Why is the ST segment elevated during myocardial infarction?

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Why ST Segment is Elevated During Myocardial Infarction

ST segment elevation during myocardial infarction represents electrical gradients caused by transmural ischemia resulting from coronary artery occlusion, reflecting severe injury to the myocardium that creates voltage differences between damaged and healthy tissue. 1

Pathophysiological Mechanism

The ST segment elevation seen during acute myocardial infarction occurs due to several key processes:

  1. Transmural Ischemia:

    • Complete coronary artery occlusion (typically from thrombus formation) causes full-thickness myocardial ischemia
    • This transmural involvement is critical for producing ST elevation 1
  2. Electrical Gradient Development:

    • Ischemic myocardium becomes electrically unresponsive
    • Voltage differences develop between the injured (electrically silent) and healthy myocardium
    • Current flows between damaged and normal zones create the ST vector 1
  3. Cellular Ionic Changes:

    • Ischemia causes:
      • Intracellular K+ loss
      • Na+ and Ca2+ accumulation
      • Cell membrane depolarization
    • These ionic shifts alter the action potential and create the characteristic ST elevation 1

Electrocardiographic Manifestations

The earliest manifestations of myocardial ischemia that may evolve to infarction include:

  • Hyperacute T-waves: Increased amplitude with prominent symmetrical T-waves in contiguous leads often precede ST elevation 1

  • ST Segment Elevation:

    • Represents the hallmark ECG finding in STEMI
    • Must be present in at least two contiguous leads 1
    • Specific voltage criteria:
      • ≥1 mm elevation in most leads
      • ≥2 mm in men and ≥1.5 mm in women for leads V2-V3 2
  • Reciprocal ST Depression: Often seen in leads opposite to the area of infarction 1

Anatomical Correlation

The location of ST elevation corresponds to the anatomical region affected:

  • Anterior/Anterolateral: ST elevation in V1-V6, I, aVL (left anterior descending artery territory)
  • Inferior: ST elevation in II, III, aVF (right coronary or circumflex artery)
  • Posterior: ST depression in V1-V3 with ST elevation in posterior leads V7-V9 2

Evolution Over Time

ST segment elevation follows a characteristic time course:

  1. Acute Phase: ST elevation appears within minutes to hours of coronary occlusion
  2. Subacute Phase: ST elevation begins to resolve as Q waves develop
  3. Chronic Phase: In most cases, ST elevation resolves within 2 weeks (95% of inferior infarctions, but only 40% of anterior infarctions) 3

Differential Diagnosis

It's important to note that ST elevation is not specific to myocardial infarction. Other conditions that can cause ST elevation include:

  • Early repolarization
  • Pericarditis
  • Left ventricular hypertrophy
  • Left bundle branch block
  • Brugada syndrome
  • Takotsubo syndrome 1, 4

Clinical Implications

The presence, location, and extent of ST elevation provide crucial information:

  • Diagnosis: Defines STEMI and guides immediate reperfusion decisions 1
  • Prognosis: Persistent ST elevation after anterior MI correlates with larger infarct size and worse outcomes 3
  • Treatment Strategy: Determines eligibility for urgent reperfusion therapy 1

Understanding the mechanism of ST elevation is essential for accurate diagnosis and timely treatment of myocardial infarction, which significantly impacts patient morbidity and mortality.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Cardiac Anatomy and Function

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

ST-segment elevation: Differential diagnosis, caveats.

Cleveland Clinic journal of medicine, 2015

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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