EXTRA COPY — ECG Blog #533: A Surprise Diagnosis — EXTRA COPY

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

https://www.powerfulmedical.com/

https://ecg-interpretation.blogspot.com/2024/08/ecg-blog-443-40s-man-with-cp-and-dyspnea.html

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Figure-2: "My Take" on defining the ST segment baseline (from Grauer K: ECG Pocket Brain-2014 ePub).

 

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Figure-3: I've labeled today's initial ECG.

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Figure-4: ECG Findings associated with acute PE (updated since ECG Blog #443).

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Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #443 and ECG Blog #496 — Review challenging cases on the ECG diagnosis of acute PE.
• ECG Blog #313 and ECG Blog #435 — Review more cases on the ECG diagnosis of acute PE.
• ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
• 
  
• ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
• ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”. 

Mohammed Elsisi <mohammedelsisi18@gmail.com> 4/24/2026
E-Mail from Mohammed 

THE CASE:

This tracing was obtained from a 45 y male pt who presented to the ER with burning chest pain on off for about 1 week with also reproduction of pain with minimal exertion along with dyspnea.

Pt was vitally stable 

I rapidly i terpreted this as sinus tachy with old inferior infarct & may be lad omi based on amputated r in rt precordial leads along with straightening of st segment with rounded peaked ample t waves. 

What's ur take? 

Thank in advance kenneth. 

MY REPLY:

Hi. This is a very worrisome tracing!

• There is sinus tachycardia (which of itself is a worrisome sign — since sinus tach is uncommon with acute MI unless “something else” [ie, heart failure, shock] is going on … ).
• As you say — there are inferior Q waves in a “qRS” pattern, which in the inferior leads almost always means an Inf. MI at some point in time.
• At the least — there is DSI ( = Diffuse Subendocardial Ischemia) — as indicated by the ST elevation in aVR, with ST depression in the other 5 limb leads.

I suspect there is a Precordial “Swirl” pattern — with clearly abnormal ST elevation & T inversion in V1 — and ST segment straightening with ST elevation in leads V2,V3 — and what looks to be some J-point depression in V6. “Swirl” typically is from acute or recent proximal LAD occlusion. The loss of R wave from V2-to-V3 suggests anterior infarction.

The difficult question is what is new vs old — and if new (as I suspect) — how new given the 1 week history of intermittent CP.

• Any prior history of heart disease in this patient?
• Any prior ECG available?
• The patient needs prompt cath — with my suspicion of an LAD “culprit” artery.

Please give me follow-up. If you can find out what happened — I would love to use this case for an ECG Blog. LET ME KNOW.  — Ken

 

= = = = = = = =

Mohammed REPLY:

Thanks ken, as u mentioned pt was admitted in the ccu as ACS. Bedside echo done showed a dilayed rv with d shaped septum thrn CTPA show bilateral pe. 

Back to the ecg one may note that prominent s in lead i ste in rt precordials & deeps in v4 to v6 along woth sinus tachy all may be ecplained with the pe as a final Dx. 

Finally echo was the only clue to us to suspect pe instead of ACS. Pt also now is stable on iv enoxaparin. We do simple work up for hidden malignancy pelviabdominal US ct chest PSA. Thanks in advance.

MY REPLY:

Hello Mohammed. Bedside Echo is invaluable !!! Once you are trained in it — you can do within minutes and you learn so much. If the etiology is an acute MI — then finding a localized wall motion abnormality is strongly supportive of that (with the 1 caveat being that when you have DSI — if there is global dysfunction, then you might not recognize the wall motion abnormality, unless overall LV function was greatly depressed in symmetric fashion).

 

In the “retrospectscope” — in addition to the sinus tachycardia (which as I said, is unusual with acute MI unless there is “something else” going on) — there are S waves everywhere !!! (in virtually all 12 leads! ) — and that can be a sign of acute right heart strain.

• That said — I did not suspect acute PE given the history of CP ….

 

So — I always like to go back in cases like this and “soul-search” and try to figure out what clues were missed. What did WE miss?

• ST elevation in lead V1 with T wave inversion in this lead can be a sign of acute RV “strain”!
• I fully admit that I still did not suspect acute PE, because the SHAPE of the ST depression in this tracing looks different that that usually seen with acute PE (ie, no T wave inversion) — and because of those inferior Q waves — and because of the ST straightening and ST elevation in V2,V3

 

KEY POINT — You did mention “dyspnea” — but you said “vitally stable”. I assumed “vitally stable" meant that the patient’s RR ( Respiratory Rate) was normal.

