August 14, 2014

REBEL ECG of the Week #8

A 52 year old female with a past medical history of type II diabetes mellitus and tobacco abuse presents with a chief complaint of chest pain.
According to the patient she had about 2 – 3 months of stuttering, substernal chest pain without any radiation.  She described the pain as pressure-like, with activity, but that it would typically resolve after a few minutes of rest.  Today she awoke with substernal chest pain that never resolved and continued in the emergency department.  She quantifies her pain as 7/10 and not relieved with 2L nasal cannula of oxygen, 325mg PO aspirin, and SL NTG x3.
BP 127/89     HR 76     RR 20      O2 sat 100% on 2L NC     Temp 99.3
Awake, A&Ox3, appears uncomfortable
Mild JVD on examination
RRR w/o m/r/g
2+ pulses in her extremities, no edema
ECG is shown (No prior ECG for comparison)…..

Before reading on, try to come up with your own interpretation of this ECG before moving on to the final impression

Wellens' Syndrome or STEMI
Rate: 68
Rhythm: Normal Sinus Rhythm
Axis: Normal Axis
QRS: Left Ventricular Hypertrophy
ST/T Waves: Biphasic T- Waves in Leads V1 – V4, but there is also ST Elevation in Leads V1 – V3
Final ECG Interpretation: Anterior STEMI
Wellens' Syndrome or STEMI
Although this is a case of Anterior STEMI, lets discuss Wellens’ Syndrome….

History of Wellens’ Syndrome

Wellens’ Syndrome was first described in 1982 [1] in which 75% of patients with t-wave inversions in V2 – V4 went on to have an acute myocardial infarction.  This was again discussed in 1989 [2], and showed that all patients with this morphology had a > 50% LAD stenosis.  In the United States, 10 – 15% of unstable angina patients admitted will have this ECG finding.

What is Wellens’ Syndrome?

  1. History of Angina
  2. ECG Changes (T-wave Inversions/Biphasic T-waves in leads V2 – V4)
  3. Normal to Minimally elevated Cardiac Enzymes
  4. No pathologic precordial q waves
  5. No loss of precordial R wave progression

What are the Types of Wellens’ Syndrome?

Types of Wellens' Waves

Image from Smith SW et al. Emerg Med Clin N Am 2006 [PMID: 16308113]

Why does Wellen’s Syndrome Matter? [3]

  • Signifies a critical high grade proximal LAD stenosis
  • Myocardial infarction occurs within a mean of 6 – 8.5 days after admission
  • Myocardial infarction occurs within a mean of 21.4 days after symptoms

What is the Specificity of inverted T waves (V1 – V4) on EKG for proximal LAD stenosis?

Remember: T-wave changes may be transient or resolve with medical management

What else can cause t-wave inversions in the anterior ECG leads?

  • Subarachnoid Hemorrhage
  • Pericarditis
  • Pulmonary Embolism
  • Takotsubo Cardiomyopathy
  • Electrolyte Abnormalities
  • HOCM
  • Pancreatitis

R.E.B.E.L. ECG of the Week: Wellens' Syndrome or STEMI - T Wave Inversion in Anterior Leads

Why should we not perform exercise stress testing in patients with suspected Wellens’ Syndrome? [4]

The only evidence for this is case reports, not large randomized control trials, but stress testing can prove fatal as there is minimal collateral circulation to the proximal anterior myocardium (i.e. “The Widow Maker”).

How do you treat Wellens’ Syndrome? [2] 

Oxygen, aspirin, nitroglycerin, and heparin or enoxaparin are the mainstay medical treatments of unstable angina, which is what Wellens’ Syndrome is, but in this specific case cardiac revascularization is also important. Specifically, how important is early revascularization vs medical management or delayed revascularization on morbidity and mortality?
R.E.B.E.L. ECG of the Week: Wellens' Syndrome or STEMI - Treatment of Wellens' Syndrome

  •  180 patients with Wellens’ ECG admitted and managed with either: Early Revascularization vs Medical Therapy
  • Less likely to die with early revascularization vs medical therapy and/or late revascularization (2.6% vs 17.9%)
  • Less likely to have AMI with early revascularization vs medical therapy and/or late revascularization (8.0% vs 30%)

Now Back to Our Patient…REBEL ECG of the Week: Wellens’ Syndrome or STEMI?

The reason our patient’s case is a STEMI and not Wellens’ Syndrome is….
Since the patient was having active symptoms and no old ECG for comparison, we activated the cath lab and the patient was found to have a 60% Left Main (LM) Artery lesion and a 100% ostial Left Anterior Descending (LAD) Artery lesion. First troponin before heart cath was 30. This turned into an evolving STEMI….or more eloquently stated a subacute anterior STEMI.
In summary our patient has:

  1. Having ACTIVE Chest Pain
  2. ST-Segment Elevation (STE) in V1 – V3
  3. Sensitive Troponin I of 30 is not minimal
  4. Absence of R waves in precordial leads

Clinical Bottom Line for Wellens’ Syndrome:

  • Wellens’ Syndrome signifies a high grade proximal LAD lesion until proven otherwise, but be sure to rule out other causes of ECG changes
  • The ECG changes of Wellens’ can be transient, so you must have a high index of suspicion
  • Stress testing, based on case reports, can induce a massive anterior myocardial infarction
  • The treatment of choice to improve both morbidity and mortality in Wellens’ Syndrome is early heart catheterization


