- Wellens’ syndrome is a pattern of deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery (LAD).
- Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next few days to weeks.
- Due to the critical LAD stenosis, these patients usually require invasive therapy, do poorly with medical management and may suffer MI or cardiac arrest if inappropriately stress tested.
Rhinehart et al (2002) describe the following diagnostic criteria for Wellens’ syndrome:
- Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6)
- Isoelectric or minimally-elevated ST segment (< 1mm)
- No precordial Q waves
- Preserved precordial R wave progression
- Recent history of angina
- ECG pattern present in pain-free state
- Normal or slightly elevated serum cardiac markers
There are two patterns of T-wave abnormality in Wellens’ syndrome:
- Type A = Biphasic, with initial positivity & terminal negativity (25% of cases)
- Type B = Deeply and symmetrically inverted (75% of cases)
The T waves evolve over time from from a Type A to a Type B pattern (see an example of this here).
Biphasic T Waves (Type A)
Deeply Inverted T Waves (Type B)
NB. There is confusion in the literature regarding the naming of the T wave patterns, with some authors using Type 1 for inverted T waves and Type 2 for biphasic. It may be better to just describe the T wave pattern!
Understanding The T Wave Changes
The following sequence of events is thought to occur in patients with Wellens’ syndrome:
- A sudden occlusion of the LAD, causing a transient anterior STEMI. The patient has chest pain & diaphoresis. This stage may not be successfully captured on an ECG recording.
- Re-perfusion of the LAD (e.g. due to spontaneous clot lysis or prehospital aspirin). The chest pain resolves. ST elevation improves and T waves become biphasic or inverted. The T wave morphology is identical to patients who reperfuse after a successful PCI.
- If the artery remains open, the T waves evolve over time from biphasic to deeply inverted.
- The coronary perfusion is unstable, however, and the LAD can re-occlude at any time. If this happens, the first sign on the ECG is an apparent normalisation of the T waves — so-called “pseudo-normalisation”. The T waves switch from biphasic/inverted to upright and prominent. This is a sign of hyperacute STEMI and is usually accompanied by recurrence of chest pain, although the ECG changes can precede the symptoms.
- If the artery remains occluded, the patient now develops an evolving anterior STEMI.
- Alternatively, a “stuttering” pattern may develop, with intermittent reperfusion and re-occlusion. This would manifest as alternating ECGs demonstrating Wellens’ and pseudonormalisation/STEMI patterns.
This sequence of events is not limited to the anterior leads — similar changes may be seen in the inferior or lateral leads, e.g. with RCA or circumflex occlusion. Also, the inciting event does not necessarily have to be thrombus formation: Wellens’ syndrome may also occur in normal coronary arteries following an episode of vasospasm, as in this case of cocaine-induced vasospasm. However, it is safer to assume the worst (i.e. critical LAD stenosis) and work the patient up for an angiogram.
The concept of occlusion/reperfusion/re-occlusion is explained by Dr Stephen Smith with some great examples here. Also check out Example 5, below.
Wellens Syndrome (Type A Pattern)
- Biphasic precordial T waves with terminal negativity, most prominent in V2-3.
- Minor precordial ST elevation.
- Preserved R wave progression (R wave in V3 > 3mm)
Wellens’ Syndrome (Type A Pattern)
- The biphasic T waves in V2-3 are characteristic of Wellens’ syndrome.
Wellens Syndrome (Type B Pattern)
- There are deep, symmetrical T wave inversions throughout the anterolateral leads (V1-6, I, aVL).
Wellens’ Syndrome (Type A Pattern)
- Biphasic T waves with minimal ST elevation in V1-5, consistent with Wellens’ syndrome.
- The patient had experienced ischaemic chest pain immediately prior to arrival in hospital and was pain free at the time the ECG was taken.
The prehospital ECG from ~15 minutes earlier demonstrates a clear anterolateral STEMI:
- This prehospital ECG was taken while the patient was still symptomatic with chest pain and diaphoresis.
- It shows unmistakable features of anterolateral STEMI, with marked precordial ST elevations and inferior reciprocal change.
- The symptom resolution and conversion to a Wellens ECG on arrival to hospital indicates reperfusion of the LAD.
This fantastic ECG series (submitted by paramedic Andrew Bishop) shows a stuttering pattern of LAD occlusion, reperfusion and re-occlusion in a middle aged lady with chest pain. The ECGs are presented in chronological order, over a 45 minute period from the prehospital environment to the cath lab.
(a) Patient experiencing chest pain and diaphoresis
- The ECG shows a clear anterolateral STEMI, with inferior reciprocal change.
