ECG Blog #505 — New? Old? vs New on Old?

The ECG is in Figure-1 was obtained from a previously healthy middle-aged man (?) — who presented to the ED (Emergency Department) with a history of intermittent CP (Chest Pain) over recent days, with the last episode occurring 1 day before the ECG shown below.

• The patient was asymptomatic and hemodynamically stable at the time ECG #1 was recorded.
• No prior ECG available …

QUESTIONS:

• On the basis of the above history and the initial ECG shown in Figure-1 — Should you activate the cath lab?
• Has this patient had an MI? If so — Is it likely that the ECG in Figure-1 represents a "new" MI? — an "old" MI? — and/or, a new MI superimposed on an old MI?

Figure-1: The initial ECG in today's case — from a middle-aged man with intermittent CP over recent days.

My Thoughts on the ECG in Figure-1:

I was not certain about what was going on from the history and ECG presented in Figure-1. I felt at the least that more clinical information — comparison with a prior ECG on this patient — and a repeat ECG would be needed for clarity.

• The rhythm in ECG #1 is sinus at ~75/minute.

PEARL #1: There is LOTS of artifact in this tracing! I favor indicating the presence of artifact in my written assessment — as it is not "our fault" if some details of the tracing are not interpretable. 

• For example, in this patient in whom we are trying to determine IF at some point there has been anterior infarction — Do the extra little deflections seen within the RED circles in leads V2,V3 of Figure-2 represent the "pseudo-Q-waves" of previous infarction? — or — Are these little extra deflections simply a reflection of artifact in the chest leads?
• Sometimes it is possible if you repeat the ECG — that you can minimize the amount of distorting artifact by attention to patient preparation details (ie, Making sure the skin is clean and dry; electrode leads might be loose; the patient may be holding some item that is moving; an extra pillow might be used to stabilize a shaking extremity; an extra blanket might reduce shivering from cold; repositioning an electrode might reduce muscle artifact, etc.). 
• KEY Point: IF we are about the base our decision of whether or not the patient in front of us needs (or does not need) cardiac cath — it is essential to get the best information possible. As a result, IF artifact is preventing optimal interpretation — Have a low threshold for immediately repeating the ECG! 

Figure-2: If artifact impairs our ability to interpret an important ECG — Consider measures to reduce artifact — and then repeat the ECG.

Continuing Our Interpretation of Figure-2:

Despite the artifact in ECG #1 — We still can interpret this tracing sufficiently to make an assessment.

• In addition to sinus rhythm — We can say that intervals (PR-QRS-QTc) and the axis look normal.
• Regarding chamber enlargement — voltage criteria for LVH are satisfied (ie, Peguero Criteria = Sum of the S wave in V3 + V4 >28 mm — per ECG Blog #73).

Regarding Q-R-S-T Waves (which I address in Figure-3):

• Q waves are seen in leads II and III (YELLOW arrows in these leads).
• R wave progression — is slightly delayed. That said — small positive initial deflections (ie, r waves) are present in leads V1,V2,V3 — with transition (where the R wave becomes taller than the S wave is deep) finally occurring between leads V5-to-V6. This delayed transition may or may not be clinically significant.

ST-T wave appearance is not normal in the chest leads:

• In lead V1 — the ST segment coving with slight elevation appears to be disproportionately “bulky” given small size of the QRS complex in this lead.
• Leads V3 and V4 are the most abnormal leads in Figure-3 — with more than 1mm of ST elevation, straightening of the ST segment takeoff — and with terminal T wave negativity.
• This terminal T wave negativity continues in subtle fashion in lateral chest leads V5 and V6 (RED arrows in these chest leads).
• Limb lead assessment is more difficult because of artifact and smaller QRST complex size — but in addition to the Q waves in leads II,III noted above — there is terminal T wave negativity in leads II and aVF, with ST segment flattening in lead aVL (BLUE arrows in these leads).

Impression: In view of the history of intermittent CP in this previously healthy middle-aged man — it is difficult to know how to interpret this initial ECG, especially given his pain-free status at the time ECG #1 was recorded.

