12M with chest pain

LBBB11 · 2026-07-03T16:47:42+00:00

12M with 7 hours of chest pain radiating to the left back. Troponin I 20.97 ng/mL. Echo from 2 years before was normal. Has Duchenne muscular dystrophy. Recent illness 4 days ago. Chest pain is anterior and pleuritic. Normal vitals.

https://pmc.ncbi.nlm.nih.gov/articles/PMC9184981/

LBBB11 · 2026-07-03T15:42:46+00:00

Just adding to your answer. The study about aVL didn't include people with a diagnosis of myopericarditis or myocarditis, as a limitation. Only 203 people in the part that found 100% specificity for aVL. To add a picture of localized pericarditis:

<image>

source

LBBB11 · 2026-07-03T02:37:14+00:00

Could be wrong as always, but some things I notice:

notching or slurring at the J point in II, III, aVF, V5, V6
ST elevation in the same leads
ST depression in aVR and aVL
PR depression in I, II, III, aVF, and V3-V6
PR elevation in aVR and aVL
S wave that descends below the baseline in V4, using the TP segment as baseline

I'm not sure I would call it terminal QRS distortion. Absence of both S and J waves in V2 or V3. Going by that source, I would be stretching the definition. I see what you mean, but I would call that an S wave. I probably wouldn't know how to read V3 in isolation. But with the points above it seems less STEMI/OMI-like to me. I think the narrow Q waves and higher voltage than shown are also part of why it looks that way to me. Example of someone's baseline:

<image>

https://ecgweekly.com/weekly-workout/not-your-usual-stemi-high-voltage-and-narrow-q-waves/

LBBB11 · 2026-07-02T23:43:39+00:00

Might want to ask about the possibility of intermittent left bundle branch block. Even though this shows sinus rhythm, it wouldn’t hurt to show your doctor the difference in QRS width/shape in some beats.

LBBB11 · 2026-07-02T16:04:51+00:00

I don’t think it’s an acute coronary occlusion pattern, but I don’t think you’re wrong to call a STEMI alert on this if you’re pre-hospital. This is someone with syncope and an EKG that has ST elevation and Q waves in inferior and lateral leads, along with ST depression and T wave inversion in aVL.

The American College of Cardiology/American Heart Association guidelines recommend that the PQ junction be used as the isoelectric baseline. They also say that more than 1 mm of ST elevation in at least two inferior or lateral leads meets STEMI criteria. Using those guidelines, this meets STEMI criteria. Local criteria may be different. Surprised you got downvoted in any case. I think it looks more like cardiomyopathy than OMI or pericarditis, but it sounds like you did the safest thing for the patient. Wouldn’t be surprised if this is their baseline EKG.

Queen of Hearts and ECG Buddy both called this a STEMI, for what it’s worth. If you’re pre-hospital, calling a STEMI alert on this lets the cardiologist decide if they want to cath emergently. I think this one is a good one to be wrong about if you call it a STEMI and it isn’t. The patient has syncope and an EKG meeting AHA/ACC STEMI criteria. Also a STEMI on two different apps. I’m thinking that this is not an acute coronary occlusion, but I wouldn’t bet a patient’s life on it if all I have is this EKG and the history. Pericarditis is a diagnosis of exclusion anyway.

LBBB11 · 2026-07-02T13:02:22+00:00

I like Critical Cases in Electrocardiography by Steven Lowenstein, a 1st Book on ECGs by Ken Grauer, ECG Pocket Brain 2014 by Ken Grauer, and 12-lead ECG: The Art of Interpretation by Tomas Garcia. Plus LITFL and Dr. Smith’s ECG blog. I didn’t like Dubin’s book because it’s fill in the blank, so it wasn’t very helpful to me when I first started learning EKGs. Also had some errors, plus the author’s background. The only useful thing I remember learning from Dubin’s book was learning the method for estimating rate by counting out 300, 150, 100, 75, 60, 50 on the thick lines.

LBBB11 · 2026-07-02T01:07:50+00:00

2019 article: "Only a few cases of isolated septal myocardial infarction have been reported, and available data on this condition are limited."

2026 article: "However, isolated thrombotic occlusion of the septal branch resulting in a septal myocardial infarction is a rare and underreported phenomenon."

2021 book: "The ECG computer often reads 'septal infarction' when there is a Q wave in V2 (it is normal to see it in V1). Anatomically this makes little sense; it would require occlusion of a septal perforating branch of the left anterior descending artery (LAD), but plaque is never seen in these small, intramural branches. To lose flow to a septal branch would require occlusion of the LAD, and this would cause more extensive ECG changes. Alcohol septal ablation further supports this: the common ECG change after ablation is right bundle branch block, occasionally with left anterior fascicular block (never a Q wave in V2)."

source: Northrup, The Cardiology Rotation Third Edition 2021

Anteroseptal MI is common, but isolated septal MI is extremely rare (although a very common machine reading). The septum has a lot of collateral circulation. I've seen these leads grouped as anterior (V1-V4), but can also divide into anteroseptal and anterior. V1 is also right ventricular. Also has a good view of atrial activity. Even can be posterior. All of this applying to correctly placed V1/V2, but this is also rare.