• In my experience — the most commonly overlooked vital sign is the respiratory rate. Much of the time — the clinician at the bedside does not take the time to COUNT the respiratory rate. Nurses also (in my experience) of do not count the respiratory rate, but instead put down 12 or 15/minute if the patient “seems OK”.
• This clearly is something that “Ya gotta be there — at the bedside” — but unless the clinician spends a moment to LOOK at the patient — it is all-too-easy to miss a patient taking rapid but small breaths unless you actually COUNT the breaths per minute — and if the patient was breathing 25-30/minute at rest — in addition to sinus tach — diffuse S waves — and that abnormal isolated ST elevation in lead V1 — acute RV failure could be all too easy to miss ….
• In retrospect — right-sided leads would probable show right-sided ST elevation.

• FINALLY — Did this patient ever have an ECG before? Comparison with a prior tracing may have been helpful. That said —it could be that ALL of the ECG findings that we see here are acute as a result of acute PE ….

   

  Bottom Line — Acute PE may present with a “Pseudo-infarction” pattern! (although usually there is more ST elevation in inferior or anterior leads in such cases … )

  • Having said all of the above — I still “fell into the trap” of thinking this ECG looked more like coronary disease than acute MI …

   

  Any more info you can provide would be helpful = What happened? How is the patient doing?

   

  MAY I WRITE this case up for an ECG Blog?

  • If so — Would you like me to acknowledge you OR do you prefer the case is anonymous?
  • If you’d like me to acknowledge you — please confirm if you’d like your name written as Mohammed Elsisi — and tell me the city and country from where you are from?

   

  THANKS! — Ken

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ECG Blog #443

https://ecg-interpretation.blogspot.com/2024/08/ecg-blog-443-40s-man-with-cp-and-dyspnea.html

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The ECG in Figure-1 was obtained from a man in his 40s — who presented to the ED (Emergency Department) because of CP (Chest Pain) and shortness of breath.

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• Based on the history and the patient's initial ECG — the cath lab was activated. Do you agree?

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

MY Thoughts on this CASE:

Not being there — I am unaware of physical exam parameters (blood pressure, respiratory rate; oxygen saturation; heart and lung auscultation, etc.). What we can comment on, given the brief history of new CP and dyspnea — is the initial ECG shown in Figure-1. I see the following:

• There is sinus tachycardia (upright P wave with fixed PR interval in lead II) — at the rapid rate of ~130/minute.
• Regarding intervals — the PR interval is normal — the QRS is of normal duration. Given the rapid rate — it is hard to say much about the QTc.
• There is RAD (Right Axis Deviation) — in that that QRS is slightly more negative than positive in lead I ( = estimated frontal plane axis about +100 degrees).

Regarding chamber enlargement — LVH is not present. Although frank criteria for RVH (Right Ventricular Hypertrophy) are not present — there are a number of ECG findings consistent (if not suggestive) of acute RV "Strain" (See Figure-2). 

• PEARL #1: Before going further — We need to consider the possibility of acute PE (Pulmonary Embolism)! Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #435 — ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).

I review the ECG diagnosis of acute RV "strain" and acute PE in the ADDENDUM below (See Figures-7, -8, -9). For now — Let's continue with ECG signs consistent with and suggestive of acute RV "Strain".

• Sinus Tachycardia and RAD — as already noted above.
• PEARL #2: In the absence of associated heart failure (cardiogenic shock) — sinus tachycardia is not a common finding in acute MI. As a result — the finding of sinus tachycardia in today's patient, who presents with both CP and shortness of breath (especially to as rapid a heart rate as the ~130/minute seen here) — should immediately prompt consideration of something other than acute coronary occlusion.
• 
  