• The poor R wave progression — clearly abnormal ST-T wave appearance in lead V1 — with significant ST elevation that is most marked in leads V3,V4 (less in other chest leads) — suggests there has been anterior infarction at some point in time. That said — the terminal T wave negativity in leads V3-thru-V6 (as well as in leads II and aVF) suggest a component of reperfusion that could be consistent with an event having occurred at any point during the “recent days” that this patient has been having intermittent CP.
• Alternatively — it could be that this previously healthy middle-aged man had a prior anterior MI that he was not aware of (ie, a “Silent” MI) — although I would not have expected this much ST elevation to still be present in leads V3,V4 from a prior infarction that over time, has evolved into a left ventricular aneurysm.
• Finally — the Q waves in leads II and III (YELLOW arrows) — together with the ST-T wave abnormalities highlighted by BLUE arrows in the limb leads, could be consistent with either old or recent inferior MI.
• 
  
• BOTTOM Line: The initial ECG that we see in Figure-3 does not distinguish between a new acute MI — vs a recent or previous MI — vs a previous MI, now with recent or acute extension of infarction. More information is needed.

Figure-3: I’ve labeled the initial ECG in today’s case.

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The CASE Continues:

The patient remained asymptomatic. Despite this, emergency providers appropriately obtained a repeat ECG some 15 minutes later.

• To facilitate comparison of these 2 ECGs in today's case — I’ve put both tracings together in Figure-4.

QUESTION:

• Does comparison between the initial ECG and the repeat ECG done just 15 minutes later — tell us what is new vs old vs new-on-top-of-old?

Figure-4: Comparison between today’s initial ECG — and the repeat ECG that was recorded ~15 minutes after ECG #1.

ANSWER: 

I'll emphasize that today's patient was not having CP at the time he presented to the ED — and was not having CP 15 minutes later when the repeat ECG shown in Figure-4 was recorded.

• PEARL #2: I am not aware of all aspects of this case. Instead — I know only that the patient was “asymptomatic” at the time he presented to the ED, and that he remained without CP at the time his initial ECG was repeated. This raises the important question of, “Why now?” (ie, Is there some reason WHY the patient presented to the ED on this day — and not on one of the previous days when he was having CP?).
• Asking the question, "Why now?" can be extremely insightful for explaining ECG changes that may be seen between serial ECGs (ie, Sometimes patients don't report subtle changes in their symptoms until specifically questioned).

With regard to Figure-4 — Looking lead-to-lead ...

• There clearly is more ST elevation in leads V3,V4.
• Subtle increases in ST elevation are also seen in Leads II,III,aVF; V1,V2.
• The terminal T wave negativity that was present in 6 leads with BLUE and RED arrows in ECG #1 — is no longer seen! 
• Instead — there is now ST segment flattening (if not slight ST depression) in lead V6!
• 
  
• PEARL #3: There have been "dynamic" ST-T wave changes during the 15 minutes that passed between the recording of ECG #1 and ECG #2. While we still cannot tell without finding a prior ECG if a previous anterior infarction had occurred at some time in the past — we now know that an acute evolving event is in progress! Prompt cath is needed!
• PEARL #4: The picture in ECG #2 suggests Precordial "Swirl" — given the coved ST elevation in lead V1 — marked ST elevation in mid-chest leads — and ST segment flattening and depression in lead V6 (See ECG Blog #482 and ECG Blog #380 — for detailed review of Precordial Swirl). This ECG picture strongly suggests acute proximal LAD occlusion!
• 
  
• PEARL #5: The fact that the terminal T wave inversion that had been seen in ECG #1 has now resolved — and has been replaced by an increase in ST elevation (most marked in leads V1,V3,V4) — tells us that the "culprit" lesion has reclosed. Clinically, spontaneous reclosure of the "culprit" artery is usually accompanied by return of chest pain — but even without return of CP, the dynamic ST-T wave changes now seen in ECG #2 are convincing!
• 
  
• PEARL #6: It was the above convincing chest lead changes that prompted me to take another closer look at limb lead changes between the 2 tracings in Figure-4. These changes are truly subtle because of the very small amplitude of limb lead QRS complexes and the large amount of baseline artifact in these leaads — but on close inspection: i) Terminal T wave inversion is no longer seen in leads II,aVF; — ii) ST-T waves look more hyperacute in each of the inferior leads; — and, iii) There is more reciprocal ST depression in high-lateral leads I,aVL. 

