EXTRA COPY — ECG Blog #530: Old or New Wellens? — EXTRA COPY

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Figure-1: The initial ECG in today's case — obtained from XXXX (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-2: XXXXX

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Figure-3: XXXXX

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Figure-4: XXXXX

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Acknowledgment: My appreciation for the anonymous submission of today's case with these tracings.

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Jennifer wanted this to be anonymous !!!

— Me to let Jennifer and Guy Janzen know whenever I publish this! —

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Jennifer Carlquist — Make this ANONYMOUS (4-18.1-2026)

Note — Guy Janzen also participated in our discussion

  — " New or Old or Wellens?" —

 

Jennifer posted this on 4/14 as, “Sent by one of our members — Is this a STEMI? — Jennifer then added that this patient had active Chest Pain with this ECG !!!

MY REPLY:

Hello Jennifer and Guy! I saw Jennifer's post on 3-Day EKG Challenge (https://www.facebook.com/groups/191541262186140/posts/1655453675794884 ) — and I see that Jennifer told Guy that there was: i) A history of previous stent; and ii) Ongoing CP. I left a Comment with several questions for the followers of 3Day EKG. Jennifer — I'd love to use this for an ECG Blog if you could get me a little more info on the case (Doesn't have to be a lot — but whatever you might be able to find out. I'm glad to acknowledge you and/or anyone who knows more about this case — and/or to make this an anonymous case. BEST to message me here (or to email me at — ekgpress@mac.com) — as I often don't get to follow up on Tabs ... P.S. Jennifer — I'll be HAPPY to discuss the questions I asked your followers — but would be GREAT if YOU could message or email me after some of your folks have answered my questions!

 

JENNIFER REPLY:

Hello good morning as it turns out this was a 52-year-old female with a history of previous PCIRCA the year prior to coming in She came in with crushing chest pain went to our left arm up to her neck with shortness of breath have been going on for two hours at this point History, hyperlipidemia, hypertension, previous nstemi

 

MY REPLY:

Hi Guy & Jennifer. GREAT corresponding with you both. Jennifer — ANY chance of getting a previous ECG? That would be the fastest way to figure out what is new vs old. (KEY POINT — So often when people post "prior ECGs" — what they FAILto get out of the chart is what the circumstancs were AT THE TIME that the previous ECG was obtained. For example, in this case — I'd want a previous ECG "after the dust had settled" from any previous event! And then you would KNOW what is new vs old! GUY — NO — There should NOT be reciprocal changes with an established aneurysm! But even without lead aVL here — the SHAPE of the ST segmets in the inferior leads is NOT the much more smooth and rounded appearance with LESS ST elevation that is characteristic of LV aneurysm. Bottom Line — in a patient with know disease who presents with this ECG and severe ongoing CP — the "Answer" is GO TO THE CATH LAB! A prior ECG will confirm what is new (and ongoing) vs what is old — but that is NOT needed to instantly know this case IMMEDIATELY should go to the cath lab. It does NOT matter what Troponins are, so do not wait for that. Finally — Jennnifer — Please confirm that I can use this case — and whether it should be anonymous — or if you'd like me to cite you and/or someone else.

 

JENNIFER:

This is a former ECG. (Presumably this former ECG was done ~9 months ago at the time of this patient’s last stent! 

MY REPLY:

This will be a GREAT case for an ECG Blog. As per Jennifer — I'll make it from anonymous.

Jennifer — Unless I missed it — My understanding is that this patient presented for CP with a Hx of previous stent. Any idea of WHEN the stent was done wrt ECG #1? 

KEY Question (if you are able to find out) — How was this initial ECG ( = ECG #1) assessed by providers and cardiology? Did they immediately recognize that this represents an acute ongoing MI?

