EXTRA COPY — ECG Blog #526: Epigastric Pain — EXTRA COPY

The ECG in Figure-1 — was obtained from a younger adult male who presented to the ED (Emergency Department) with new epigastric pain. The patient had a history of prior PCI (Percutaneous Coronary Intervention).

• The cardiology team was consulted — but felt there was no indication of a STEMI, and that the tall chest lead T waves represented a repolarization variant in this patient whose presenting symptom was abdominal pain.

QUESTIONS:

• Do YOU agree with the cardiology consultant's opinion?
• What would you do? 

Figure-1: The initial ECG in today's case — obtained from a younger adult male with epigastric pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

It’s always challenging when you disagree with your consultant and the patient’s well-being is dependent on a timely correct diagnosis. There are many reasons why the Cardiology Team’s opinion is not correct. These include: 

• i) The “focus” is wrong. In a patient who presents to the ED for new-onset of a potential “CP (Chest Pain) Equivalent” symptom — the onus is on medical providers to rule out an acute event, rather than having to “rule it in”. (This is especially true in a patient with known coronary disease, given prior PCI).
• ii) The diagnosis of a “repolarization variant” — is a diagnosis of exclusion (ie, to only be made after you have ruled out the possibility of an acute event). While I have seen very tall, peaked, non-hyperkalemic T waves represent a benign repolarization variant — this is rare! Instead — the presence of overly tall, peaked chest lead T waves in a patient who presents to the ED with new symptoms should be suspected as representing a form of deWinter-like T waves until proven otherwise (See the ADDENDUM below).  
• 
  
• iii) The morphology of the chest lead ST-T waves is diagnostic! As shown below in Figure-2 — these T waves are symmetric (Benign repolarization variants tend to be asymmetric — with slower rising and more rapid downsloping of the ascending and descending T wave limbs). In addition — the T wave peaks become “fatter”-than-they-should-be” as one more toward chest leads more lateral than lead V3. Finally — straightening of the ST segment takeoff in lead V6 indicates hyperacuity in a patient with new symptoms.
• iv) STEMI Criteria are satisfied in Figure-2 (ie, the dotted RED lines in leads V4,V5 show 2 mm of J-point ST elevation). To Emphasize: STEMI criteria are not needed to justify the need for prompt cath in today’s patient — but these criteria are nevertheless satisfied.
• v) Limb lead findings confirm that today’s ECG is not a repolarization variant! This is because: a) There is clearly abnormal ST segment straightening with angulation of the T wave onset in leads III and aVF (These represent subtle “reciprocal” changes to the chest lead T wave peaking); — and, b) There is equally subtle-but-real ST elevation in lead aVL — and — a “bulky” (hyperacute) T wave in lateral lead I.

Bottom Line: In a patient who presents to the ED with new symptoms — today’s ECG is strongly suggestive of acute LAD occlusion (LAD OMI) until proven otherwise! 

Figure-2: I've labeled today's ECG.

What to Do?

If your cardiology consultant does not agree with your interpretation — Consider the following:

• Repeat the ECG within 10-20 minutes! Especially in the presence of ongoing symptoms — it is often surprising how quickly acute ECG finding may evolve. Seeing “dynamic” ST-T wave changes in a patient with new symptoms should serve to convince the most skeptical of interventionists of an acute evolving event in need of prompt cath.
• And, if your 1st repeat ECG fails to show significant changes — Continue to order timely additional repeat tracings (which in a patient with ongoing symptoms will usually show changes).
• Find a prior ECG for comparison! Given the history of previous PCI — We know that this patient has previous ECGs. If the ECG in Figure-2 represents a new acute event — there is no way that a previous ECG will show such overly tall, peaked T waves (ie, You can immediately prove that the ST-T wave changes in Figure-2 are new if these findings are not seen on a previous tracing).
• Perform bedside Echo. If your patient who shows the extensive ECG abnormalities seen in Figure-2 continues to have ongoing symptoms — a bedside Echo will almost always show a localized wall motion abnormality that is diagnostic of an acute event.
• Realize that any elevation in Troponin is significant in a patient with persistent new symptoms. 