  1. de Zwaan C et al. 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. PMID: 6121481
  2. de Zwaan C et al. Angiographic and Clinical Characteristics of Patients with Unstable Angina Showing an ECG Pattern Indicating Critical Narrowing of the Proximal LAD Coronary Artery. Am Heart J 1989. PMID: 2784024
  3. Hanna EB et al. ST-Segment Depression and T-Wave Inversion: Classification, Differential Diagnosis, and Caveats. Cleve Clin J Med 2011. PMID: 21632912
  4. Sowers N. Harbinger of Infarction: Wellens Syndrome Electrocardiographic Abnormalities in the Emergency Department. Can Fam Physician 2013. PMID: 23585602

For more on Wellens’ Syndrome Checkout:


Cite this article as: Salim Rezaie, "REBEL ECG of the Week #8", REBEL EM blog, August 14, 2014. Available at:
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Salim Rezaie

Emergency Physician at Greater San Antonio Emergency Physicians (GSEP)
Creator & Founder of REBEL EM
  • Pik Mukherji
    Posted at 10:13h, 14 August Reply

    Really nice Salim but must check out Jason West’s review on the JacobiEM site. It has great historical overview and notes that as Wellen’s is a reperfusion dynamic EKG change, CP free pts. w abnl EKGs are common.

    • Salim Rezaie
      Posted at 10:49h, 14 August Reply

      Hey Pik,
      Do you have a link to the post. Will give it a look. TY for the comment, always love your thoughts.

  • Eric
    Posted at 13:03h, 14 August Reply

    great post. key here is the ACTIVE chest pain.
    would just make an addition to the anterior t wave inversion list – include cerebral t waves, if you’re going to include pancreatitis

    • Salim Rezaie
      Posted at 13:41h, 14 August Reply

      Agreed Eric. In my mind include that with SAH. Appreciate the post-pub peer review. 🙂

  • Ken Grauer
    Posted at 05:36h, 15 August Reply

    Nice case by Salim that emphasizes some features of what Wellens Syndrome is and is not. I’d add the following comments:
    I have always thought of “Wellens’ Syndrome” – as a way to predict a tight proximal LAD lesion BEFORE an infarct occurs. So while 2 types of this syndrome are often described – I focus on Type II.
    Type I = deep symmetric T wave inversion in anterior leads. As emphasized by Salim – this ECG pattern is not at all specific, as many other entities may cause it (as you listed). I think it confusing (and not clinically helpful) to consider Type I ECG anterior symmetric T inversion together with Type II changes ….
    True Type II ECG changes can be diagnostic of Wellens syndrome – and predictive with ~90% accuracy of a proximal LAD lesion that should prompt cath with probable need for timely reperfusion. That said – we do not have that picture in this case …..
    In my opinion – the lead V2 picture shown above in your schematic figure for “Type II” Wellens is not optimally drawn by the artist. The T wave is simply too peaked (almost looks like the beginning of a DeWinter T wave …. ).
    The infarct has already occurred in this patient. Instead of small anterior r waves – there are deep QS complexes in the anterior leads – and as mentioned, ST segment elevation is present in V1 and clearly more than the no-more-than-minimal amount that should be seem with typical Wellens. These are reperfusion T waves in this case following this patient’s anterior MI (and not the “pre-infarction” picture of a typical Wellens case presentation).
    Again – NICE case! Thank you for presenting – : )

    • Salim Rezaie
      Posted at 12:33h, 15 August Reply

      Hello Ken,
      It has been a while. 🙂 TY for your comments as always. Will see if I can get my hands on a better representation of Type I and Type II Wellens’. Your knowledge, comments, and post-publication review is always welcomed and appreciated.

  • Ken Grauer
    Posted at 14:37h, 15 August Reply

    Hi Salim. Since you ask – Here is my web page on Wellens – – and this is my web page on Giant T Wave Syndrome – – Feel free to use any figures you might like from either of these pages – 🙂 Ken

  • Stephen Smith
    Posted at 07:50h, 16 August Reply

    Let me say it again: this type I and type II classification is bogus. Wellens’ classified biphasic T-waves as “Pattern A” and deep symmetric as “pattern B”. Someone, I think Tandy, got it reversed. And it is an important distinction, because, over time, biphasic evolves into deep symmetric. Wellens’ waves always evolve. And they don’t evolve from “II” to “I” (that would be a strange evolution, going backwards); they evolve from “A” to “B”.
    Steve Smith

    • Salim Rezaie
      Posted at 13:28h, 16 August Reply

      TY Steve,
      I just looked up the original 1982 Wellens’ paper and you are right. The types are backwards. I will get this fixed ASAP in the post.
      Here is the link to the original paper if anyone else wants to see it:

  • Stephen Smith
    Posted at 07:54h, 16 August Reply

    Also, these specificities can be very deceiving. If you take all patients with such T-waves, the specificity is poor: 1) if high voltage, then LVH can cause false positives, 2) if patient still has chest pain, these will be false positives, 3) if there is no R-wave, these T-waves will be false positives, 4) if there was no chest pain (SOB, weakness, etc.) these T-waves are likely to be false positives. EM physicians often want to diagnose Wellens based on the T-waves alone, and they are getting it wrong. Then they get the “crying wolf” syndrome with the cardiologists.
    Steve Smith

    • Salim Rezaie
      Posted at 13:35h, 16 August Reply

      Hello Again Steve,
      I agree with the false positives associated with the LVH, active CP, and lack of R waves. I hope I emphasized this point in the post.
      I always appreciate your input, and knowledge. TY for reading over the post and your comments. I always welcome the feedback and the conversation on the site.

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  • Inka
    Posted at 16:06h, 05 January Reply

    thank you for this case on Wellen syndrome. I was really enjoying how you presented your case: question-guess-answer. Interesting and easy to read, easy to follow your thought. Thank you again.

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