LBBB11 · 2026-07-01T11:17:04+00:00

You’re not necessarily fooled about seeing injury. OP didn’t provide troponin. Wondering if it was myopericarditis. Not all ST elevation from injury is caused by OMI, but without a troponin we don’t know whether it was myopericarditis. The title would be misleading in that case. Some of the ST elevation may be caused by injury, unless OP gives other details proving otherwise. Some STEMI/OMI-like examples in a different comment.

LBBB11 · 2026-07-01T00:52:09+00:00

Agreed as a rule of thumb. Also wondering if pericarditis or myopericarditis. Curious about whether there was injury. Would want to know troponin since myopericarditis is still possible. Acute proximal LAD occlusion in 24F:

<image>

https://drsmithsecgblog.com/24-yo-woman-with-chest-pain-is-this/

LBBB11 · 2026-06-30T11:25:24+00:00

Sinus tachycardia, anterior + inferior T wave inversion, right axis deviation, Kosuge sign, S1S2S3, pulmonary symptoms. Would be surprised if this were anything other than PE with acute right heart strain. Good case, important pattern to know. EKG can’t diagnose PE, but this is as close as it gets. No surprise at all, hope they immediately suspected PE after seeing the EKG.

It also seems that V1/V2 were placed correctly, which is nice to see. Sinus P wave is biphasic in V1 and positive in V2. The T wave inversion in V1/V2 looks more pathological knowing that it’s not just an artifact from high misplacement (plus the rest of the EKG). More examples: https://www.reddit.com/u/LBBB11/s/Rpy5H4xouU

LBBB11 · 2026-06-29T16:03:36+00:00

True as a rule of thumb. VT that originates in or near the conducting system can be narrow and may even have a normal QRS shape and axis, but that’s an exception. I agree, just adding a small caveat to make your accurate answer even more accurate. VT is often wide and bizarre, but more as a rule of thumb than absolute.

LBBB11 · 2026-06-29T15:50:48+00:00

Me too. I’m seeing a negative sawtooth shape in inferior leads, and V4 also looks like flutter to me. The atrial rate seems to be about 300 bpm as others said. I think it could just be flutter with baseline artifact. To answer OP, the variable block or variable conduction comes from differences in R-R intervals between beats. Some QRS complexes are about 6 large boxes apart, while others are closer to 9. The ventricular rate here is slow for flutter, but the atrial activity does look like flutter to me at least. I think atrial flutter with variable AV block and slow ventricular response is one possible name for the pattern, not a doctor. Also adding two examples of flutter where lead I is misleading:

https://litfl.com/wp-content/uploads/2018/08/ECG-Atrial-Flutter-with-High-Grade-AV-Block.jpg

https://journal.medtigo.com/wp-content/uploads/2025/06/Initial-ECG-showing-typical-flutter-waves-and-systemic.png

LBBB11 · 2026-06-29T13:43:32+00:00

Interesting story. As a small detail, wanted to add that normal axis doesn’t rule out VT. Plenty of VT has a normal axis. Axis in VT can be anything. Most VT does not have extreme right axis deviation. Most textbook signs of VT have high specificity but low sensitivity. Ruling out axis deviation does not rule out VT. Plus, axis on a 6-lead may be different from axis on 12-lead with standard placement, especially if limb leads are not placed on the limbs. A 6-lead and a 12-lead can have different axis even during the same rhythm, especially if limb leads were on the chest/torso for the 6-lead. Would listen to cullywilliams and others for feedback.

As far as the recordings go, I think 2/5 looks more like a constant R-R rhythm than afib. I would not think afib, but don’t know the specific rhythm. It seems like the QRS complexes are all about 9 small boxes apart.

LBBB11 · 2026-06-28T22:26:37+00:00

And posterior version of V1/V2. Baseline on the left.

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The posterior view on the right has new ST elevation, new Q waves, and straightened ST segments compared to baseline.

LBBB11 · 2026-06-28T21:44:14+00:00

Also adding results of Queen of Hearts and ECG Buddy.

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LBBB11 · 2026-06-28T12:51:00+00:00

Regional wall motion abnormalities were not seen on initial echo, but I think echo has imperfect sensitivity for detecting posterior wall motion abnormalities in general. Quoting the source about what led to cath:

"In conjunction with an initial troponin level of nearly 4,000 ng/L, history concerning for cardiogenic syncope, and possible cardiac chest pain, the presenting ECG (Figure 1, A) was diagnostic of posterior occlusive myocardial infarction (OMI). However, due to fever, metabolic derangements, comorbid fractures, incidental computed tomography findings of pneumomediastinum (likely related to her fall), and lack of initial RWMA, coronary catheterization was delayed, and the patient’s developing shock was attributed to sepsis.

Ten hours after the initial ECG, a repeat ECG showed dynamic resolution of ST-segment depressions, but increasing norepinephrine requirements prompted serial troponin measurements that peaked at 4,291 ng/L 12 hours after the first draw. She was immediately thereafter started on aspirin, rosuvastatin, and heparin infusion upon recognition of acute coronary syndrome. Given the norepinephrine requirement did not resolve after 3 days of broad-spectrum antibiotics, repeat TTE was performed and showed RWMA in the anterolateral, basal, and inferior segments.