So — Finding the prior tracing that you sent us TELLS a STORY! We can go back to the Previous ECG ( = ECG #2) — and as per Guy, ECG #2 shows an Inf. MI with Inf. ST coving,still slight ST elevation and LARGE inf. Q waves — with deep symmetric T wave inversion = Reperfusion T waves! Together with the minimal residual inf. ST elev. and the minimal reciprocal ST dep in aVL — this is reperfusion, potentially obtained anywhere from a few hours after reperfusion (either from PCI, thrombolytics or sponaneous) — together with an overly tall T wave in V2 + reperfusion ST-T wave changes in V4-6.

Now when you compare this to the NEW ECG ( = ECG #1) — Inf. lead ST segments are actively rising with HYPERACUTE ST segment straightening and mirror-image opposite reciprocal changes in leads I,aVL. In the chest leads — all reperfusion changes are less (ie, given the NEW CP ==> this is absolutely diagnostic of acute reocclusion ==> Need for Cath ASAP.

So Jennifer — any "detective work" you can do to figure out how long it took providers to realize acute reocclusion would be insightful! (P.S. NO problem if you are unable to learn any more about this case — as these 2 ECGs alone is more than enough for an instructive case! — :)

 

JENNIFER:

The last stent was 9 months ago. I believe this ECG was done at the time of the last stent, which was ~9 months ago!

 

MY REPLY:

That helps! ECG #2 probably done prior to hospital discharge (since it really suggests fairly recent reperfusion). So with the history of new severe CP at the time of the NEW ECG ( = ECG #1) — providers ideally would instantly recognize this is acute reocclusion with need for immediate cath — :)

 

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BELOW is What I Wrote on Jennifer's 3-Day EKG Site (4/20/2026):

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GREAT case for discussion! These were questions that I posed earlier:

— Is this Wellens' Syndrome? (and ... WHY or Why Not?)
— What will a previous ECG show?
— Why is there NO P wave in the long lead V1 rhythm strip?
= = = = = = = 
My ANSWERS:
— As so often is the case, the answer is, "It DEPENDS" — but the KEY for the astute clinician is know ON WHAT does it depend — 🙂

— For TRUE "Wellens' Syndrome — the patient must be ASYMPTOMATIC at the time that the ECG is done. What Wellens' Syndrome actually represents is that there already HAS BEEN coronary occlusion, but not for long enough to cause significant loss of myocardium. So true Wellens' Syndrome is a "warning" — that tells you that the "culprit vessel" is unstable — and that since the patient is now pain-FREE, that the "culprit" vessel has spontaneously opened, but that this "culprit" vessel is at risk at ANY time of spontaneous reclosure — which is why prompt cath with PCI is urgently needed.

— Although we are all familiar with Wellens' Syndrome occuring in the LAD distribution — it can occur ANYWHERE — so this type of terminal T wave inversion in the inferior leads could be Wellens IF the ECG was previously normal, if there was CP (Chest Pain) that is now relieved — and if instead of the marked ST elevation that we see here in the inferior leads, there was only minimal or no ST elevation. But that is not what we see here, because there is TOO MUCH ST elevation to be Wellens (and TOO MUCH ST elevation for this to be an inferior wall aneurysm). And since this patient was having new severe CP — this ECG represents an ongoing infarction.

— KEY POINT: True Wellens may look identical to an MI that has occurred! This is why the patient MUST BE pain-FREE for an ECG to represent Wellens.

As to what a previous ECG might show? THIS is the KEY. In this particular case — this patient had a prior MI, ST segments had been up and were coming down — and now they are rising again in association with recurrence of CP — so this ECG turned out to represent acute RE-OCCLUSION, with need for prompt cath.

Finally and EASY to overlook — the rhythm is not sinus. The negative P in the inferior leads indicates a junctional rhythm. Lead V3 shows that there IS a negative P wave before the QRS — so we can assume that the reason we don't see a P wave in lead V1 is that the retrograde P wave in this lead is isoelectric with the baseline. But the simultaneous long lead V1 confirms that this is a junctional rhythm! ( = another complication of recurring acute OMI.