• Although criteria for RAA (Right Atrial Abnormality) are not strictly satisfied (P wave amplitude in lead II does not attain 2.5 mm in amplitude) — the P wave in lead II is more peaked and pointed than it usually is (within the RED oval in Figure-2). In the context of a suggestive clinical history and other ECG signs of acute RV "strain" — I interpret more-than-expected inferior lead P wave peaking as suggestive of RAA, therefore another supportive (albeit subtle) indication of RV "strain" (See ECG Blog #75 — for more regarding ECG criteria for RAA).
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• S1Q3T3 — Whereas the diagnostic value of this pattern is limited when seen as an isolated finding — a definite S1Q3T3 pattern (as seen in Figure-2) — is very helpful in today's case, given association with other ECG evidence pointing to the possibility of acute PE. 
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• PEARL #3: ST-T wave findings of acute RV "Strain" — are most often seen in the form of anterior T wave inversion (and/or anterior ST depression). The other ECG area to look for RV "strain" — is in the inferior leads, though it is less common in my experience to only see RV "strain" inferiorly without also seeing ST-T wave changes anteriorly.
• As a result — I admittedly, was initially deterred from the diagnosis of acute PE because of the lack of anterior T wave inversion in ECG #1. That said — ST-T wave changes of acute RV "strain" are present in each of the inferior leads (BLUE arrows in leads II,III,aVF in Figure-2).
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• PEARL #4: Instead of anterior lead T wave inversion — there is some ST elevation in leads V1 and V2, with ST segment straightening in lead V3. On occasion — such anterior lead ST elevation (instead of T wave inversion) can be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016). 
• Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2 in Figure-2).

PEARL #5: The KEY for being able to suspect acute PE from the ECG — is when you see a constellation of ECG findings potentially consistent with this diagnosis (as listed below in the ADDENDUM in Figure-7) — in a patient with a suggestive history. 

• Today’s patient presented to the ED not only with chest pain — but also with shortness of breath, therefore with a history potentially consistent with the diagnosis. 
• Easily attainable bedside findings that further support the diagnosis of acute PE include a low oxygen saturation — and — an increased respiratory rate. To emphasize — Count the respiratory rate yourself! (Reading the respiratory rate off of nursing notes is not necessarily accurate in my experience — so spending 15-20 seconds simply looking at the patient breathing and counting breaths is well worth this short amount of your time).
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• ECG Signs (in addition to those already mentioned above) — that are consistent with acute PE in today’s tracing (as per the Table in Figure-7) include: i) Poor R wave progression, with persistence of S waves through to lead V6; and, ii) The rSr' morphology seen in lead V1, which in association with the narrow terminal s waves in lateral leads I and V6 — is consistent with a IRBBB proxy (See labeled Figure-2 below).

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

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QUESTION: 

Although today’s initial ECG is potentially consistent with acute PE — I would not be 100% convinced of this diagnosis from the tracing shown in Figure-2 alone.

• What could be done at the bedside within no more than a few minutes to verify the diagnosis of acute PE?

ANSWER:

• A POC (Point-Of-Care) ECHO — will sometimes be diagnostic of acute PE. When it is — this may greatly expedite clinical decision-making for anticoagulation and/or thrombolysis.
• The sensitivity of POC Echo is not perfect. That said — the specificity of Echo for acute PE can be excellent IF certain echocardiographic findings are present. This is especially true for larger, more hemodynamically significant PEs — with prognostic insight provided depending on the degree of impairment of RV function (On and Park — Korean J Intern Med: 38(4);456-470, 2023 and Hritani et al — Cleveland Clin J Med 85(110: 826-828, 2018).

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The ECHO on Today's Patient:

In Figure-3 — I've labeled the 4-chamber view from the Echo on today's patient. In Figure-4 — I've included the video recording of this view. What do you think?

Figure-3: Still picture of the Echo 4-chamber view.

Figure-4: Video recording of this 4-chamber view. I include a slow-motion section to facilitate recognition of the diagnostic Echo sign described below.

Figures-3 and -4 on Today's Echo:

For orientation — the 4 chambers are shown in Figure-3:

• The RV (Right Ventricle) is clearly dilated, and appears to be even larger than the LV. As a result of RV overload — the IVS (InterVentricular Septum) is shifted toward the left side of the heart. In a patient with a suggestive history and ECG findings consistent with acute PE — seeing this degree of RV dilation on Echo strong favors acute PE as the diagnosis. That said — seeing RV dilation on Echo does not distinguish between acute vs chronic causes of RV "strain".
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• PEARL #6: In contrast to the finding of RV dilation (that could be a longstanding condition) — the McConnell Sign is a dynamic echocardiographic finding that is specific for conditions causing acute RV "strain", such as acute PE. 
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• A McConnell Sign is said to be present when 2 echocardiographic findings are seen: i) There is RV free wall akinesis (seen as per the YELLOW arrow in Figure-3 — as an outward movement of the RV free wall as a result of increased pressure in the dilated RV chamber); and, ii) The RV apex manifests hypercontractility, as a result of being "tethered" to the LV (RED arrow moving inward). This sign is positive in the video recording shown in Figure-4 — in which the RV apex has been described as "a trampoline bouncing up and down while the rest of the RV remains still."
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• References on Echo for PE Diagnosis: Oh and Park - Korean J Intern Med 38(4):456-470, 2023 — and — Hritani et al - Cleveland Clin J Med 85(11):826-828, 2018 — and — IF you want an excellent 5-minute video review on recognition of the McConnell Sign on Echo — WATCH_this_VIDEO by Dr. Christopher Voscopoulos.

