ischemia because of oxygen supply/demand imbalance 
    • Coronary artery spasm, microvascular dysfunction
    • Coronary embolism
    • Coronary artery dissection
    • Sustained bradyarrhythmia
    • Hypotension or shock
    • Respiratory failure
    • Severe anemia Increased myocardial oxygen demand, eg,
    • Sustained tachyarrhythmia
    • Severe hypertension with or without left ventricular hypertrophy
  • Other causes of myocardial injury
    • Heart failure
    • Myocarditis
    • Cardiomyopathy (any type)
    • Takotsubo syndrome
    • Coronary revascularization procedure
    • Cardiac procedure other than revascularization
    • Catheter ablation
    • Defibrillator shocks
    • Cardiac contusion
    • Sepsis, infectious disease
    • Chronic kidney disease
    • Stroke, subarachnoid hemorrhage
    • Pulmonary embolism, pulmonary hypertension
    • Infiltrative diseases, eg, amyloidosis, sarcoidosis
    • Chemotherapeutic agents
    • Critically ill patients
    • Strenuous exercise

Types of Myocardial Infarction:

  1. Type 1 MI – Troponin elevation  with at least 1 of the following:
    • Symptoms of acute myocardial ischemia;
    • New ischemic ECG changes;
    • Development of pathological Q waves;
    • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology;
    • Identification of a coronary thrombus by angiography including intracoronary imaging or by autopsy.*
  2. Type 2 MI – Troponin elevation and imbalance between myocardial oxygen supply and demand unrelated to acute coronary atherothrombosis, requiring at least 1 of the following:
    • Symptoms of acute myocardial ischemia;
    • New ischemic ECG changes;
    • Development of pathological Q waves;
    • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
  3. Type 3 MI – “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.”
  4. Type 4 MI – Cardiac procedural myocardial injury with troponin elevation, or increase of 20% above baseline if chronically elevated.  
    • 4a- < 48 hrs post post procedure
    • 4b-  stent/scaffold thrombosis documented by angiography or autopsy 
    • 4c- in-stent restenosis, or restenosis following balloon angioplasty in the infarct territory. 
  5. Type 5 MI- CABG-related MI with troponin elevation or increase >20% if chronically elevated. In addition, 1 of the following elements is required:
    • Development of new pathological Q waves*;
    • Angiographic documented new graft occlusion or new native coronary artery occlusion;
    • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.
    • Isolated development of new pathological Q waves meets the type 5 MI criteria if cTn values are elevated and rising but <10 times the 99th percentile URL
  6. Silent/Unrecognized MI – Any 1 of the following criteria meets the diagnosis for prior or silent/unrecognized MI:
    • Pathological Q waves as described in Table 3, with or without symptoms, in the absence of nonischemic causes;
    • Imaging evidence of loss of viable myocardium in a pattern consistent with ischemic etiology;
    • Pathological findings of a prior MI.

ECG Suggestive of Acute Myocardial Ischemia (In the Absence of LVH and BBB) 

  • New ST-elevation
    • ST-elevation at the J-point in 2 contiguous leads with the cut-point: ≥1 mm in all leads except V2-V3 (or >1mm from prior baseline)
    • ST elevation V2 –V3
      • ≥2 mm in men ≥40 years
      • ≥2.5 mm in men <40 years
      • ≥1.5 mm in women regardless of age.
  • ST-depression and T wave changes
    • New horizontal or downsloping ST-depression ≥0.5 mm in 2 contiguous leads
    • T wave inversion >1 mm in 2 contiguous leads with prominent R wave or R/S ratio >1.
  • Specific to LAD occlusion :
    • Tall symmetrical T waves in the precordial leads with up-sloping ST-segment depression >1 mm at the J-point. (DeWinter)
    • ST-segment elevation (>1 mm) in lead aVR
    • Symmetrical, often deep (>2 mm), T wave inversions in the anterior precordial leads (Wellens)
  • ST-elevation in lead aVR >1 mm may accompany anterior or inferior STEMI, and is associated with increased 30-day mortality in patients with acute MI
  • “In patients with LBBB, ST-segment elevation ≥1 mm concordant with the QRS complex in any lead may be an indicator of acute myocardial ischemia. Similar findings can be useful in detecting ECG evidence for acute myocardial ischemia in patients with right ventricular paced rhythms”

ECG Changes Associated With Prior Myocardial Infarction (In the Absence of Left Ventricular Hypertrophy and Left Bundle Branch Block) 

  • Any Q wave in leads V2 –V3 >0.02 s or QS complex in leads V2 –V3 .
  • Q wave ≥0.03 s and ≥1 mm deep or QS complex in leads I, II, aVL, aVF or V4 –V6 in any 2 leads of a contiguous lead grouping (I, aVL; V1 –V6 ; II, III, aVF).*
  • R wave >0.04 s in V1 –V2 and R/S >1 with a concordant positive T wave in absence of conduction defect.

Takotsubo Syndrome

  • Is a STEMI mimic
  • Found in 1% to 2% of patients presenting with suspected STEMI.
  • Often triggered by intense emotional or physical stresses.
  • Over 90% of patients are postmenopausal women.
  • Cardiovascular complications occur in 50% of patients.
  • Inpatient mortality is similar to STEMI (4% to 5%) due to
    • cardiogenic shockventricularrupturemalignant arrhythmias. 
  • ST-segment elevation is frequent (44%), but the extent is usually widespread across the lateral and precordial leads, beyond that of a single coronary artery distribution. 
  • ST-segment depression occurs in <10% of patients
  • After 12 to 24 hours, deep, symmetric T wave inversion and QTc prolongation are typically observed.
  • Troponin elevation is usually transient (>95% of cases) and typically modest.

Takotsubo syndrome “should be suspected when the clinical manifestations and ECG abnormalities are out of proportion to the degree of (troponin) elevation … and when the distribution of the LV wall motion abnormalities does not correlate with a single coronary artery distribution. However, coronary angiography and ventriculography are often needed to secure the diagnosis. In most cases, the coronary arteries are angiographically normal, and where CAD is present (15% cases) it is not sufficient to explain the observed pattern of regional wall motion abnormalities.”

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