ECG Blog #502 (Video): Is this Wellens' Syndrome?

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 — Today's case is an ECG Video!

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The ECG in Figure-1 is from an older patient who was awakened by severe CP (Chest Pain) in the middle of the night. The CP was intermittent throughout the night — with her again awakened by very severe CP that morning.

• The patient called EMS that morning — but her CP had almost disappeared by the time the paramedics arrived (which is when the ECG in Figure-1 was recorded).

QUESTIONS:

• Is this Wellens' Syndrome? 
• — or — Is it something else?

Figure-1: The ECG in today's Case.

Below is the Video presentation of today's case (6 minutes):

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Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome. 
• ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).
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• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
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• ECG Blog #350 — another case of Wellens' Syndrome.
• ECG Blog #326 — Reviews a case that was missed.
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• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
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• See the October 15, 2022 post (including My Comment at the bottom of the page) — for review and illustration of the concept of "Precordial Swirl" (due to proximal LAD OMI).

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ADDENDUM (10/25/2025): I excerpted what follows below from My Comment in the August 12, 2022 post in Dr. Smith's ECG Blog).

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The History of Wellens' Syndrome:

It's hard to believe that the original manuscript describing Wellens' Syndrome was published over 40 years ago! I thought it insightful to return to this original manuscript (de Zwaan, Bär & Wellens: Am Heart J 103: 7030-736, 1982):

• The authors (de Zwaan, Bär & Wellens) — studied 145 consecutive patients (mean age 58 years) admitted for chest pain, thought to be having an impending acute infarction (Patients with LBBB, RBBB, LVH or RVH were excluded). Of this group — 26/145 patients either had or developed within 24 hours after admission, a pattern of abnormal ST-T waves in the anterior chest leads without change in the QRS complex.
• I've reproduced (and adapted) in Figure-2 — prototypes of the 2 ECG Patterns seen in these 26 patients. Of note — all 26 patients manifested characteristic ST-T wave changes in leads V2 and V3.
• Most patients also showed characteristic changes in lead V4.
• Most patients showed some (but less) ST-T wave change in lead V1.
• In occasional patients — abnormal ST-T waves were also seen as lateral as in leads V5 and/or V6.
• 
  
• Half of the 26 patients manifested characteristic ST-T wave changes at the time of admission. The remaining 13/26 patients developed these changes within 24 hours after hospital admission.
• Serum markers for infarction (ie, CPK, SGOT, SLDH) were either normal or no more than minimally elevated.

ECG Patterns of Wellens' Syndrome:

The 2 ECG Patterns observed in the 26 patients with characteristic ST-T wave changes are shown in Figure-2:

• Pattern A — was much less common in the study group (ie, seen in 4/26 patients). It featured an isoelectric or minimally elevated ST segment takeoff with straight or a coved (ie, "frowny"-configuration) ST segment, followed by a steep T wave descent from its peak until finishing with symmetric terminal T wave inversion.
• Pattern B — was far more common (ie, seen in 22/26 patients). It featured a coved ST segment, essentially without ST elevation — finishing with symmetric T wave inversion, that was often surprisingly deep.

Figure-2: The 2 ECG Patterns of Wellens' Syndrome — as reported in the original 1982 article (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982).

ST-T Wave Evolution of Wellens' Syndrome:

I've reproduced (and adapted) in Figure-3 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose serial ECGs are shown in Figure-3 — is a 45-year old man who presented with ongoing chest pain for several weeks prior to admission. His initial ECG is shown in Panel A — and was unremarkable, with normal R wave progression. Serum markers were negative for infarction. Medical therapy with a ß-blocker and nitrates relieved all symptoms.
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• Panel B — was recorded 23 hours after admission when the patient was completely asymptomatic. This 2nd ECG shows characteristic ST-T wave changes similar to those shown for Pattern B in Figure-3 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).
• 
  
• Not shown in Figure-3 are subsequent ECGs obtained over the next 3 days — that showed a return to the "normal" appearance of this patient's initial ECG (that was shown in Panel A of Figure-3). During this time — this patient remained asymptomatic and was gradually increasing his activity level.
• 
  
• Panel C — was recorded ~5 days later, because the patient had a new attack of severe chest pain. As can be seen — there is loss of anterior forces (deep QS in lead V3) with marked anterior ST elevation consistent with an extensive STEMI. Unfortunately — this patient died within 12 hours of obtaining this tracing from cardiogenic shock. Autopsy revealed an extensive anteroseptal MI with complete coronary occlusion from fresh clot at the bifurcation between the LMain and proximal LAD.