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Diagnostic CTPA on Today's Patient:

Final confirmation of acute PE in today's case was obtained by CTPA ( = Pulmonary Angiography in Figure-5). 

• Excellent review of diagnostic testing for acute PE (Moore et al — Cardiovasc Diagn Ther 8(3):225-243, 2018).
• For a 10-minute video review on reading Pulmonary CT Scan — WATCH_this_VIDEO by Dr. Jake Gibbons.

Figure-5: CTPA view in today's case — showing large clot burden in the right and left main pulmonary arteries.

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CASE Follow-Up:

The "good news" in today's case — is that the patient received thrombolytics, and ultimately did well. That said — the diagnosis of acute PE was delayed for a number of hours, because providers were initially more concerned about an acute MI. As a result — diagnostic Echo was not performed until after cardiac cath was found to be normal.

• PEARL #7: Echo at the bedside is a fast test that takes only minutes! In today's case — the Echo could have been done while waiting for cath facilties to get ready. Had this been done — the dramatic RV dilation and positive McConnell Sign seen in Figures-3 and -4 — would have allowed immediate confirmation of acute PE that could have avoided any need for cardiac cath, thereby expediting initiation of thrombolytic therapy.

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Repeat ECG After Thrombolytic Therapy:

I found it of interest to compare the follow-up ECG obtained after successful thrombolytic therapy (Figure-6).

• Sinus tachycardia has resolved.
• Right axis deviation in ECG #2 is much less (predominant positivity of the R wave in lead I has returned).
• RV "strain" is no longer evident (resolution of ST depression in the inferior leads).
• Right-sided ST elevation that had been present in leads aVR, V1,V2 of ECG #1 — is no longer seen in the repeat tracing.
• S waves no longer persist through to lead V6.

Figure-6: Comparison between the initial ECG in today's case — with the repeat ECG obtained following thrombolytic therapy.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #313 and ECG Blog #435 — Review cases on the ECG diagnosis of acute PE.
• ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
• 
  
• ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
• ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”. 

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ADDENDUM #1 (8/16/2024): 

I've included below some review material regarding the ECG diagnosis of acute PE (Pulmonary Embolus) and RV "strain".

Figure-7: ECG Findings associated with acute PE (from ECG Blog #435).

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PEARL #8: The "Note" under the S1Q3T3 finding in Figure-7 — refers to data from Kosuge et al (Am J Cardiol 99(6): 817-821, 2007 — and the March 4, 2023 post in Dr. Smith's ECG Blog) — that state that when there is T wave inversion in the chest leads, if T waves are also inverted in leads III and V1 — then acute PE is far more likely than acute coronary disease (See the Addendum ECG in Figure-10 below).

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Figure-8: Summary of KEY findings in the ECG diagnosis of acute PE (from my ECG-2014-ePub).

Figure-9: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

 

ADDENDUM #2 (8/17/2024): 

My thanks to Konstantin Tikhonov (from Moscow, Russia) — who sent me the following illustrative ECG and case the very next day after I posted this ECG Blog #443.

• The patient whose ECG is shown in Figure-10 — had progressively increasing dyspnea over a 10 day period.
• Considering the ECG findings shown above in Figure-7 (with attention to PEARL #8) — How many ECG findings of acute PE can you identify?

Figure-10: Addendum ECG (My thanks to Konstantin Tikhonov for sending me this case). 

ANSWER:

The ECG in Figure-10 shows the following findings in favor of acute PE:

• Sinus tachycardia.
• S1Q3T3.
• Persistent precordial S waves (through to lead V6).
• Acute RV "strain" (here in the form of deep, symmetric chest lead T wave inversion that is maximal in leads V2,V3,V4 — and as per PEARL #8, shows T wave inversion in lead V1 and lead III, as well as in lead aVF).

Follow-Up: Pulmonary CT scan confirmed an acute submassive PE.

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.

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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).
• 
  
• 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.
•  
• 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).
• 
  
• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
• 
  
• ECG Blog #326 — Reviews a case of Wellens' Syndrome that was missed.
• ECG Blog #350 — another case of Wellens' Syndrome.
• 
  
• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
• 
  
• 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.
• 
  
• 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.
•  
• 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-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.
• 
  
• 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.