To Emphasize: Waiting for serum Troponin to rise takes longer than the time it should take to repeat the ECG, find a prior tracing (if PCI was done in the same hospital) — and/or do bedside Echo. 

• CAVEAT #1: As noted in ECG Blog #508 — Although one may be momentarily comforted by an initial normal hs-Troponin value — this in no way rules out an acute cardiac event. Wereski et al (JAMA Cardiology, 2020) — found that 14% of patients with an acute STEMI had a normal initial hs-Troponin (and ~25% had hs-Troponin levels below the infarction “rule-in” level). 
• Therefore — IF serial ECGs show "dynamic" ST-T wave changes — or, a prior ECG looks different — or, bedside Echo shows a localized wall motion abnormality — then waiting for an elevated Troponin wastes precious time (and precious myocardium).
• 
  
• CAVEAT #2: Bedside Echo is only helpful in lowering the likelihood of an acute event IF: a) LV contractility is completely normal; and, b) The patient is having symptoms at the time the Echo is done (Nothing is ruled out if the patient is pain-free at the time the Echo is done).

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CASE Follow-Up:

• Bedside Echo showed reduced contractility.
• The patient continued to have severe pain.
• As a result — cardiac cath was performed and showed a "culprit" lesion in the LAD (Left Anterior Descending) coronary artery. The patient's pain was relieved following PCI — and he has done well in follow-up.

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Acknowledgment: My appreciation to Nirdosh Rassani (from Quetta, Pakistan) for the case and this tracing.

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ADDENDUM (4/4/2026): 

• See ECG Blog #183 for review of the original 2008 NEJM manuscript by deWinter and colleagues.
• ECG Blog #341 is equally insightful (There are many other examples of deWinter-like T waves on this Blog).

MY Observations regarding De Winter T Waves: 

Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

• Many (most) of these cases do not fit strict definition of “de Winter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, giant T waves are limited.
• ECG changes in many of these cases are not “static” until reperfusion, as was initially reported in 2008 by de Winter et al. Nevertheless, cath follow-up routinely confirms LAD occlusion.
• 
  
• MY "Take": I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. What will be seen on the ECG depends greatly on when during the process the ECG was obtained. While many of these patients do not manifest “true de Winter T waves” (because their ECG pattern does not remain static until reperfusion by coronary angioplasty) — for the practical purpose of promptly recognizing acute OMI — I don’t feel ( = my opinion) that it matters whether a “true” de Winter T wave pattern vs simple “hyperacute” T waves (that are deWinter-like) is present.

 

—  —

TODAY’s ECG Media PEARL #1 (3:00 minutes Audio): — relates to the phenomenon of deWinter-like T waves.

EXTRA COPY- ECG Blog #525- Another Wide Tachycardia- EXTRA COPY

The ECG in Figure-1 was obtained from an older woman who presented with new-onset palpitations. She was hemodynamically stable in association with this tracing.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How specific can you be with your interpretation?
• What is the treatment of choice? 

Figure-1: The initial ECG in today's case.

MY Thoughts on this Tracing:

The ECG in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at a rate of ~185/minute without clear sign of atrial activity.

• QRS morphology is consistent with LBBB conduction in the chest leads (ie, predominantly negative QRS in the anterior leads — with an all-positive QRS in lateral chest leads) — with an inferior frontal plane axis (as determined by the all-positive QRS in inferior leads — with an equiphasic QRS in lead I).

Impression:

The above description is virtually diagnostic of RVOT VT (Right Ventricular Outflow Track Ventricular Tachycardia).

• PEARL #1: Once you are familiar with the entity of RVOT VT — You should be able to make this diagnosis with high accuracy within seconds of seeing an ECG that looks like today’s tracing. 
• As we’ve shown on multiple posts on this ECG Blog — RVOT VT is one of the two most common forms of idiopathic VT (See ECG Blog #489 — Blog #346 — Blog #323 — among many others). This term “idiopathic” VT simply refers to the ~10% of patients who present with VT without underlying heart disease.