Figure-3: Representative sequential ECGs from one of the patients in the original 1982 article. 
— Panel A: The initial ECG on admission to the hospital; 
— Panel B: The repeat ECG done 23 hours after A. The patient had no chest pain over these 23 hours. NOTE: 3 days after B — the ECG appearance of this patient closely resembled that seen in A ( = the initial tracing). 
— Panel C: 5 days later — the patient returned with a new attack of severe chest pain. As seen from this tracing (C) — this patient evolved a large anterior STEMI. He died within hours from cardiogenic shock (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982 — See text).

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Relevant Findings from the 1982 Article:

The ECG pattern known as Wellens' Syndrome was described over 40 years ago. Clinical findings derived from the original 1982 manuscript by de Zwaan, Bär & Wellens remain relevant today.

• One of the 2 ECG Patterns shown in Figure-3, in which there are characteristic anterior chest lead ST-T wave abnormalities — was seen in 18% of 145 patients admitted to the hospital for new or worsening cardiac chest pain.
• Variations in the appearance of these 2 ECG patterns may be seen among these patients admitted for chest pain. Serial ECGs do not show a change in QRS morphology (ie, no Q waves or QS complexes developed). Serum markers for infarction remained normal, or were no more than minimally elevated.
• Among the subgroup of these patients in this 1982 manuscript who did not undergo bypass surgery — 75% (12/16 patients) developed an extensive anterior STEMI from proximal LAD occlusion within 1-2 weeks after becoming pain-free.

LESSONS to Be Learned:

At the time the 1982 manuscript was written — the authors were uncertain about the mechanism responsible for the 2 ECG patterns of Wellens' Syndrome.

• We now know the mechanism. A high percentage of patients seen in the ED for new cardiac chest pain that then resolves — with development shortly thereafter of some form of the ECG patterns shown in Figure-1 — had recent coronary occlusion of the proximal LAD — that then spontaneously reopened.
•  The reason Q waves do not develop on ECG and serum markers for infarction are normal (or at most, no more than minimally elevated) — is that the period of coronary occlusion is very brief. Myocardial injury is minimal (if there is any injury at all).
• BUT: What spontaneously occludes, and then spontaneously reopens — may continue with this cycle of occlusion — reopening — reocclusion — reopening — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).
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• Clinically: We can know whether the "culprit" artery is either open or closed by correlating serial ECGs with the patient's history of chest pain. For example — resolution of chest pain in association with reduction of ST elevation suggests that the "culprit" vessel has spontaneously reopened. And, if this is followed by return of chest pain in association with renewed ST elevation — the "culprit" artery has probably reclosed.
• The importance of recognizing Wellens' Syndrome — is that it tells us that timely cardiac cath will be essential IF we hope to prevent reclosure. In the de Zwaan, Bär & Wellens study — 75% of these pain-free patients with Wellens' ST-T wave changes went on to develop a large anterior STEMI within the ensuing 1-2 weeks if they were not treated.
• Thus, the goal of recognizing Wellens' Syndrome — is to intervene before significant myocardial damage occurs (ie, diagnostic criteria for this Syndrome require that anterior Q waves or QS complexes have not developed — and serum markers for infarction are no more than minimally elevated).
• It is not "Wellens' Syndrome" — IF the patient is having CP (Chest Pain) at the time one of the ECG patterns in Figure-2 are seen. Active CP suggests that the "culprit" artery is still occluded.
• Exclusions from the 1982 study were patients with LBBB, RBBB, LVH or RVH. While acute proximal LAD occlusion can of course occur in patients with conduction defects or chamber enlargement — Recognition of the patterns for Wellens' Syndrome is far more challenging when any of these ECG findings are present.

A final word about the 2 ECG Patterns in Figure-2. 