= = = = = = = = = = = = 

ECG Blog #453 — Is this Wellens' Syndrome?

https://ecg-interpretation.blogspot.com/2024/10/ecg-blog-453-is-this-wellens-syndrome.html

= = = = = = = = = = = =

The ECG in Figure-1 was obtained from a middle-aged man who presented with a 2 week history of progressively increasing CP (Chest Pain) with exertion. He had his most severe episode of CP the day before he was seen with this ECG. His CP was much less compared to the day before — but it had not yet completely resolved.

• An initial Troponin drawn less than 1 hour after the ECG in Figure-1 was recorded was over 10,000.

 

QUESTIONS:

• Given this history — How would YOU interpret this ECG?
• Is this Wellens’ Syndrome?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today’s CASE:

The rhythm for the ECG in Figure-1 is sinus at ~85/minute. The PR and QRS intervals are normal; the QTc appears to be borderline prolonged (counting the terminal negative part of the T waves in V3,V4). There is no chamber enlargement. 

Regarding Q-R-S-T Wave Changes:

• Small q waves are seen in each of the inferior leads. The q wave in lead III is a bit wider than usual for a normal septal q wave — so I was uncertain if these inferior q waves might be of clinical significance.
• That said — there is a definite QS complex in lead V3 (See Figure-2). This QS complex takes on additional significance because there is loss of r wave from lead V2-to-V3. As a result of this QS in V3 — I interpreted the small Q wave in lead V4 as also significant.
• Small and narrow q waves of uncertain significance are seen in lateral chest leads V5 and V6.
• R Wave Progression is delayed because of the loss of anterior forces in leads V3 and V4.

Regarding ST-T Wave Changes:

• There is ST segment straightening with slight ST elevation in lead V2.
• The ST segment take-off in lead V3 is slightly elevated and coved in shape — with sharp descent into terminal T wave negativity (BLUE arrow in this lead in Figure-2).
• Similar ST segment straightening with terminal T wave negativity continues in lead V4, and to a lesser extent in lead V5 (Blue arrows in these leads).
• There is nonspecific ST-T wave flattening in lead V6 — and in the limb leads.

My Impression of ECG #1 given Today's History:

In this middle-aged man with a 2-week history of CP — with his most severe episode the day before ECG #1 was recorded — and with reduced (but not completely resolved) CP at the time this ECG was recorded — this tracing suggests there has been anterior infarction.

• My "eye" was immediately drawn to the 2 leads within the RED rectangles in Figure-2 — which highlight the QS complex in lead V3 and the Q in V4 that indicate infarction.
• NOTE: Preservation of the initial positive deflection (that is the r wave) in leads V1,V2 — suggest the septum is still intact.
• The initial Troponin of >10,000 confirms infarction has occurred — perhaps the day before ECG #1 was recorded, since CP was most severe at that time.
• The modest amount of residual ST elevation in anterior leads, in association with terminal T wave inversion in leads V3,V4,V5 and greatly reduced CP — suggest there has been some spontaneous reperfusion.

BOTTOM Line: Clinical correlation with today's ECG point to LAD (Left Anterior Descending) occlusion, now with reperfusion T waves (in association with the reduction of CP). 

• The above said, this is not Wellens' Syndrome — because a large infarction has already occurred! (See below for full explanation).
• P.S.: Cardiac cath was performed — and showed a distal LAD "culprit" lesion that was successfully stented. Echo revealed an ejection fraction of 35-40%.

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

What is Wellens’ Syndrome?

When we talk about Wellens’ Syndrome — It is all about timing. As reviewed in ECG Blog #350 — the clinical significance of Wellens' Syndrome — is that its recognition tells you that the patient has a high-grade LAD narrowing with presumably "hot" thrombus having high propensity to propagate and/or totally occlude the LAD at any point in time (including immediately). 