I review the KEY distinguishing points of the idiopathic VTs in the ADDENDUM to today’s post (See my summary info sheet in Figure-4 — and my 8-minute Audio Pearl below).

• Many (admittedly not all) of the idiopathic VTs are readily recognizable by their QRS morphology (described in Figure-4).
• Because the QRS complex in idioventricular VT is typically not overly wide — and because of the resemblance to QRS morphologic features of known conduction blocks (ie, RBBB + Hemiblock for fasicular VTs — and LBBB for outflow track VTs) — there is a tendency to misdiagnose the idiopathic VTs as some form of reentry SVT with aberrant conduction (instead of recognizing them as VT).

PEARL #2: One of the most helpful clues that a regular WCT without P waves is likely to be idiopathic VT (and not some form of reentry SVT with aberrant conduction) — is that there are subtle atypical features that are not consistent with any known form of conduction block. For example — in Figure-1:

• Although the predominant negativity of the QRS complex in leads V1,V2 is consistent with LBBB conduction — with typical LBBB, transition tends to occur later than what is seen in Figure-1 (ie, with simple LBBB — no more than a tiny r wave usually persists past lead V3 — and this R wave does not become predominant until at least lead V5). Instead, as we look at Figure-1 — the R wave is already enlarging in lead V3, and it is predominant in lead V4.
• With LBBB — septal depolarization moves right-to-left (instead of left-to-right) — followed by slow, progressive leftward depolarization of the left ventricle (that overwhelms electrical activity arising from the much smaller right ventricle). As a result — the QRS vector in left-sided leads V6 and in lead 1 manifest an all-positive widened R wave. The small, isoelectric QRS complex in lead I of Figure-1 should not be seen with LBBB (unless there has been prior infarction and/or extensive scarring or myocardial infiltration). The fact that this small isoelectric complex in lead I begins with a negative deflection — and the finding of an all negative QRS in high-lateral lead aVL are especially atypical for LBBB conduction.
• To Emphasize: It’s impossible from Figure-1 alone to be 100% certain that this ECG represents VT. But the findings of LBBB-like conduction in the chest leads with an inferior frontal plane axis are completely typical for RVOT VT — and — the atypical QRS morphology features described in this PEARL #2 strongly suggest VT until proven otherwise.

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The CASE Continues:

Today's patient was successfully cardioverted — but the WCT rhythm in Figure-1 returned. Lasting conversion to sinus rhythm was finally achieved after a 2nd cardioversion (as shown in Figure-2).

QUESTIONS:

• Does the ECG in Figure-2 solidify the diagnosis of VT for the initial ECG that was seen in Figure-1?
• What other interventions might have been considered?

Figure-2: The repeat ECG, recorded after the 2nd cardioversion.

My Thoughts:

The repeat ECG in Figure-2 shows restoration of a normal sinus rhythm (RED arrows in Figure-3 highlighting upright sinus P waves in the long lead II) — with the exception of a single early wide beat toward the end of the tracing ( = beat "X").

• PEARL #3: We know with 100% certainty from Figure-3 that beat X is a PVC (Premature Ventricular Contraction) and not an aberrantly conducted supraventricular beat — because underlying "on time" sinus P waves continue thoughout this long lead II rhythm strip (ie, The PINK arrow P wave shows continuation of these "on time" sinus P waves — and this can only happen if the wide beat originates "from below", since a supraventricular beat would have delayed the next sinus P wave).
• 
  
• PEARL #4: Note that QRS morphology in Figure-3 of the PVC is identical in simultaneously-recorded leads V4,V5,V6 (within the BLUE rectangle) — to QRS morphology in leads II,V4,V5,V6 during the WCT rhythm in ECG #1. This finding highlights the utility of the post-conversion ECG for retrospectively making a definitive diagnosis of the etiology of a WCT rhythm if one or more similar QRS morphology PVCs are seen.

Figure-3: Comparison between the 2 ECGs in today's case.