- The artery is occluded at this point.
(b) Resolution of pain
- The ECG now shows a typical Wellens pattern of biphasic T waves in V2-3, plus improvement in the anterolateral ST elevation.
- This indicates spontaneous reperfusion of the LAD — i.e. the artery has re-opened.
(c) Recurrence of chest pain and diaphoresis
- With recurrence of pain there is pseudo-normalisation of the precordial T waves: the previously biphasic T waves have become prominently upright (= “hyperacute” T waves).
- This apparent normalisation of the T waves indicates re-occlusion of the LAD artery.
(d) Ongoing ischaemic symptoms
- Following re-occlusion of the artery, there is further evolution of the anterolateral ST changes, with evolving anterior STEMI.
(e) Symptoms improving
- Once again there is reperfusion of the artery, only this time the ST changes are slower to resolve.
(f) Now Pain Free
- Now the T waves are starting to become biphasic again (Wellens Pattern A).
Shortly after this series of ECGs was taken, this patient suffered a VF arrest that was refractory to defibrillation. She was placed on a mechanical CPR device and taken to the cath lab, where she was found to have a 100% proximal LAD stenosis. This was stented, she was successfully cardioverted and subsequently made a good neurological recovery!
Differential Diagnosis of Wellen’s Syndrome
While the morphology of the T wave changes in Wellens’ syndrome is often quite distinctive, there are numerous other conditions that may produce similar patterns of precordial T-wave inversion, including:
Explore the links above to appreciate the similarities and differences between these ECG patterns.
This ECG was initially posted as an example of Wellens’ syndrome. What do you make of it?
Note the following features:
- Tachycardia (~100bpm)
- Rightward axis (+90)
- T wave inversions in the right precordial leads (V1-4) plus lead III
- The ST / T-wave morphology is identical to this example of pulmonary embolism
Apologies for the misinformation… As you can see, these two conditions can be difficult to tell apart!
What about this example?
This is an example of Pseudo-Wellens syndrome due to left ventricular hypertrophy.
- LVH by voltage criteria (SV1 + RV6 > 35mm)
- The pattern of inverted and biphasic T waves is different to Wellens’ syndrome, affecting multiple leads (i.e. any lead with a tall R wave) rather than V2-3.
- In this case, the Wellens-like T waves are just a variant on the repolarisation abnormality (LV “strain” pattern) that is seen with LVH.
This pattern of T wave changes:
- Is most commonly seen in the lateral leads (V5-6, I, aVL).
- Typically occurs in patients with high QRS voltages, e.g. due to LVH, or in young black males with benign early repolarization.
Learn from the Experts!
Consolidate your learning with lessons from the masters of ECG interpretation. Follow the links below for expert commentary, video lessons, case-based discussion and detailed explanations to take your learning to the next level.
- Amal Mattu’s Emergency ECG Video of the Week — Wellens’ Syndrome (video lessons)
- Amal Mattu’s Emergency ECG Video of the Week — PseudoWellens (video lesson)
- Dr Smith’s ECG Blog — Wellens’ Syndrome (case discussions)
- Dr Smith’s ECG Blog — Wellens Mimics (case discussions)
- John Larkin’s ECG of the Week — Wellens’ Syndrome (case discussion)
- Salim Rezaie at ALiEM — Wellens’ Syndrome (blog post)
Check out these other pages from the LITFL ECG library.
- de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. PMID: 6121481.
- Chan TC, Brady WJ, Harrigan RA, Ornato JP and Rosen PR. ECG in Emergency Medicine and Acute Care. Elsevier 2005.
- Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bär FW, Wellens HJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol. 1995 Jun 15;75(17):1206-10. PubMed PMID: 7778540.
- Haines DE, Raabe DS, Gundel WD, Wackers FJ. Anatomic and prognostic significance of new T-wave inversion in unstable angina. Am J Cardiol. 1983 Jul;52(1):14-8. PubMed PMID: 6602539.
- Mattu A, Brady W. ECGs for the Emergency Physician 1, BMJ Books 2003.
- Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.
- Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II. BMJ. 2002; 324: 963-6. [full text]
- Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002 Nov;20(7):638-43. PubMed PMID: 12442245.
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.
- Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome. Ann Emerg Med. 1999 Mar;33(3):347-51. Review. PubMed PMID: 10036351.
- Wehrens XH, Doevendans PA, Ophuis TJ, Wellens HJ. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J. 2000 Mar;139(3):430-6. PubMed PMID: 10689257.