The above said — Wellens' Syndrome remains a misunderstood and often misdiagnosed clinical entity. The following are the KEY clinical and ECG features that establish the diagnosis of Wellens' Syndrome:

• There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
• There should be no more than minimal (if any) troponin elevation. 
• There are no new infarction Q (or QS) waves. R wave progression should be preserved (so there is not loss of anterior forces).
• There may be slight (but not marked) ST elevation in one or more of the chest leads.
• There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4).
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• CAVEAT: The diagnosis of Wellens' Syndrome should be made with caution (if at all) in a patient with marked LVH and ST-T wave changes of LV "strain". This is because the ECG finding of increased QRS amplitude that occurs in association with abrupt precordial transition from predominantly negative to predominantly positive QRS complexes — may result in an ST-T wave appearance identical to the biphasic T wave with terminal negativity characteristic of Wellens' changes (See ECG Blog #209 and Blog #254 and Blog #309 — for several examples of this "false positive" appearance).

Why Today's ECG does Not represent Wellens' Syndrome:

Appreciation of the pathophysiology of Wellens' Syndrome facilitates understanding why today's case does not qualify. 

• The characteristic biphasic T wave with rapid T wave descent into terminal T wave negativity — is indication that there has been brief total occlusion of the LAD, which has now spontaneously reperfused. This ECG finding is a "reperfusion T wave". It may look identical to the ST-T wave appearance seen after a STEMI with marked troponin elevation, that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).
• The Chest Pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. The reason the patient is pain-free at the time the defining ECG is done — is that the "culprit" LAD lesion is now open. IF the "culprit" LAD lesion was still occluded — then rather than a warning of impending infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
• The reason there is no more than minimal (if any) troponin elevation with Wellens' Syndrome — is because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. In contrast, if Troponin is significantly elevated — this implies significant myocardial damage has already occurred (which by definition means you are dealing with a completed infarction — and not with the "warning" of an impending large infarction).
• For this same reason — there should not be new infarction Q (or QS) waves, which would imply completed infarction.
• The reason there is no more than slight ST elevation — is because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).
• The clinical risk posed by Wellens' Syndrome — is that it is proof there has already been acute thrombotic occlusion of the LAD (albeit brief in duration and followed by spontaneous reopening of the vessel). BUT — What has spontaneously occluded and then spontaneously reopened — is at high-risk of another spontaneous reocclusion (with no guarantee that there will again be spontaneous reopening this next time that the vessel occludes).

Regarding Today's CASE: 

Reread the history in today's case (in the opening paragraph above) — and Take another LOOK at the ECG in Figure-2.

• Loss of r wave from lead V2-to-V3, so as to form the large QS complex in lead V3 (with Q wave also in lead V4) — indicates that significant anterior infarction has already occurred in today's patient, whose CP has not yet completely resolved — and whose initial Troponin value is already markedly increased (at over 10,000). This indicates completed infarction — and does not fit the definition of Wellens' Syndrome.

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Acknowledgment: My appreciation to Josep Serra Tarragon (from Tarragona, Spain) 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 #326 — Reviews a case of Wellens' Syndrome that was missed.
• ECG Blog #350 — another case of Wellens' Syndrome.
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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 (10/26/2024): 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-3 — 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.
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• 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-3:

• 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-3: 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-4 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose ECGs are shown in Figure-4 — 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).
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• Not shown in Figure-4 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-4). During this time — this patient remained asymptomatic and was gradually increasing his activity level.
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• 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-4: 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).
• 
  
• 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-3 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.
• Finally, a word about the 2 ECG Patterns in Figure-3. 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 the example in Figure-3 — Pattern B may be limited to symmetric T wave inversion without the finding of steep T wave descent into terminal negativity in any lead. Deep, symmetric T wave inversion per se is seen in a number of other conditions, and is 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.

 

EXTRA COPY- ECG Blog #529: Should Prompt Cath be Done? (4-21.1-2029) - EXTRA COPY

The ECG in Figure-1 was obtained from an older woman — who presented following an episode of severe epigastric pain, associated with nausea, vomiting and dyspnea. This ECG was obtained a number of hours after the episode had subsided.