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Final Thought: Regarding treatment of the WCT rhythm in ECG #1: 

• There is no single "correct" answer for how best to treat the regular WCT rhythm that today's patient presented with. And, the treatment path chosen in today's case was successful.
• Synchronized cardioversion is clearly the intervention of choice if there is any concern about hemodynamic stability in association with a WCT rhythm. Sometimes, "Ya just gotta be there" to judge when to go ahead with synchronized cardioversion.
• That said — today's patient was stable on presentation, so options are available. As noted below in Figure-4 — RVOT VT often responds to Adenosine, which could have been tried.
• Recurrence of the WCT after the 1st synchronized cardioversion in today's case was a signal that a longer-acting intervention (ie, perhaps IV Amiodarone) might be needed to maintain sinus rhythm, rather than repeat cardioversion.
• I do not have further follow-up as to whether or not this patient was referred for EP evaluation. 

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Acknowledgment: My appreciation to Kianseng Ng (from Kluang, Johore, Malaysia) for making me aware of this case and allowing me to use this tracing.

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ADDENDUM (3/XXX/2026):

• Below — More on idiopathic VT:

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? 

— WHY do we care? Special attention to the 2 most common forms 

= RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

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EXTRA COPY — ECG Blog #524: A little bit of Jadwar — EXTRA COPY

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NOTE: Today's post is from our publication in JACC Case Reports — 

(Nirdosh Rassani, MBBS & Ken Grauer, MD — Jan, 2026) (https://www.jacc.org/doi/10.1016/j.jaccas.2026.107164)

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The patient in today's case is a man in his late 20s — who presented to the ED about 6 hours after ingesting a finger-breadth piece of Jadwar (Figure-1).

Figure-1: Photograph of Delphinium denudatum (Jadwar). 

Details of today's case can be found in our JACC Case Reports article (available at the above link). 

• Suffice it to say that the patient's symptoms at the time of presentation were limited to mild flushing, increased sweating and palpitations. 
• He was alert — with stable vital signs.

On seeing this patient's initial ECG (that I've reproduced in Figure-2) — it is easy to understand his chief complaint of "palpitations".

QUESTION:

• How would you interpret this initial ECG?

Figure-2: The initial ECG in today's case — obtained from a man in his 20's who ingested Jadwar. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-2:

This patient's initial ECG is extremely worrisome. That's because there is a constantly changing QRS morphology. It's hard to tell if there any "normal" beats.

• To facilitate assessment in Figure-3 — I've numbered the beats in the long lead II rhythm strip.
• Can you tell what is going on? (See below).

Figure-3: I've numbered the beats in today's initial ECG.

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

The Long-Lead II Rhythm Strip:

This is a complicated rhythm strip. I outline my stepwise "thought process" for assessment below:

• The rhythm is irregularly irregular.
• As noted — QRS morphology is constantly changing throughout the long lead II rhythm strip. Many of the beats are wide.
• There are some narrow beats. Three of these narrow beats look similar and are upright in the long lead II (ie, beats #5,12,18). Presumably these 3 beats are supraventricular!
• A short pause precedes beats #5 and 18 — but I see no sign of atrial activity. If P waves were present — I would expect to see them in the short pause that precedes beats #5 and 18. Given the overall irregularity with occasional narrow beats but no sign of P waves — I suspect that the underlying rhythm is AFib (Atrial Fibrillation).
• There are multiple wide beats in the long lead II. Other than beats #5,12,18 — all of the other positive QRS complexes are clearly wide (ie, beats #1,2,3,4; #6; #9,10,11; #14; #19). Each of these beats look to be of ventricular etiology.
• Fortunately — the long lead II rhythm strip is simultaneously recorded with the 12-lead tracing above it. The reason this is so helpful in this tracing — is that this allows us to view the QRS complexes that are negative in the long lead II in other simultaneously-recorded leads. For example — although beat #13 looks fairly narrow in the long lead II — it is actually a wide (presumably ventricular) beat when viewed in simultaneously-recorded leads V2,V3.
• Beat #16 is all negative and appears to be slightly widened in the long lead II — but it looks much wider, and clearly of ventricular etiology in simultaneously-recorded leads V1,V2,V3.
• Beat #15 in the long lead II looks intermediate in QRS morphology between beats #14 and #16. Is the intermediate QRS shape of beat #15 the result of fusion between beats arising from 2 different ventricular sites?
• On the other hand — not only is beat #21 narrow in the long lead II — but it appears to also be narrow in simultaneously-recorded leads V4,V5,V6. This suggests that beat #21 may be supraventricular, with its negative QRS morphology in the long lead II explained by aberrant conduction. Perhaps other fairly narrow, negative complexes in the long lead II are also supraventricular with aberrant conduction?

