Dr. Smith's ECG Blog: A woman in her 50s with acute chest pain

Sunday, June 15, 2025

A woman in her 50s with acute chest pain

Written by Pendell Meyers

A woman in her 50s with no significant past medical history experienced acute anterior chest pain that woke her from sleep and radiated to her back. She described it as "stabbing", 8/10, constant, and associated with nausea. She denied preceding symptoms or recent illnesses.

Here is her triage ECG during active pain:

What do you think?

This ECG was recorded 30 minutes later with ongoing pain:

Queen of Hearts says no signs of STEMI or Equivalent for both:

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The physician was worried about possible acute coronary occlusion, and activated the cath lab.

The angiogram showed no significant coronary disease:

First troponin I was 10 ng/L.

Second troponin was 23 ng/L. None further were measured during this hospitalization.

Echocardiogram showed normal EF, no wall motion abnormalities, no pericardial effusion.

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There is a lot of data now to show that the Queen reduces false positives by a lot.

1. Decreased prehospital false positives (retrospectively) by 58%.

2. Midwest STEMI Consortium: decreased false positives by 33% (presented at ACC Quality Summit San Antonio 2024)

3. Willy Frick, from St. Louis University, presented at Heart Rhythm Society: 1 month of chest pain in the ED. 528 chest pain patients, 14 with culprits lesions. Queen detected 11/14 with zero false positives. Cardiologist detected 6/14 with 3 false positives.

4. Macherey-Meyer S. Presented at German Society of Cardiology. 1770 chest pain patients. 56 OMI. Specificity 0.967. Negative predictive value 98.4% and Positive predictive value was 34.1%. Subgroup analysis of patients ruled-out following 0/1h hs-cTnT algorithm identified misclassification as false-positive in 1% of ECGs by AI model. Specificity and accuracy both were 0.989 (95% CI: 0.983-0.994, see table 2). Negative predictive value was 100% (95% CI: 100-100).

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Here is the ECG the next day:

(QoH gets this one wrong, calls it STEMI/OMI, understandably based on the STE in III with STD in aVL.)

She was given colchicine and discharged.

She returned with similar symptoms about 1 month later.

Repeat echocardiogram at this visit revealed a small pericardial effusion.

Cardiac MRI was read as:
Acute pericarditis with signs of early constrictive physiology. The pericardium is diffusely thickened. There is diffuse late gadolinium enhancement of the parietal and visceral pericardial layers consistent with pericardial inflammation. There is a small circumferential pericardial effusion. There are no signs of tamponade physiology. There is ventricular interdependence as demonstrated by mild septal bounce, and the IVC is dilated to 2.9 cm with less than 50% collapse with inspiration - these findings suggest early constrictive physiology. There is no myocardial LGE to suggest inflammation, infiltration, or infarction of the LV myocardium.

Two troponins were drawn, both less than 6 ng/L.

She was given an extended course of colchicine and ibuprofen.

Rheumatologic and infectious workups were negative.

This ECGs was recorded on day 4 of the hospitalization:

This ECG was recorded on day 6 of hospitalization:

Her diagnosis was recurrent idiopathic pericarditis. She was discharged.

Here is her ECG 6 months later, at an outpatient visit with no active symptoms:

The "four stages of pericarditis on ECG" are typically taught as:

Stage 1: wide spread STE and PR depression

Stage 2: ST segment return to baseline with T wave flattening

Stage 3: T wave inversion

Stage 4: Normalization

Of course, these stages may not follow a typical time course, may not have serial ECGs timed correctly to catch each stage, etc.

However, this patient seems to fulfill the classic sequence as shown in her second admission.

Please understand that actual pericarditis is incredibly rare compared to normal variant baseline ST elevation.

And please be careful: the harm of one delayed diagnosis of OMI, incorrectly diagnosed as pericarditis, far outweighs the benefit of quickly making many true positive diagnoses of pericarditis. OMI is common, while pericarditis is rare. As Dr. Smith says, "you diagnose percarditis at your peril!"

See these cases if you don't understand how dangerous it can be:

You Diagnose Pericarditis at your Peril (at the Patient's Peril!)

Watch what happens when "pericarditis" and morphine cloud your judgment

24 yo woman with chest pain the morning after binge drinking: Is it Pericarditis?

