Wellens' syndrome

• First described in 1982
  • Subset of patients fared poorly with medical management of “impending myocardial infarction” (unstable angina)
    • At risk for extensive anterior wall myocardial infarction due to proximal LAD stenosis[1]
    • Shared characteristic ECG changes
      • T wave abnormality associated with critical LAD stenosis[2]
  • Findings can be transient (persists for hours after pain has resolved and then disappears)

• Symptoms of Myocardial infarction or ischemia
• Symptoms have often resolved at presentation
• May have previous recent episodes of angina or anginal equivalents
• Initial cardiac enzymes are frequently normal or slightly elevated[3][4]
• Cocaine use may cause pseudo-Wellens due to vasospasm without critical stenosis[5]

• High voltage
• PE
• RBBB
• Hypokalemia
• CNS Injury
• Persistent Juvenile T-wave pattern
• Digitalis Effect
• "Normal variant" STE with biphasic T-wave[6]
  • Common in young, healthy, Black males
  • Patterns that are NOT found in Wellen's
    • High voltage complexes
    • Notching at J-point ("fishhook")
    • Concave upward ST segment followed by steep drop in T wave

• History of chest pain
• Normal or slightly-elevated cardiac enzymes
• No precordial Q-waves
• Isoelectric or <1mm ST-segment elevation
• Wellens' pattern present in pain-free state

Two T-wave Characteristics (at times terms are reversed in the literature or labeled Type I and II):

• Type A (25%)
  • Biphasic T-wave in V2/V3
• Type B (75%)
  • Deep, symmetrically inverted T-waves in V2/V3

Note Wellens criteria should not be applied to patients with LVH

• Urgent cardiac catheterization
• Stress testing contraindicated

• Admit

• STEMI equivalents

Mattu ECG Case - Wellens' Syndrome

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