My Impression of Figure-3: 

This is an extremely complicated tracing. My assessment:

• The underlying rhythm appears to be AFib.
• There are multiple wide beat QRS morphologies that most-likely represent non-sustained runs of PMVT (PolyMorphic Ventricular Tachycardia).
• Those beats that are narrower in the long lead II exhibit beat-to-beat variation in QRS morphology, suggestive of aberrant conduction and/or fusion with ventricular ectopy.
• 
  
• PEARL #1: What counts in assessment of Figure-3 is the overall "Gestalt" of what is likely to be happening. It simply is not worth spending excessive time trying to "dissect" the etiology of every beat in this tracing — as this is a thankless, if not impossible task. Instead, our goal for interpreting the rhythm is to arrive at an overall assessment — and this appears to be underlying AFib with non-sustained runs of PMVT.
• 
  
• PEARL #2: As noted above — beat #21 is probably supraventricular with aberrant conduction. As a result, I looked closely at ST-T wave morphology and the QT interval for this beat. Note within the RED rectangle in Figure-3 — that there appears to be marked ST depression in leads V5,V6 for beat #21 (BLUE arrow) — as well as QT prolongation considering the overall rapid rate.
• 
  
• PEARL #3: The unusual rhythm in Figure-3 is best interpreted in light of the clinical situation. This clinical situation is that today's patient ingested Jadwar prior to the onset of his symptoms! 

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

About Jadwar:

Jadwar (Delphinium denudatum) is a traditional medicinal herb widely used in South Asia as a "universal antidote" for treating a wide variety of neurologic, analgesic and gastrointestinal conditions. Among its attributed actions include pain relief, an anti-inflammatory effect, reduced fatigue, antidote properties (for snake or scorpion bites), addiction recovery (to help manage narcotic dependency) — as well as for treatment of URIs and other common infections.

• Although Jadwar itself is generally considered safe and of low toxicity when used appropriately — Jadwar may sometimes be adulterated with aconite (which can occur if/when herbal medicines are improperly prepared).
• Aconite ingestion may be highly toxic and even fatal. The mechanism stems from binding to and persistently activating voltage-sensitive sodium channels in excitable cells (including myocardial, nerve and muscular tissue). This results in sustained sodium influx with persistent sodium channel activation (Chan — Clin Toxicol 47(4):279-285, 2009).
• Patients with aconite ingestion may present with a combination of neurologic features (paresthesias with facial or limb numbness) — motor effects (muscle weakness) — and cardiovascular effects that may be severe (hypotension, chest pain, palpitations from a variety of arrhythmias including refractory ventricular tachycardia and ventricular fibrillation).
• Management of aconite poisoning is largely supportive until effects of ingestion have worn off. IV Lidocaine was successfully used in our case for its sodium-channel blocking effect that counteracts aconitine toxicity.

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

CASE Follow-Up:

Detailed description of today's presentation is covered in our JACC Case Reports article. In brief — laboratory evaluation of this patient was largely normal, with exception of low-normal serum Mg++ (treated with IV Mg++ replacement). Serum Troponins were negative and Echo showed surprisingly normal LV function despite the arrhythmia.

