Wellens' syndrome

Background

• First described in 1982, a set of EKG changes specific for critical, proximal stenosis of LAD
  • At risk for extensive anterior wall myocardial infarction due to proximal LAD stenosis
    • In the original study, a subset of patients fared poorly with medical management of “impending myocardial infarction”
    • 75% of patients with these findings will later develop anterior MI (if not treated with PCI)
  • Characteristic EKG changes: T wave abnormality (2 types, shown below) associated with the stenosis
• Commonly described as a STEMI equivalent, but per the 2022 ACC Expert Consensus Decision Pathway, it's instead categorized as an ischemic change
  • This is because patient is not currently having an MI; rather, it's a post-ischemic change

Clinical Features

• 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
• Cocaine use may cause pseudo-Wellens due to vasospasm without critical stenosis

Differential Diagnosis

• High voltage
• PE
• RBBB
• Hypokalemia
• CNS Injury
• Persistent Juvenile T-wave pattern
• Digitalis Effect
• "Normal variant" STE with biphasic T-wave
  • 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

ST Elevation

• Cardiac
  • ST-segment elevation myocardial infarction (STEMI)
  • Post-MI (ventricular aneurysm pattern)
  • Previous MI with recurrent ischemia in same area
  • Wellens' syndrome
  • Coronary artery vasospasm (eg, Prinzmetal's angina)
  • Coronary artery dissection
  • Pericarditis
  • Myocarditis
  • Aortic dissection in to coronary
  • Left ventricular aneurysm
  • Left ventricular pseudoaneurysm
  • Early repolarization
  • Left bundle branch block
  • Left ventricular hypertrophy (LVH)
  • Myocardial tumor
  • Myocardial trauma
  • RV pacing (appears as Left bundle branch block)
  • Brugada syndrome
  • Takotsubo cardiomyopathy
  • AVR ST elevation
• Other thoracic
  • Pneumomediastinum
  • Pneumothorax
  • Pulmonary embolism
• Metabolic
  • Drugs of abuse (eg, cocaine, crack, meth)
    • Cocaine chest pain
  • Hyperkalemia (only leads V1 and V2)
  • Hypothermia ("Osborn J waves")
• Medications
  • Tricyclic (TCA) toxicity
  • Digoxin

Evaluation

• History of chest pain
  • ECG may be normal during episode of pain
• Normal or slightly-elevated cardiac enzymes
• No precordial Q-waves
• Isoelectric or <1mm ST-segment elevation
• Wellens' sign present in pain-free state
  • Wellens' sign during pain-free state plus recent history of angina and normal to slightly elevated cardiac enzymes = Wellen's syndrome
  • Findings can be transient (persists for hours after pain has resolved and then disappears)

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

• IF there is acute occlusion MI, Wellens T wave patterns may normalize and convert to ST elevations
• Note Wellens criteria should not be applied to patients with LVH

Management

• Treat similarly to MI, including antiplatelets and anticoagulation
• Urgent cardiac catheterization is the definitive treatment
• Stress testing contraindicated
  • Can precipitate an acute myocardial infarction and sudden death

Disposition

• Admit

See Also

• STEMI equivalents

External Links

Mattu ECG Case - Wellens' Syndrome