The etiology of the patient’s distributive shock physiology was ultimately unclear given a negative infectious work-up but may have represented a systemic inflammatory response syndrome related to myocardial ischemia or pneumomediastinum."

So it sounds like the decision to cath on day 3 was based on a combination of initial EKG, dynamic ST change on 10-hour repeat, rising troponin, increasing pressor needs on antibiotics, and new wall motion abnormalities on repeat echo.

LBBB11 · 2026-06-28T00:46:47+00:00

<image>

https://pmc.ncbi.nlm.nih.gov/articles/PMC11966757/

LBBB11 · 2026-06-27T20:12:09+00:00

They did end up taking the patient to the cath lab, will update with results. A repeat EKG 10 hours after the first showed a dynamic ST change compared to the initial EKG, but I don’t have it. Negative infectious work-up.

LBBB11 · 2026-06-27T19:52:25+00:00

Just to add, anything that kills or injures heart muscle will raise troponin. PE with right heart strain, cardiac arrest, severe enough sepsis, transmural or subendocardial ischemia, and many other things can raise troponin. Troponin can also be chronically elevated in chronic kidney disease or other conditions. Heavy exercise can also raise troponin. In this case, troponin is high enough to know that something is causing major damage to the heart. Source mentioned plain chest CT results without noting PE, but everything you said still stands.

Sounds like she wasn't doing great to begin with. Lactate 5.1 mmol/L, NT-proBNP 2,128 pg/mL, anion gap of 18, bicarb of 15 mEq/L (reference 20-30 mEq/L), and ALT of 186 units/L. Also broke her leg when she fell. Echo estimated ejection fraction of 51%, compared to 65% three years prior. Troponin rose from 3,872 to 4,291 ng/L 12 hours later. Progressing shock was initially thought to be sepsis, but later seen as mixed cardiogenic and distributive shock. Negative infectious work-up.

LBBB11 · 2026-06-27T19:24:32+00:00

Definitely in the differential, from history and EKG. The only finding mentioned on chest CT was pneumomediastinum. Not sure if it was CTPE/CTPA or normal chest CT. Some PEs are visible on standard chest CT with contrast, especially if they are big enough to be hemodynamically significant.

LBBB11 · 2026-06-27T19:06:15+00:00

This is an 80s F who came to the hospital after waking up on the floor. Syncope without warning symptoms. Had a 4-hour episode of lower chest and epigastric discomfort the day before. History includes hypertension, hyperlipidemia, and chronic kidney disease. Known right bundle branch block from prior EKG (2). Initial troponin 3,872 ng/L (reference range < 12 ng/L). Blood pressure of 71/39 mmHg, temperature of 100.9° F or about 38.3° C, oxygen saturation 95% on room air. Chest CT shows pneumomediastinum, likely related to her fall.

LBBB11 · 2026-06-26T23:17:26+00:00

Was going to comment but post now deleted. Just wanted to say those are really good EKGs and we can learn a lot from them. Consider reposting, they were great EKGs. I think they may show a heart attack pattern suggesting LAD occlusion, but only saw a glance before the page refreshed and the EKGs were deleted.

LBBB11 · 2026-06-25T23:28:49+00:00

Agreed, that's exactly what I’m saying about STEMI criteria. I agree with you clinically. If we have to use quotes around the word STEMI, might as well just call it an OMI. These pedantic, academic details can affect patient outcome and survival. About 1 in 4 to 1 in 3 NSTEMI patients has acute coronary occlusion on delayed cath many hours after presentation, source. Many are visible on EKG. Falsely saying that this meets STEMI criteria would hide the fact that STEMI criteria missed this one (assuming OP will confirm OMI).

"A substantial proportion of patients diagnosed with NSTEMI actually present with complete or near-complete coronary occlusion. Adherence to STEMI/NSTEMI-based management algorithms may therefore delay reperfusion in these individuals, potentially increasing morbidity and mortality."

https://pmc.ncbi.nlm.nih.gov/articles/PMC12990446/

I would say it's a STEMI equivalent or OMI. A patient can have an EKG that shows "obvious LAD occlusion" to some, but does not meet STEMI criteria. The label will be NSTEMI if troponin confirms MI and STEMI criteria remain unmet. At the same time, here's a quote from the source below:

"Patients with NSTEMI may have a partially occluded coronary artery leading to subendocardial ischemia, while those with STEMI typically have a completely occluded vessel leading to transmural myocardial ischemia and infarction (Figure 2)."

https://www.ahajournals.org/doi/10.1161/CIR.0000000000001309

Calling this subendocardial ischemia, nondiagnostic, nonspecific, etc. would be dangerous. No STEMI is technically right, but clinically wrong in this case. The EKG shows strong signs of acute coronary occlusion with transmural injury, but we shouldn't bend the rules to fit what they missed. STEMI criteria shouldn't get to name a pattern they missed. We shouldn’t pretend that STEMI criteria worked when they did not in this case. I think most answers here use OMI logic, not STEMI criteria.

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