Cardiac Cath was quickly performed:  

• Severe multi-vessel disease was present. Balloon angioplasty was performed on the 1st Diagonal Branch — and a drug-eluting stent was placed in the proximal LAD. 
• Considering the diffuseness of cardiac cath findings — I suspect this "previously healthy" patient had longstanding largely "silent" coronary disease, and presented now with acute anterior infarction.

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Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) 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 #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
• ECG Blog #424 — Another example of when marked LVH may manifest anterior ST elevation.
• ECG Blog #461 — Another example of the differential diagnosis between LVH vs acute anterior MI vs LV aneurysm.
• ECG Blog #380 and Blog #482 — on Precordial "Swirl".
•  
• For cases similar to today, in which LVH may mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.
• 
  
• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

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ADDENDUM (11/15/2025):

• 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).
• 
  
• 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.
• 
  
• 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.

ECG Blog #504 (Video) — A Challenging Rhythm ...

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 — Today's case is an ECG Video!

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The 3 successive lead II rhythm strips shown in Figure-1 — are from a 10-year old child with palpitations.

QUESTIONS:

• What is the rhythm? 
• What to consider clinically?

Figure-1: Succesive rhythm strips from a 10-year old child with palpitations.

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Below is the Video presentation of today's case (9 minutes):

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Acknowledgment: My appreciation for today's case — sent to me from an anonymous follower.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #188 — Reviews how to read and draw Laddergram (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
• ECG Blog #192 — AV Dissociation by Usurpation — Default — or by AV Block?

 

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ADDENDUM (11/8/2025): 

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The 2:30 minute ECG Video below reviews:

• The Ps,Qs,3R Approach — for systematic rhythm interpretation.
• Some additional general tips on rhythm interpretation.

ECG Media PEARL #9 (4:45 minutes) — reviews the 3 Causes of AV Dissociation — and emphasizes why AV Dissociation is not the same thing as Complete AV Block.

ECG Blog #503 (14,57) — The Cause of the Pause

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NOTE: I’ve decided to update and republish several of my favorite cases from years past. (Today's post is an improved version of ECG Blogs #14,57 — initially published in 2011).

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QUESTIONS: Interpret the rhythm below in right-sided Lead MCL-1.

• There is group beating in Figure-1.  Is this Wenckebach?
• Extra Credit: Why is the PR interval before beat #7 shorter than the PR interval before beat #6 (and also shorter than the PR interval before the other sinus beats in this tracing?).

Figure-1: Is the group beating here due to Wenckebach?

MY Thoughts on the Rhythm in Figure-1:

The rhythm in Figure-1 is not regular, but does manifest a pattern of group beating (with 2 short pauses between beats #2-3 and #6-7). 

• The QRS complex for each of the 9 beats in this tracing is narrow (ie, not more than half a large box in duration = not more than 0.10 second in duration). 
• The underlying rhythm appears to be sinus, with similar-looking P waves showing a fixed PR interval preceding all beats except for beat #7.
• Despite the presence of group beating — there is no evidence of Wenckebach or other form of AV block on this tracing.  Instead, the "cause" of the pause lies partially hidden within the T waves of beats #2 and 6.

PEARL #1: It's important to remember that the most common Cause of a Pause is a blocked PAC. Although most premature supraventricular beats ( = PACs or PJCs) are conducted normally to the ventricles (ie, with a narrow QRS complex that looks like other sinus-conducted beats) — this is not always the case. Instead, PACs (or PJCs) may sometimes occur so early in the cycle as to be "blocked" (non-conducted) because the conduction system is still in an absolute refractory state.

• This is the situation for premature impulse A in Figure-2 — which shows impulse A occurring during the ARP (Absolute Refractory Period).
• At other times — premature (early beats may occur during the RRP (Relative Refractory Period) — in which case aberrant conduction (with a wide and different-looking QRS) occurs. This is the situation for premature impulse B in Figure-2.
• Because impulse B occurs during the RRP — part (but not all) of the ventricular conduction system has recovered. Most often PACs occurring at Point B will conduct with some form of bundle branch block and/or hemiblock (reflecting that part of the conduction system which has not yet recovered).
• Premature impulse C in Figure 2 occurs after the refractory period is over.  As a result — a PAC occurring at Point C will conduct normally (ie, with a narrow QRS that looks identical to other sinus beats on the tracing).