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 — obtained from an older womman following an episode of severe epigastric pain. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The ECG in Figure-1 shows a fairly regular sinus rhythm at ~90/minute. The PR and QRS intervals are normal — and the QTc is at most borderline prolonged. The frontal plane axis is normal at about 0 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: None.
• R Wave Progression: Delayed. Transition (where the R wave becomes taller than the S wave is deep) does not occur until between lead V5-to-V6. That said — at least a small R wave is present in each of the chest leads, with gradual increase in R wave size until transition occurs.

Regarding ST-T Wave Changes:

As highlighted in Figure-2 — ST-T wave appearance is clearly of concern — with abnormal findings in almost all leads.

• ST segments in multiple leads are flat. Most remarkable is the shelf-like ST depression that is maximal in leads V2,V3,V4 (within the RED rectangle in Figure-2). 
• A lesser degree of flat ST depression is seen in the remaining chest leads (ie, in leads V1;V5;V6).
• There is terminal T wave positivity in all 6 chest leads.

In the Limb Leads:

• There is nonspecific ST-T wave flattening with slight depression in high-lateral leads I and aVL (BLUE arrows in these leads).
• In the inferior leads — leads II and aVF show nonspecific ST-T wave flattening. KEY Point: The 3rd inferior lead (which is lead III) — shows ST segment coving, with a hint of ST elevation.
• The remaining limb lead (which is lead aVR) — shows a very slight amount of ST elevation. 

My Impression: 

If today's patient had presented with the ECG in Figure-2 and a history of new-onset chest pain — then this tracing would be especially worrisome.

• Instead — this patient presented with severe epigastric pain, associated with nausea, vomiting and dyspnea. That said — in view of the fact that the symptoms reported could represent a CP (Chest Pain) “equivalent” symptom — Consideration has to be given to the possibility of an acute ongoing cardiac event.
• ST depression is seen in 8/12 leads in Figure-2 (leads I,aVL; and the 6 chest leads). Even without any more than the minimal ST elevation in lead aVR — these findings suggest DSI (Diffuse Subendocardial Ischemia). As discussed in ECG Blog #483 and ECG Blog #400 — DSI may be the result of either non-cardiac causes (ie, anemia, GI bleeding, marked hypotension, "sick" patient, etc.) — or — significant coronary disease, which could be acute.
• As suggested by the RED arrows (within the RED rectangle in Figure-2) — ST depression appears to be maximal in leads V2,V3,V4 — which strongly suggests the possibility of acute or recent posterior OMI.
• In this context — the ST segment coving with slight ST elevation in lead III could reflect associated inferior OMI in the setting of underlying multi-vessel disease (ie, similar to an Aslanger Pattern — as described in detail at the bottom of this page).
• 
  
• BOTTOM Line: Although more information is clearly needed to better define what is going on — one needs to consider the possibility of an acute occlusion infarction (ie, an "OMI") until proven otherwise.

Figure-2: I've highlighted key findings in today's ECG.

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CASE Follow-Up:

Clinical details are unfortunately lacking in today's case. That said, from what I am aware of — the possibility of an acute MI was not considered until a serum Troponin came back markedly elevated.

• At that point — the MI was declared a NSTEMI (Non-ST Elevation Myocardial Infarction). In the absence of ST elevation — cardiac catheterization was deemed to be "not necessary".
• An Echo was not done until later. It showed an inferolateral wall motion defect with significant LV dysfunction. At this point — cardiac cath was finally recommended, but not performed because the patient refused the procedure.
• The patient's condition deteriorated — but with full informed consent, she still refused cardiac cath. Eventually, after a complicated hospital course — her condition improved and the patient was discharged from the hospital.
• The patient never underwent cardiac catheterization ( = her informed consent decision not to undergo cath). A number of weeks later on follow-up — she appeared stable on her new medical treatment regime for heart failure. We can only wonder if the heart failure resulting from this patient's extensive infarction might have been prevented had prompt cath with PCI been done.