• Within 30 minutes of administering IV Lidocaine (IV bolus followed by IV infusion) — there was a dramatic reduction in the frequency and duration of PMVT episodes — with complete suppression of ventricular ectopy achieved by 6 hours.
• IV Lidocaine infusion was continued for 24 hours — followed by observation on telemetry for an additional 24 hours, after which the patient was discharged from the hospital.

To facilitate comparison in Figure-4 — I've added the discharge ECG below this patient's initial tracing. This discharge tracing reflects what was seen on telemetry during the last 40+ hours of observation.

• Note return of normal sinus rhythm (RED arrow P waves in the long lead II of ECG #2) — and the complete absence of ventricular ectopy!
• The lateral chest lead ST depression in ECG #2 is now minimal — with normalization of the QT interval.
• PEARL #4: In support of my suspicion that beat #21 in the initial tracing was indeed a supraventricular beat — is the finding of similar QRS morphology for this beat in leads V5,V6 of ECG #1 — with QRS morphology in leads V5,V6 after restoration of sinus rhythm in ECG #2. This suggests that the reason beat #21 was negative in the long lead II of ECG #1 was indeed aberrant conduction.
• The "PEARL" — is that sometimes the etiology of certain beats or rhythms of uncertain etiology in an initial tracing may become clear by careful comparison of morphology on subsequent tracings.

Figure-4: Comparison of today's initial ECG — with the discharge ECG recorded 48 hours later.

FINAL Thoughts:

Today's case proved satisfying by the complete recovery made by this patient who had ingested a potentially lethal dose of medicinal herb.

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Related Material:

• ECG Blog #231 — reviews the various types of VT terminology.
• 
  
• See Viskin et al (Circulation 144:823-839, 2021) — for an in-depth review of PMVT.

EXTRA COPY — ECG Blog #523: Is there a "Culprit"? — EXTRA COPY

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The ECG in Figure-1 was obtained from an older woman — who presents to the ED (Emergency Department) with CP (Chest Pain) that began ~2 hours earlier.

QUESTIONS:

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

Figure-1: The initial ECG in today's case.

MY Thoughts on Today's CASE:

Given the history of new CP — this is an extremely worrisome ECG:

• The  rhythm is sinus at ~80/minute. Regarding intervals — the PR interval and QRS duration are both normal, with the QTc no more than of borderline duration. Regarding chamber enlargement — the S wave of >20 mm in lead V2 is consistent with voltage for LVH (See Figure-7 in the Addendum of ECG Blog #73).

Regarding Q-R-S-T Changes:

• A small and narrow Q wave is seen in lead aVL.
• R wave progression — is normal (Small but definite initial r waves are seen in both leads V1,V2 — with transition occurring normally between leads V3-to-V4).

The remarkable findings relate to ST-T waves:

• My attention was immediately drawn to the ST-T waves in the 3 inferior leads — which show eyecatching straightened and downsloping ST segments (RED arrows in leads II,III,aVF in Figure-2). Each of these leads show terminal T wave positivity (upright YELLOW arrows) — with this down-up T wave appearance in a patient with new CP being an especially worrisome sign of hyperacuity.
• Support for our concern is forthcoming from the hyperacute ST-T wave appearance in lead aVL (with ST segment straightening, subtle-but-real ST elevation given small size of the QRS — and a disproportionately "fattened" T wave with wide base).

In the Chest Leads: 

• Lead V1 is notable for ST segment straightening — which is especially remarkable in light of the distinctly abnormal 1-2 mm of flat ST segment depression in leads V3,V4,V5,V6 (BLUE arrows in these leads). Each of these 4 chest leads show significant terminal T wave positivity — which in this patient with new CP strongly suggests hyperacuity.
• I found lead V2 especially interesting as a "transition" lead — in that it shows neither J-point depression or elevation. This is most probably because lead V2 is situated between lead V1 (which is remarkable for its hyperacute-looking ST segment straightening) — and leads V3,V4,V5,V6 (each of which show unmistakeable ST segment flattening and depression with terminal T wave positivity).
• Finally — there is slight-but-real ST elevation in lead aVR.

