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STEMI Infarction - ECG

ST Elevation Myocardial Infarction, STEMI Heart Attack

Infarct Nomenclature

• Myocardial infarction is myocardial necrosis
• Releases troponin
  
  
• According to ECG, we differentiate between 2 types of infarctions
• STEMI infarction
• NSTEMI infarction
  
  

STEMI Infarction

• Occurs due to occlusion
• Necrosis is:
• Subepicardial
• Later transmural
• On ECG, there are ST elevations

NSTEMI Infarction

• Occurs due to stenosis
• Necrosis is:
• Subendocardial
• Not transmural
• On ECG, there are ST depressions

• The following nomenclature is obsolete
• It is not used because the extent of myocardial necrosis does not always correlate with the ECG findings:
• Transmural Infarction
• Is an obsolete term for STEMI
• STEMI usually results in transmural necrosis, but this is not always the case
• Q Infarction
• Is an obsolete term for STEMI
• STEMI usually creates transmural necrosis and a pathological Q wave, but this is not always the case
• Non-Transmural Infarction
• Is an obsolete term for NSTEMI
• NSTEMI usually results in non-transmural necrosis, but this is not always the case
• Non-Q Infarction
• Is an obsolete term for NSTEMI
• NSTEMI usually results in non-transmural necrosis and does not produce a pathological Q wave, but this is not always the case

Troponin and Infarction

• Troponin (TnT) is the main laboratory marker for infarction
• It is specific to myocardium
• It is released into the blood during an infarction (due to cardiomyocyte breakdown)
• It is not released during myocardial ischemia
• Other enzymes (CK, AST, LDH) are not as specific
• Because they are also found in other organs
• Troponin levels
• Start to rise 2-4 hours after occlusion
• Peak at around 12-24 hours
• Remain elevated for about 7 days

ST Elevations (STE) in STEMI

• STEMI is characterized by
• Convex STE
• Horizontal STE
• Rarely, ST elevations (STE) can be:
• Descending
• Ascending
• STEMI (subepicardial or transmural ischemia)
• Never creates concave (smiling) STE elevations

Dynamics of ST Elevations in STEMI

Classification of STEMI by Stage

• In clinical practice, STEMI is classified into 3 stages based on the EKG findings:
• Acute STEMI
• Characterized by ST elevations without Q waves
• Duration: minutes - hours
• Subacute STEMI
• Characterized by ST elevations and Q waves
• Duration: hours - days
• Old STEMI
• Characterized by Q waves without ST elevations
• Duration: > week

ECG and Size of ST Elevations in STEMI

• ST elevations must be present in at least 2 adjacent leads
• Men ≥ 40 years:
• ≥ 2mm (V2-V3)
• ≥ 1mm in other leads
• Men < 40 years:
• ≥ 2.5mm (V2-V3)
• ≥ 1mm in other leads
• Women (regardless of age)
• ≥ 1.5mm (V2-V3)
• ≥ 1mm in other leads
• Men and Women (V4R, V3R)
• ≥ 0.5mm
• Men < 30 years ≥ 1mm
• Men and Women (V7-V9)
• ≥ 0.5mm

Reciprocal Changes and STEMI

• Reciprocal changes are caused by only STEMI infarction (not NSTEMI)
• STEMI shows ST elevations in at least 2 adjacent leads
• Towards which the ischemic vector is directed
• Reciprocal changes are
• ST depressions in opposite leads
• Because the vector is directed away from opposite leads
• Opposite lead
• Looks at the vector from the exact opposite side (180°)
• However, EKG only has 12 leads
• Therefore, the ischemic vector rarely points precisely
• To a specific lead
• From a specific lead
• No EKG lead has an exact (180°) opposite lead
• Leads are incompletely opposite
• Posterior wall infarction
• Shows only reciprocal ST depressions (V1-3) on standard EKG
• Then leads V7-9 are placed
• The heart has a specific shape (it is neither a sphere nor a cube)
• You need to imagine the heart in 3D space along with the EKG leads
• Reciprocal changes are therefore seen in incompletely opposite leads
• If a patient has STEMI and ST depressions in opposite leads
• These are reciprocal ST depressions
• It is not a second subendocardial ischemia
• Subendocardial ischemia alone causes ST depressions

STEMI by Location

• Infarction occurs in the myocardium behind the occlusion
• The infarct zone is "viewed" by EKG leads
• In which ST elevations occur
• Only STEMI infarction can be localized, not NSTEMI
• Standard 12-lead EKG does not provide a view
• Of all parts of the myocardium
• In case of suspected infarction
• Right ventricular infarction is evaluated with V3R-V6R leads
• Posterior wall infarction is evaluated with V7-V9 leads
  
  
• Basic coronary artery supply:
• RCA (Right Coronary Artery)
• LCA (Left Coronary Artery)
• LAD (Left Anterior Descending artery)
• LCx (Left Circumflex artery)
• PDA (Posterior Descending artery)

Hyperacute Anterior STEMI

• Sinus Rhythm
• Hyperacute high T waves (V2-V4)
• Persist for only several minutes after occlusion
• The patient later exhibited typical STEMI EKG dynamics
• Laboratory tests showed high troponin
• This is a hyperacute anterior STEMI

Pseudonormalization - Hyperacute STEMI

• This is an EKG from a previous patient
• The patient experienced severe angina
• T waves and ST segment are normal
• The patient had an LAD occlusion
• Resulted in a hyperacute anterior STEMI
• Hyperacute T waves developed in the setting of previously negative T waves
• Thus, T waves appear normal
• Later, the patient had elevated troponin and STEMI EKG dynamics

Subacute Anterior STEMI

• ST elevations in the anterior leads (V2-V5)
• Pathological Q wave (V2-V3) - indicates the subacute stage
• It is due to occlusion of the LAD (left anterior descending artery)
• This is a subacute anterior STEMI
• Duration hours - days

Subacute Inferior and Lateral Wall STEMI

• ST elevations in the inferior and lateral leads (II, III, aVF, V5-V6)
• Pathological Q waves (II, III, aVF)
• The patient had an occlusion of the dominant LCx (ramus circumflexus)
• ST elevation II > III
• This is a subacute inferior and lateral - left wall STEMI
• Duration hours - days