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COMMENT:

There are lessons-to-be-learned from this case.

• It is well established that not all patients with an acute MI have CP (Chest Pain). Instead, some patients have other "CP-equivalent" symptoms (ie, epigastric pain, dyspnea) — while others have no symptoms at all (See ECG Blog #228).
• That today's patient had a recent (ongoing) MI was not appreciated until her Troponin came back markedly elevated. This possibility should have been realized as soon as her initial ECG (shown in Figure-1) was recorded. Yet a few days passed before this possibility was considered.
• Given the less typical presentation (ie, epigastric rather than chest pain) — I would interpret today's initial ECG as suspicious but non-diagnostic. The diffuse ST depression (present in 8/12 leads in Figure-2) — clearly indicates DSI (Diffuse Subendocardial Ischemia). As noted above — DSI often (but not always) indicates severe underlying coronary disease.

The situation of having to determine if a patient with a non-diagnostic initial ECG is having an acute MI is common. 

• "Time is Muscle (myocardium). If the cause of an acute MI is acute occlusion of a major coronary vessel (ie, an "OMI" = Occlusion-associated Myocardial Infarction) — then we need to appreciate that the more time that passes until the occluded vessel is reperfused (either by cardiac cath with PCI or by use of thrombolytic agents) — the greater the amount of myocardium that will be lost.
• As repeatedly shown in Dr. Smith's ECG Blog (See My Comment in the February 8, 2026 post) — the most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in up to 60% more myocardium infarcted).

There are 2 main types of acute myocardial infarction: 

• Type 1 MI's — which are caused by a ruptured plaque that results in acute occlusion of a major coronary vessel. 
• Optimal treatment of Type 1 MI's consists of reopening the acutely occluded artery (ie, reperfusion by cardiac cath with PCI — or with use of thrombolytic agents). 
• Sometimes (if not often) — the acutely occluded artery may spontaneously reopen (which is why the patient's symptoms and ECG abnormalities may suddenly improve — even before any treatment is given).
• But what spontaneously reperfuses — may just as easily spontaneously reclose (which is why with a Type I MI, even if symptoms and the ECG suddenly improve [or completely resolve] — definitive treatment with PCI may still be needed to prevent reclosure).

• Type 2 MI's — which are not the result of a ruptured plaque, but instead are due to an oxygen supply-demand mismatch (which may be seen with "high-demand" states, in which the heart requires more oxygen than it receives — as may occur with marked stress states, septicemia, severe anemia, sustained tachyarrhythmias, or shock, among other causes).
• Optimal treatment of Type 2 MI's is to find and "fix" the cause of the supply-demand mismatch (Neither PCI nor thrombolytics benefit a Type 2 MI).
• If it is not clear from history and serial ECGs — then cardiac cath may occasionally (not often) be needed to distinguish between a Type 1 vs Type 2 MI.

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Is "NSTEMI" a Useful Term?

The reason today's ECG was called a NSTEMI (Non-ST Elevation Myocardial Infarction) — is because Troponin was significantly elevated, but no ECG satisfied sufficient millimeter-based ST elevation criteria to qualify as a STEMI.

