Types of Myocardial Infarction (MI)

Part 1: Clinical Classification (Universal Definition - Types 1-5)

Type 1 - Spontaneous MI (Atherothrombotic)

• The patient usually has underlying severe coronary artery disease (CAD), though occasionally nonobstructive or no CAD is found.
• This is the classic "heart attack" most people envision.

Type 2 - MI Secondary to Ischemic Imbalance (Non-Atherothrombotic)

• Coronary endothelial dysfunction
• Coronary artery spasm (vasospastic/Prinzmetal's angina)
• Coronary embolism
• Tachyarrhythmia or bradyarrhythmia
• Anemia, respiratory failure
• Hypotension or severe hypertension with/without LV hypertrophy

Type 3 - MI Resulting in Death Before Biomarkers Available

Type 4a - MI Related to Percutaneous Coronary Intervention (PCI)

• Elevation of cardiac troponin (cTn) >5× the 99th percentile URL in patients with normal baseline
• OR a rise >20% if baseline cTn is elevated and stable/falling
• Plus at least one of: new ischemic ECG changes, new pathologic Q waves, imaging evidence of new loss of viable myocardium, or angiographic procedural complication

Type 4b - MI Related to Stent Thrombosis

Type 4c - MI Related to Restenosis

Type 5 - MI Related to Coronary Artery Bypass Grafting (CABG)

Part 2: Anatomopathological Classification

Based on Depth of Necrosis

1. Transmural MI

• Definition: Necrosis involves the full thickness of the ventricular wall (>50% of wall thickness)
• Cause: Permanent epicardial vessel occlusion from atherosclerosis + acute thrombosis (Type 1 MI mechanism)
• Nearly all involve at least part of the LV and/or interventricular septum
• 15-30% involving the posterior wall also extend to the RV
• ECG: Typically produces ST elevation (STEMI) and develops pathological Q waves
• Classic pattern: Q-wave MI

2. Subendocardial (Nontransmural) MI

• Definition: Necrosis limited to the inner third of the myocardium (endocardium + intramural myocardium), without reaching the epicardium
• Cause: Plaque disruption followed by thrombus that is lysed before necrosis becomes transmural; or global hypoperfusion (the subendocardium is most vulnerable to hypoxia because it has the highest wall stress and the lowest perfusion pressure)
• Subtypes:
  • Regional subendocardial - from partial/transient coronary obstruction
  • Circumferential subendocardial - from global hypotension superimposed on fixed 3-vessel disease
• ECG: Usually no ST elevation, no Q waves - but this is not absolute (see below)

3. Microscopic Infarcts (Microinfarcts)

• Occur with small-vessel occlusions - vasculitis, emboli (from valve vegetations or mural thrombi), vasospasm from catecholamines (cocaine, pheochromocytoma)
• May show no diagnostic ECG changes
• (Robbins & Kumar Basic Pathology, p. 355-356)

Part 3: ECG-Based Classification

STEMI (ST-Elevation MI)

• ST-segment elevation in 2+ contiguous leads indicates acute transmural ischemia
• Signifies complete, persistent occlusion requiring emergent reperfusion (PCI or thrombolytics)
• Usually evolves into Q-wave MI if not reperfused

NSTEMI (Non-ST-Elevation MI)

• No ST elevation on presenting ECG
• Biomarkers (troponin) ARE elevated - distinguishes it from unstable angina (UA), which has no biomarker rise
• Usually subendocardial in depth
• May show ST depression, T-wave inversions, or even normal ECG

Q-wave MI vs. Non-Q-wave MI

"Abnormal Q waves were once considered markers of transmural myocardial infarction, whereas subendocardial infarcts were thought not to produce Q waves. However, transmural infarcts may occur without Q waves, and subendocardial (non-transmural) infarcts may be associated with Q waves."

(Harrison's Principles of Internal Medicine 22E)

Part 4: By Location (Regional Anatomy)

Part 5: Gross Pathology & Temporal Sequence

Part 6: Wellens Syndrome (Special ECG Variant)

Quick Summary Table

• STEMI ≈ transmural ≈ Q-wave MI (statistically, but not always)
• NSTEMI ≈ subendocardial ≈ non-Q-wave MI (again, not a perfect correlation)
• Type 2 MI is increasingly recognized in hospitalized patients with anemia, sepsis, or tachyarrhythmia - management differs from Type 1 (anticoagulation/PCI may not be appropriate)
• The subendocardium is always the most vulnerable zone because it has the highest wall tension, lowest perfusion pressure, and longest diffusion distance from epicardial vessels

ECG Interpretation

Patient Details (from printout)

• Patient: Mrjuna Khatun
• Date: 19/06/2026, 17:10-48
• Hospital: Chanchal Sub-Division & S.S. Hospital, Chanchal, Malda (Govt. of West Bengal)
• Machine: ClarityMed ECG-100C

Machine-Measured Parameters

Systematic Interpretation

1. Rate & Rhythm

• Rate: 66 bpm - Normal sinus rate
• Rhythm: Regular rhythm, sinus P waves present (positive in I, II, aVF; negative in aVR)
• Impression: Normal sinus rhythm

2. Axis

• P axis: 42° - Normal
• QRS axis: 69° - Normal (0° to +90°)
• T axis: 32° - Normal

3. Intervals

• PR interval: 136 ms - Normal (no heart block, no pre-excitation)
• QRS duration: 72 ms - Normal (no bundle branch block)
• QTc: 449 ms - Borderline prolonged (upper limit of normal for females is 440-460 ms; this is at the borderline)

4. P Waves

• Normal morphology and axis - no evidence of atrial enlargement

5. QRS Complexes

• QRS duration normal (72 ms) - no BBB
• Normal QRS axis (69°)
• Looking at the precordial leads: there appears to be poor R-wave progression in V1-V3, with small R waves in early precordial leads

6. ST Segments & T Waves

• Leads I, II, III, aVF, aVL: ST segments appear isoelectric (no clear elevation or depression)
• T waves appear upright in I, II, aVF

• V1-V4: There appear to be T-wave changes - the T waves in V1-V3 appear flattened or inverted, which is a notable finding
• V5-V6: T waves appear relatively upright

7. Q Waves

• No pathological Q waves (>25% of R wave height or >40 ms wide) are clearly visible in this tracing

Key Findings & Impression

Clinical Interpretation

1. Borderline QTc prolongation (449 ms): This is at the upper limit of normal for a female patient. Causes to consider include electrolyte imbalance (hypokalemia, hypomagnesemia), medications, and rarely congenital long QT syndrome. It warrants checking electrolytes.
2. T-wave flattening in anterior leads (V1-V3): This is a non-specific finding but can indicate:
   • Non-specific T-wave changes (most common, benign)
   • Early or resolving anterior ischemia
   • Right ventricular strain
   • Electrolyte disturbance

• Acute STEMI (no ST elevation)
• Acute NSTEMI pattern (no ST depression)
• Pathological Q waves (no completed MI pattern)
• Bundle branch block
• Complete AV block

Recommendation

This ECG does not show acute MI. However, given the anterior T-wave changes and borderline QTc:

• Correlate with the patient's symptoms (chest pain, dyspnea, palpitations?)
• Check serum electrolytes (K⁺, Mg²⁺, Ca²⁺)
• Check medications (any QT-prolonging drugs?)
• If symptomatic, serial ECGs and troponin are warranted to rule out NSTEMI

⚠️ This is an AI-assisted interpretation for educational purposes. Final clinical decisions must be made by the treating physician with full clinical context.