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

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Putting It All Together:

• I'd immediately activate the cath lab. The history of new-onset CP in this older woman whose initial ECG shows significant ST-T wave abnormalities in no less than 11/12 leads indicates an acute cardiac event until proven otherwise.

The question arises as to what the "culprit" artery might be? 

• The only lead showing ST elevation is lead aVL. In the absence of ST elevation in other lateral leads — I thought acute LCx (Left Circumflex) occlusion to be less likely.
• ST elevation is commonly seen with proximal LAD (Left Anterior Descending) occlusion — but other than the ST segment straightening in lead V1 — there is no anterior lead ST elevation.
• Instead — the predominant finding in Figure-2 is the very acute-looking ST depression with terminal T wave positivity in 7 leads (leads II,III,aVF; and leads V3,V4,V5,V6) — with transition lead V2 — and with ST elevation in lead aVR.
• 
  
• PEARL #1: The most logical explanation for this series of acute-looking ST-T wave abnormalities without suggestion of a specific "culprit" artery — is that there is severe multi-vessel disease.
• I suspected acute LAD occlusion given findings of ST straightening in V1 + transition lead in V2 with lateral chest lead ST depression suggesting a Precordial "Swirl" pattern (See ECG Blog #380). Supportive findings of ST elevation in aVL with reciprocal inferior lead ST depression is consistent with proximal LAD occlusion — with the diffuseness of the ST depression reflecting impossible-to-account-for attenuation effects from multi-vessel involvement.
• Bottom Line: None of this matters. What counts is simply that prompt cath with PCI is needed. Specific anatomy to be revealed by cardiac cath.

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The CASE Continues:

• Cardiac cath was performed — and revealed severe multi-vessel disease (with an 80% ostial LMain lesion — a 95% "culprit" mid-LAD lesion + RCA disease).
• The initial hs-Troponin-I came back with borderline elevation. The repeat Troponin was clearly elevated.

PEARL #2: It does not matter what Troponin shows in today's case. This is because regardless of what the 1st and 2nd Troponin assays show — prompt cath with PCI will be needed given the history of new-onset CP and today's initial ECG showing diffuse acute-looking ST-T wave changes in 11/12 leads!

• The initial hs-Troponin may be negative or non-diagnostic in up to 25% of acute STEMI patients (Wereski et al — JAMA Cards 5(11):1302, 2020).
• "Time is Muscle (myocardium)". As repeatedly shown in Dr. Smith's ECG Blog (See My Comment in the February 8, 2026 post) — The most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in 60% more myocardium infarcted).
• Serum Troponin values provide a rear-view mirrow of what has already happened — and not of what is about to happen.
• PEARL #3: The decision to perform cardiac cath in today's case can be made as soon as the initial ECG is seen.

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A 2nd ECG was recorded ~3 hours after ECG #1 (shown in Figure-3):

• ECG #2 was obtained prior to cardiac cath — at a time when the patient's symptoms had decreased. Dual antiplatelet therapy (DAPT) and Heparin were ongoing.

QUESTIONS:

• Given that the patient's CP was less at the time ECG #2 was recorded — How would you interpret this repeat ECG?

Figure-3: Comparison between the 2 ECGs in today's case.

MY Thoughts on ECG #2:

Compared to ECG #1 — the repeat ECG in Figure-3 shows reperfusion changes in virtually all leads that previously looked acute:

• Most remarkable in ECG #2 is the anterior lead ST segment coving, now with deep, symmetric T wave inversion in lead V2.
• The horizontal ST depression previously seen in leads V3,V4,V5,V6 has essentially resolved.
• Reciprocal reperfusion changes are now seen in the inferior leads — in which downsloping ST depression has been replaced by tall, "bulky" positive T waves.
• Deep symmetric T wave inversion is seen in lead aVL.
• PEARL #4: Especially in view of reduced CP — I interpreted the evolutionary changes in ECG #2 as confirming acute LAD occlusion as the "culprit" artery in this patient with underlying multi-vessel disease.

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Acknowledgment: My appreciation to Chun-Hung Chen (from Taichung City, Taiwan) for the case and this tracing.

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