• As suggested from data in the original 1982 manuscript, Pattern A — is far less common, but more specific for Wellens' Syndrome IF associated with the "right" history (ie, prior chest pain — that has now resolved at the time ST-T wave abnormalities appear).
• Unlike Pattern A in Figure-2 — Pattern B may be limited to symmetric T wave inversion in a number of chest leads without an initially positive T wave, that then steeply descends into terminal negativity. The diagnostic problem — is that deep, symmetric T wave inversion may be seen in a number of other conditions, and is therefore much less specific for Wellens' Syndrome.

In Conclusion: The 145 patients studied by de Zwaan, Bär & Wellens in 1982 continue to this day to provide clinical insight into the nature of Wellens' Syndrome.

 

ECG Blog #499 — An Athlete with Chest Pain ...

I was shown the ECG in Figure-1, obtained from a previously healthy, middle-aged man — who presented to the ED (Emergency Department) with new, severe CP (Chest Pain).

• Of note — the patient is an active endurance athlete.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Should you activate the cath lab?

Figure-1: The initial ECG in today's case — from a middle-aged man with CP. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Today's CASE:

The history in today's case is worrisome. In this context — I would interpret the ECG in Figure-1 as suggestive of acute proximal LAD occlusion until proven otherwise.

• The rhythm in ECG #1 is sinus at ~65/minute. All intervals (PR-QRS-QTc) and the axis are normal. No chamber enlargement.

Regarding Q-R-S-T Wave Changes:

• There appear to be tiny (probably insignificant) Q waves in leads III and aVF.
• R wave progression is normal (with transition, where the R wave becomes taller than the S wave is deep — occurring normally between leads V3-to-V4).
• ST-T wave changes — The most remarkable finding on this tracing is the disproportionate increased size of T waves in the chest leads (See RED arrows in Figure-2). Especially given modest size of the QRS complex in leads V2,V3,V4 — the T waves in these leads clearly appear larger-than-expected — which in the context of a patient with new CP — qualifies these T waves as hyperacute until proven otherwise!
• In isolation, I probably would not have interpreted the T waves in leads V5,V6 as abnormal. However, in the context of new CP and the hyperacute-appearing T waves in neighboring leads V2,V3,V4 — I thought the T waves in leads V5,V6 represented an extension of this process (BLUE arrows in Figure-2).

PEARL #1: When I have any doubt from the chest leads about the clinical implications of ST-T wave findings in a patient with symptoms — I look extra closely at ST-T wave appearance in the limb leads.

• To Emphasize: Not all cases of acute LAD occlusion manifest abnormal limb lead findings. Most often — it is those proximal LAD occlusions that are most likely to manifest at least some ST elevation in lead aVL and/or reciprocal ST depression in the inferior leads.
• Therefore: If you do not see ST-T wave abnormalities in the limb leads — this does not rule out the possibility of acute LAD occlusion. BUT — IF you do see clear ST-T wave abnormalities in the limb leads — this strongly supports that what you may be questioning in the chest leads is a valid indicator of an acute ongoing process.

QUESTION:

Take another LOOK at the ECG in Figure-2:

• How would you assess ST-T wave findings in the limb leads?

Figure-2: I've labeled the initial ECG in today's case.

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PEARL #2: It's important to recognize the difficulty in assessing the validity of what you are seeing when there is as much variability in ST-T wave appearance as we see for beats #1,2,3 in leads II,III; and in leads aVL,aVF (within the broken-lined PURPLE rectangles in Figure-2).

• Which of these first 3 beats in the limb leads reflects the "true" appearance of the ST-T waves in these leads? If it is beat #3 (that shows marked ST depression in the inferior leads with subtle ST elevation in aVL) — then there is no doubt about the hyperacuity of the T waves in the chest leads! 
• BUT — Our assessment might be less certain if beats #1 and #2 reflect the true ST-T wave appearance in leads II,III; and aVL,aVF.

Fortunately — The ST-T waves for the last 2 beats in the limb leads of Figure-2 look to be more consistent in appearance — so I made my assessment largely based on what I see for beats #4 and #5 in Figure-2:

• The ST segment in leads III and aVF for beats #4 and 5 looks straightened.
• Given tiny size of the QRS in lead aVL — the upright T wave for beats #4 and 5 in this lead looks disproportionately large.
• And — all 5 beats in lead I look consistent in appearance — all showing some ST segment straightening with a more "voluminous"-than-expected T wave.
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• Impression: In this patient with new severe CP — I interpreted this ECG as suggestive of acute proximal LAD occlusion until proven otherwise. My thoughts when I was shown this tracing were to activate the cath lab.
• If providers on the scene had any doubts about the need to activate the cath lab — quick search for a prior ECG on this patient or repeat ECG within 10-15 minutes mght be helpful options.

