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Clinician

Blog articles for clinicians and other medical professionals.

Clinical Overview of Wellens Syndrome

April 3rd, 2025

Failure to recognize this syndrome can result in catastrophic cardiac events, making it essential for clinicians to identify and appropriately manage affected patients.

Pathophysiology

Wellens syndrome is characterized by transient ischemia of the LAD territory, likely secondary to temporary obstruction of the LAD coronary artery, according to the National Library of Medicine.

This is usually caused by the rupture of an atherosclerotic plaque, which leads to characteristic ECG findings prior to significant biomarker elevation or persistent ST-segment elevation. If untreated, progression to complete occlusion can result in extensive anterior wall MI, often with devastating consequences.

Mechanisms of ischemia and infarction

The narrowing of the LAD artery in Wellens syndrome occurs due to a variety of atherosclerotic processes, including:

  • Plaque rupture and thrombosis: Unstable plaques can rupture, leading to platelet aggregation and thrombus formation.
  • Endothelial dysfunction: Decreased nitric oxide production and increased oxidative stress contribute to vasoconstriction and impaired perfusion.
  • Microvascular dysfunction: Although Wellens syndrome is primarily a large-vessel phenomenon, microvascular dysfunction can contribute to transient ischemic episodes.

These mechanisms culminate in transient ischemia, reflected by characteristic ECG changes, even before complete occlusion occurs. The presence of Wellens syndrome serves as a warning sign, emphasizing the urgency of intervention before irreversible myocardial damage occurs.

Epidemiology

  • This typically affects middle-aged adults, with a male predominance.
  • Patients often present with a history of chest pain that has resolved, misleadingly suggesting clinical stability.
  • The condition is underdiagnosed, especially in emergency settings where chest pain syndromes are frequent and diverse.
  • Risk factors include smoking, a family history of coronary artery disease, hypertension, diabetes, and hyperlipidemia.

Clinical presentation

Patients with Wellens syndrome may present with:

  • Intermittent, self-resolving chest pain in the days preceding evaluation
  • Absence of chest pain at the time of ECG assessment
  • Minimal or no elevation of cardiac biomarkers upon initial presentation
  • No hemodynamic instability unless progression to infarction has occurred
  • History of previous CAD or known risk factors
  • Reports of chest discomfort associated with exertion, stress, or heavy meals

Detailed symptom analysis

While classic anginal symptoms include pressure-like chest pain, Wellens syndrome can also present with:

  • Atypical symptoms, such as jaw pain, arm discomfort, nausea, or diaphoresis.
  • Silent ischemia, particularly in diabetic patients.
  • Epigastric discomfort, mimicking gastrointestinal reflux disease (GERD).

Electrocardiographic features

ECG findings are paramount in diagnosing Wellens syndrome.

According to the National Library of Medicine, diagnostic criteria include:

  • Presence of deeply inverted T waves in leads V2 and V3 (This can also be visible in leads V1, V4, V5, and V6) or biphasic T waves (coupled with initial positivity and terminal negativity) in V2 and V31

These signs can also be presented alongside the above:1

  • Isoelectric or minimally elevated ST segment, less than 1 mm
  • Preservation of precordial R-wave progression and no precordial Q waves
  • Recent history of angina
  • ECG pattern present in a pain-free state
  • Normal or slightly elevated cardiac indicators

Two classic patterns

Type A (25% of cases)

  • Biphasic T waves in leads V2 and V3
  • Less common but still highly specific for proximal LAD involvement
  • May be the initial manifestation before evolving into Type B

Type B (75% of cases)

  • Deep, symmetrical T-wave inversions in leads V2 and V3
  • May extend to V1, V4, or V5 in more extensive disease
  • Indicative of prolonged ischemia and a higher likelihood of progression to infarction

Additional ECG findings

  • Absence of significant ST-segment elevation
  • Preserved R-wave progression (distinguishing it from evolving anterior STEMI)
  • No pathological Q waves, indicating the absence of completed infarction
  • Occasional mild ST depression, which may be overlooked

Diagnostic workup

Recognizing Wellens syndrome on ECG mandates urgent further evaluation, even if the patient is pain free. The following diagnostic steps should be taken:

1. Serial ECGs

  • Repeat ECGs to monitor for dynamic changes.
  • Watch for evolving ST elevation, which signals infarction.
  • Compare with prior ECGs, if available, to assess progression.

2. Cardiac biomarkers

  • This is initially normal or only mildly elevated troponin levels.
  • Serial monitoring is necessary, as elevation may indicate infarction progression.
  • High-sensitivity troponin assays may detect subtle ischemic changes earlier.

3. Coronary angiography (gold standard)

  • This is required to confirm proximal LAD stenosis.
  • This should be performed emergently if symptoms recur or if troponins rise.
  • Intravascular ultrasound (IVUS) or optical coherence tomography (OCT) may be used to assess plaque characteristics.

4. Stress testing (Contraindicated)

  • Exercise or pharmacologic stress testing is dangerous and can precipitate MI.
  • Instead, urgent angiography should be prioritized.
  • If ischemia is unclear, a non-invasive CT coronary angiogram may be considered.

Differential diagnosis

While ECG findings are highly suggestive, other conditions may mimic Wellens syndrome, including:

  • Pulmonary embolism
  • Hypertrophic cardiomyopathy
  • Early repolarization syndrome (benign T-wave changes, typically in younger patients)
  • Bundle branch blocks (which can obscure Wellens findings)
  • Raised intracranial pressure
  • Hypokalemia

Management

Once Wellens syndrome is identified, immediate intervention is required to prevent infarction.

1. Hospital admission

  • Patients should be admitted for continuous cardiac monitoring.
  • Serial ECGs and troponin measurements should be performed.

2. Medical therapy (bridge to revascularization)

  • Aspirin (325 mg loading dose, then 81 mg daily)
  • P2Y12 inhibitors (e.g., ticagrelor 180 mg loading, then 90 mg BID)
  • Anticoagulation (unfractionated heparin or enoxaparin if no contraindications)
  • Beta-blockers (unless contraindicated, e.g., in acute decompensated heart failure)
  • Nitrates for symptom control if needed
  • ACE inhibitors or ARBs, particularly in patients with diabetes or hypertension

3. Urgent coronary angiography and revascularization

  • PCI with stenting is the preferred strategy for most patients.
  • CABG may be indicated in extensive multi-vessel disease or complex LAD stenosis.

Prognosis

With prompt recognition and appropriate management, the prognosis of Wellens syndrome is favorable. However, delays in diagnosis or failure to intervene can lead to:

  • Anterior STEMI with significant myocardial loss
  • Heart failure and reduced ejection fraction
  • Arrhythmias and sudden cardiac death

Wellens syndrome represents an ECG emergency that should never be overlooked. Clinicians must maintain a high amount of suspicion in patients presenting with transient chest pain, even if symptoms have resolved.

Early recognition, urgent coronary angiography, and timely revascularization are essential to prevent infarction and improve patient outcomes.

References

  1. Miner, B., Grigg, W. S., & Hart, E.H. (2023). Wellens syndrome. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK482490/
  2. Cadogan, M. & Buttner, R. (2021). Wellens syndrome, Retrieved from https://litfl.com/wellens-syndrome-ecg-library/