Wellens’ Syndrome

Clinical Significance

 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.

Diagnostic Criteria

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).

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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!

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Classification of Wellens ECG patterns, from the original paper. 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.

Understanding The T Wave Changes

The following sequence of events is thought to occur in patients with Wellens’

syndrome:

1. 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.
2. 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.
3. If the artery remains open, the T waves evolve over time from biphasic to deeply
inverted.
4. 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.
5. If the artery remains occluded, the patient now develops an evolving anterior
STEMI.
6. 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.

Example ECGs

Example 1

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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)

Example 2

Wellens’ Syndrome (Type A Pattern)

 The biphasic T waves in V2-3 are characteristic of Wellens’ syndrome.

Example 3

Wellens Syndrome (Type B Pattern)

 There are deep, symmetrical T wave inversions throughout the anterolateral

leads (V1-6, I, aVL).

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Example 4

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.

Example 5

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.

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(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.
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(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:

 Pulmonary embolism
 Right bundle branch block
 Right ventricular hypertrophy
 Left ventricular hypertrophy
 Hypertrophic cardiomyopathy
 Raised intracranial pressure
 Normal paediatric ECG
 Persistent juvenile T wave pattern
 Brugada syndrome
 Hypokalaemia

Explore the links above to appreciate the similarities and differences between these
ECG patterns.

Wellens?

This ECG was initially posted as an example of Wellens’ syndrome. What do you make of
it?

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Reveal Answer

As ECG expert Steve Smith from Dr Smith’s ECG Blog pointed out in a recent email to me, this ECG
is more consistent with a diagnosis of pulmonary embolism!

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!

Pulmonary embolism, example :

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What about this example?

Reveal Answer

This is an example of Pseudo-Wellens syndrome due to left ventricular hypertrophy.

Note:

 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.

Steve Smith discusses pseudo-Wellens due to LVH here. Amal Mattu discusses pseudo-Wellens due
to BER here.

Be cautious when diagnosing Wellens syndrome in patients with high voltage QRS
complexes

 There is a normal variant pattern, seen in young males

 Commonly mimics wellens syndrome & seen mostly in African-Americans
 Look for a fishhooked J-points & concave upward STE before a steep T-wave drop