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!
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• 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. 
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• 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".
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• 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.
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• 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).
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• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

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

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 Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1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• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.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