Figure-2: Absolute and Relative Refractory Periods (ARP & RRP) — explaining why beat A is blocked — and beat B is conducted with aberration.

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Returning to the Questions in Today's Case: 

Take another LOOK at Figure-1.

• Is the group beating in Figure-1 due to Wenckebach?
• Why is the PR interval before beat #7 so short?

Figure-1: Taking another look at Figure-1 ...

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ANSWERS:

There is no AV block in Figure-1. The PR interval as one moves from beat #3 to beats #4,5 and 6 is not increasing, as it would if Mobitz I (which is 2nd-degree AV block of the Wenckebach type) was present.

• Instead (as per PEARL #1) — The cause of the pause that we see between beats #6-7 in Figure-1 is a blocked PAC. We show this in Figure-3 — in which the RED arrow in the T wave of beat #6 highlights the "telltale notching" of a PAC buried in this T wave. 
• Note that a similar very early-occurring PAC (corresponding to a PAC occurring at point A in Figure 2) can be seen notching the T wave of beat #2.

PEARL #2: How do we know that the pointed deflection highlighted by the RED arrow in Figure-3 is truly a PAC — and not artifact? The KEY is that none of the normally conducted sinus P waves in this tracing manifest anything resembling an "extra" deflection (ie, The T waves of beats #1; 3,4,5; 7,8,9 are all smooth — and it is only the T waves of beats #2 and 6 that manifest this extra pointed deflection). 

• Thus, we need to first determine what the normal T wave for a sinus-conducted beat looks like — before we can determine if a PAC is partially hidden within the T waves of other beats.

Figure-3: Answer to Figure-1.

PEARL #3 — is related to PEARL #1: 

• Because the most common cause of a pause is a blocked PAC, it turns out that in clinical practice — blocked PACs are much more common than any form of AV block.
• That said — blocked PACs are often subtle and difficult to detect. As a result — they are often overlooked. But — blocked PACs will be found IF looked for (they'll often be hiding and/or notching a part of the preceding T wave — as seen above in Figure-3).

NOTE: The occurrence of a PAC depolarizes the rest of the atria — and therefore resets the SA Node. As a result — a brief pause usually follows after a premature P wave. These relationships are schematically illustrated in the laddergram shown in Figure-4:

• The rhythm in Figure-4 begins with 2 normally sinus-conducted beats (beats #1 and 2).
• The PINK circles in the Atrial Tier of the laddergram represent the 2 PACs that are not conducted to the ventricles, because they occur so early as to fall within the ARP (corresponding to impulse A, as was shown in Figure-2).
• Note the brief pause that follows each of these blocked PACs (ie, the pauses that occur between beats #2-3 and between #6-7).
• Unlike AV Wenckebach (in which the underlying P wave rhythm remains regular) — We can see that the sinus P wave before beat #3 ( = the 3rd RED circle in Figure-4) is delayed. When this 3rd RED arrow sinus P wave finally occurs — this P wave is conducted to the ventricles with a normal PR interval.
• There follow 3 more on-time sinus P waves (producing sinus-conducted beats #4,5,6) — until the next very early-appearing PAC occurs (the RED arrow highlighting this 2nd blocked PAC that notches the T wave of beat #6).
• Once again — a brief pause is seen after this 2nd blocked PAC. But note that when the next sinus P wave finally occurs — the PR interval before beat #7 is shorter than all other PR intervals on this tracing! (as per the open RED circle showing this very short PR interval before beat #7).

PEARL #4: The PR interval before beat #7 is too short to conduct. But since the QRS of beat #7 is narrow and virtually identical in morphlogy to all of the other sinus-conducted beats on this tracing — beat #7 must be a junctional escape beat! (schematically represented by the BLUE circle within the AV Nodal Tier).

