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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