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The CASE Continues:

• The initial Troponin came back normal.
• The patient was given IV paracetamol — which significantly reduced his pain. 
• Feeling better, the patient was convinced his CP was the result of an intense endurance session the day before. As a result — he left the ED after 30 minutes against medical advice (such that no repeat ECG or repeat Troponin was done).

MY Thoughts:

When told the above — I wrote back the following:

• I would have activated the cath lab on the basis of the initial ECG that we see in Figure-1.
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• It would have been very helpful to see a follow-up ECG recorded within 15-to-30 minutes of the 1st tracing. IF the ECG in Figure-1 truly represents an acute evolving MI — it is very likely that a 2nd ECG done within the next 30 minutes would have shown "dynamic" ST-T wave changes (ie, deflation of the hyperacute chest lead T waves) — and that would have been diagnostic of an ongoing acute event!
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• PEARL #3: A normal initial Troponin does not rule out an acute MI (because up to 25% of STEMI+ infarctions fail to satisfy "rule-in" values on the initial Troponin — Wereski et al — JAMA Cardiology, 2020). Thus, although elevation of the initial Troponin would have been helpful to confirm an ongoing acute event — a normal initial Troponin would not have changed my impression that the cath lab should be activated.
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• PEARL #4: In patients with new CP, in whom you are suspicious of an acute cardiac event — it is best not to administer analgesics (ie, IV Morphine) — until a decision is made to either activate the cath lab or that an acute OMI has been definitely ruled out. This is because partial (or total) CP relief with IV Morphine may produce a false sense of security — when it reality what it does is delay the diagnosis of acute coronary occlusion in need of definitive treatment = prompt cath with PCI ( = this CASE, and many others in Dr. Smith's ECG Blog).
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• I asked if it would be possible to get follow-up on this patient?

Final Follow-Up:

Medical providers reached out and were able to contact the patient by phone a few days later.

• The patient was actually doing well since leaving the hospital against medical advice. He was convinced that his CP was a result of a muscular injury from his intense athletic training.
• Several weeks later — the patient did come in for a follow-up visit. He reported being able to continue his endurance training — albeit with intermittent discomfort that he felt was related to certain torso movements.
• The was no previous ECG in this patient's file for comparison as his previous "baseline".
• Repeat ECG on this follow-up visit was essentially the same as the ECG in Figure-1!
• Echo in the office at this time was completely normal (normal chamber size and normal cardiac function).
• CT coronary angiography was performed — and was without significant disease. Normal LV function.

CASE Conclusion:

Based on the above follow-up to this case — We concluded that the ECG picture in Figure-1 represents an unusual repolarization variant in this highly trained endurane athlete, who is otherwise healthy and in excellent physical condition.

• PEARL #5: I like to give a copy of unusual ECGs, such as today's initial tracing to the patient to either keep in their wallet or to be scanned for their cell phone — such that if ever in the future they present again for emergency care — they can show of copy of their baseline tracing that is "normal for them". This was done for today's patient — who continued his regular athletic training.
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• PEARL #6: Sometimes the workup (including cardiac cath) will be normal. It's important to appreciate that a normal cardiac catheterization does not mean that the catheterization should not have been done. On the contrary — sometimes the only way to ensure the absence of coronary disease is by complete evaluation, that may at times include cardiac catheterization.

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Acknowledgment: My appreciation to Lorenzo Kapetis (from Lamaca, Cyprus) for the case and this tracing.

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ADDENDUM #1 (10/5/2025):

• For More Material — regarding the ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion). NOTE: The timed-contents of this Podcast #2 facilitate quickly finding whatever key concepts you wish to review.
• Check out near the top of the "My ECG Videos" page, those videos from my MedAll ECG Talks that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
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• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
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• KEY Clinical Reality: Many of the acute coronary occlusions that we see never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.