• Normal sinus rhythm then resumes for the last 2 beats in Figure-4 ( = beats #8 and 9).
• To Emphasize: The occurrence of a junctional escape beat in Figure-4 is perfectly appropriate. The R-R interval preceding beat #7 is slightly more than 6 large boxes in duration, which corresponds to a junctional escape rate of slightly less than 50/minute — which means that the AV node is doing what it is "supposed to do" — namely, putting out an escape beat at the appropriate junctional escape rate of between 40-60/minute if and when the next sinus P wave is delayed.
• 
  
• Beyond-the-Core for a Very Advanced Point: Extra credit to any readers who used calipers, and on carefully measuring the R-R intervals of both pauses in Figure-4 — detected that the R-R interval for the 1st pause (between beats #2-3) — is actually slightly longer than the R-R interval for the 2nd pause. Since most of the time — the junctional escape rate is quite regular, I would have expected the junctional escape beat in this tracing ( = beat #7) to be preceded by a longer pause than the pause that precedes beat #3 which is sinus-conducted — but the opposite occurs. I attribute this unexpected finding to the slight variation in regularity that may occasionally be seen with escape rhythms.

Figure-4: Laddergram illustration of the rhythm from Figure-1. The cause of the 2 brief pauses (between beats #2-3 and #6-7) are blocked PACs. The PR interval preceding beat #7 is too short to conduct — which tells us that beat #7 is a junctional escape beat.  

Part 2 in Today's CASE: 

To emphasize the clinical importance of today's case — I present another challenging rhythm that I show in Figure-5.

QUESTIONS: 

Interpret the rhythm below in right-sided Lead MCL-1:

• What kind of AV block is present?
• Is a pacemaker likely to be needed?

Figure 5: Lead MCL-1 rhythm strip. Is this Mobitz I or Mobitz II? 

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ANSWER:

Hopefully you did not fall into the trap. There is no AV block in Figure-5. 

• As always — I find it easiest to be systematic. I favor the Ps,Qs,3Rs Approach (See ECG Blog #185).
• 
  
• The ventricular rhythm in Figure-5 is quite Regular at a Rate of ~50/minute for the first 6 beats. I'll defer attention to beat #7 for the moment.
• The QRS for these first 6 beats is narrow in this single lead rhythm strip. Assuming the other 11 leads in a 12-lead tracing confirm that the QRS is narrow — this would tells us that the rhythm is supraventricular.
• P waves are present! (ie, the colored arrows in Figure-6).
• The 5th parameter in the Ps,Qs,3R Approach addresses whether P waves are Related to neighboring QRS complexes — which they are for the first 6 beats, because the PR interval preceding beats #1-thru-6 is constant (RED arrow P waves in Figure-6). Thus, there is sinus conduction!
• But — every-other-P-wave is not conducted (No QRS follows the BLUE arrow P waves in Figure-6).

PEARL #5: The rhythm in Figure-6 is not a form of AV block! There are several reasons why we know this:

• The shape of the P waves highighted by the RED and BLUE arrows is different! (RED arrow P waves have an initial pointed positive deflection, followed by a wider, rounded negative deflection — vs — BLUE arrow P waves that have a triphasic negative-positive-negative morphology). This is consistent with atrial bigeminy (every-other-P-wave being a PAC) — because P wave morphology will be different when P waves arise from different atrial sites.
• The P-P interval is irregular! While true that 2nd- and 3rd-degree AV blocks often manifest slight P-P interval variation — the degree of P-P interval variation with this type of "ventriculophasic sinus arrhythmia" is generally not nearly as marked as the variation in P-P intervals seen in Figure-6.
• Beat #7 is a PAC that is conducted to the ventricles, here with a wider QRS complex due to aberrant conduction. P wave morphology of this last premature P wave is identical to the P wave morphology of each of the preceding BLUE arrow P waves — suggesting that all of these P waves are PACs.
• 
  
• CONCLUSION: The commonest cause of a pause is a blocked PAC, and not some form of AV block. There is no AV block in Figure-6. Instead — the rhythm is atrial bigeminy (every-other-P-wave is a PAC) — with the first 4 BLUE arrow P waves highlighting blocked PACs — and the last BLUE arrow representing a PAC that conducts with aberration (similar to impulse B in Figure-2).

Figure 6: Colored arrows highlight each P wave in Figure 5.

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.
•  
• 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 #350 — another case of Wellens' Syndrome.
• ECG Blog #326 — Reviews a case that was missed.
• 
  
• 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 (10/25/2025): 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).
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• 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.
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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-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.