• It was on this basis (ie, that no STEMI was present) that the recommendation for acute cardiac catheterization was delayed for more than a day. As discussed above — the patient consistently refused cardiac cath — so this delay did not influence the ultimate outcome. That said — it is nevertheless important to consider WHY the recommendation for cardiac cath was so greatly delayed.
• Practically speaking — the diagnostic designation, "NSTEMI" — serves no useful purpose. On the contrary — the "default diagnosis" of calling cases such as the one in today's post a NSTEMI is not only without utility — But it is potentially harmful — because for clinicians who are "stuck" in the outdated STEMI Paradigm, declaring that an MI is a "NSTEMI" provides a false sense of security that prompt cath with PCI is not needed — and this all-too-often results in significant delay until cardiac cath is finally done (and as stated above, "Time is Muscle" = lost myocardium).
• The Clinical Reality: Up to 35% of "NSTEMIs" are found (on their delayed cath) to have had acute coronary occlusion despite a lack of ST elevation on one or more ECGs (Aslanger, Smith et al- IJC Heart & Vasculature, Vol. 30, 2020 — Chi-Sheng Hung et al- Critical Care 22:34, 2018 — Khan et al- Eur Heart J 38(41): 3082-3089, 2017 — and — Avdikos, Michas, Smith- Arch Acad Emerg Med 10(1), 2022).
• And even in those cases in which STEMI criteria are eventually met: i) Waiting for ST elevation to finally develop often results in a delay of too many hours (with loss of too much myocardium); — and, ii) As documented in many cases on Dr. Smith's ECG Blog — for many of these slow-to-develop STEMI cases, the provider still somehow ends up writing "NSTEMI" on the discharge diagnosis.

BOTTOM Line: The millimeter-based "STEMI Paradigm" is flawed — because it misses at least 25% of acute coronary occlusions (which is the group of acute MI's that we care about — because these are the MI's that benefit from prompt reperfusion by either cath with PCI or with thrombolytics). 

• We would all be better served if the outdated and misleading term, "NSTEMI" — was no longer accepted as a diagnosis.
• We would be BEST served if instead of insisting on millimeter-based ST elevation criteria before considering cath with PCI or thrombolytics — if we instead adopted those ECG and clinical clues that have been shown to predict acute coronary occlusion (ie, an acute OMI) without having to wait for sufficient ST elevation (that might never come) before doing so (See detailed discussion in my ECG Blog #337 — in the July 31, 2020 Dr. Smith post — as well as in numerous additional posts in this ECG Blog and in Dr. Smith's ECG Blog).

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What is Aslanger's Pattern?

I introduced the concept of Aslanger's Pattern in ECG Blog #258 and ECG Blog #322. The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

• ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
• ST depression in one or more of the lateral chest leads (V4, V5, V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
• ST elevation in lead V1 that is more than any ST elevation in lead V2.
• There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
• The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

Regarding Today's CASE:

The ECG in Figure-2 does not satisfy all of the above features of Aslanger's Pattern (ie, Instead of ST elevation in leads V1 and V2 — there is ST depression in these leads). That said — the elements of today's case that do resemble this pattern are:

• There is DSI (Diffuse Subendocardial Ischemia).
• The ST segment is coved and slightly elevated in lead III, but not in the other inferior leads.

Bottom Line: Today's patient presented with severe new-onset symptoms potentially consistent with a "CP-equivalent" syndrome. The initial serum Troponin was markedly elevated — thus confirming an acute MI. 

• ST depression is maximal in leads V2,V3,V4 — suggesting an acute posterior OMI (and acute posterior OMI is very commonly associated with acute inferior involvement).
• The diffuseness of ST depression in Figure-2 suggests severe underlying coronary disease.
• In this context, although not strictly satisfying all features of Aslanger's Pattern — I interpreted the ST coving and slight elevation in lead III as suggestive of acute inferior involvement.
• Regardless — Given the history and the markedly elevated initial Troponin — indication for prompt cath seemed apparent as soon as the initial ECG was recorded.
• An Echo was not done until later. If providers had any doubt about the need for prompt cath after seeing the ECG in Figure-2 — seeing the hypokinetic inferolateral wall motion defect on a bedside Echo could have established a definite need for prompt cath within minutes after seeing the initial ECG.

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Acknowledgment: My appreciation to Ahmed Marai (from Anbar, Iraq) for making me aware of this case and allowing me to use this tracing.

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Me to go back to Blog #337 to see how I described this - OMI criteria !!!!

Me to REDO/UPDATE my Comment in the 7/31/2020 SSmith post !!!!

https://drsmithsecgblog.com/omi-nomi-paradigm-established-as-better/