"Pericarditis" strikes again

See our other cases involving pericarditis here:

A young woman in her early 20s with syncope

Severe Atypical Chest Pain in a Young Woman: Series of Pericarditis ECGs

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MY Comment, by KEN GRAUER, MD (6/15/2025):

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Medicine is humbling. And while I definitely included acute pericarditis in my differential diagnosis when I first saw today's case — I did not think pure pericarditis (without a component of myocarditis) was likely. Instead — I thought this patient had acute LCx occlusion.

For clarity in Figure-1 — I've reproduced today's initial ECG.

Why I Thought: "Acute MI Until Proven Otherwise" ...

The ECG in Figure-1 shows sinus rhythm at ~90/minute — normal intervals and axis — no chamber enlargement — and lots of ST elevation.

This 50-something woman was awakened from sleep by new, severe CP (Chest Pain) — which prompted her ED presentation. As per Dr. Meyers — statistically, acute MI is abundantly more common than acute pericarditis in this setting (and potential morbidity and mortality from missing acute MI far exceeds that for missing acute pericarditis). As a result — Assume acute MI until proven otherwise!

Regarding ECG findings in Figure-1 that suggest acute MI until proven otherwise:

Q waves are present in multiple leads in ECG #1 — and these are the same leads that show ST elevation.
The ST elevation seems to correlate with acute infero-lateral infarction (I suspected acute occlusion of a dominant LCx ... ).
Lead aVL seems to show reciprocal ST changes (albeit the amount of ST depression in aVL is not as much as I'd normally expect, given the amount and acuity of the ST elevation in lead III ).
More than just ST elevation — lead V3 (and to a lesser extent, lead V4) look hyperacute (BLUE arrow highlighting the disproportionately "fat" T wave peak and "bulkier"-than-expected T wave dimensions in this V3 lead).
I initially thought there was T-QRS-D (Terminal QRS Distortion) in lead V4. If true — this would all-but-confirm acute infarction (See My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog for more on T-QRS-D).
Bottom Line: While more data was needed — my initial impression of ECG #1 was acute infero-lateral STEMI in progress with need for prompt cath.

Figure-1: The initial ECG in today's case (with magnified view in the 2 inserts below of leads V4 and V6).

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ECG Findings For and Against Acute Pericarditis:

I did not think today's initial ECG was suggestive of pure acute pericarditis. It clearly could be consistent with acute myopericarditis — as the ECG picture of acute myocarditis can manifest virtually anything, and be indistinguishable from the ECG of acute MI. Consider the following:

As Drs. Smith and Meyers have repeatedly emphasized in this ECG Blog — You diagnose acute pericarditis "at your peril" — for the simple reason that in an unselected emergency setting, acute MI is so much more common than pericarditis (and the potential morbidity and potential mortality of missing an acute MI is so much greater than for missing acute pericarditis).
In favor of the ECG diagnosis of acute pericarditis — is the diffuse ST elevation (seen in leads I,II,III,aVF; and in leads V3,V4,V5,V6).

Against the ECG diagnosis of acute pericarditis are the following findings:

Diffuse Q waves are seen in almost all leads in which there is ST elevation. Although these Q waves are small and narrow: i) These Q waves are indistinguishable from the early Q waves of acute infarction in which ST segments are acutely rising; and, ii) Although inferior lead "normal septal q waves" may be seen in leads II,III,aVF — this usually only occurs with an inferior axis (which is not present in ECG #1) — and, if the inferior Q waves that we see in ECG #1 were the result of "normal septal q waves" — then we should not also see the Q wave that is present in lateral lead I.
One of the most characteristic ECG features of acute pericarditis in my experience — is that the ST-T wave appearance in lead II resembles the ST-T appearance in lead I (vs the situation with acute inferior MI — in which the ST-T wave appearance in lead II is much more similar to what we see in lead III, than it is to the lead I ST appearance).
T-QRS-D is not present in lead V4 of Figure-1 (As shown in the magnified insert — When we look closely, the BLUE arrow highlights a definite notch at the J-point that negates the possibility of T-QRS-D).
Although the ST/T wave ratio in lead V6 is "positive" for pericarditis (ie, the ST/T ratio = 0.33, which is over 0.25) — I did not feel this was a convincing result because the amount of ST elevation in lead V6 is only 1 mm, and therefore potentially subject to error pending minimal change in the point of reference chosen for measurement (See Figure-3 in My Comment in the June 8, 2022 post for more on the ST-T wave ratio in lead V6 for pericarditis diagnosis).
With the "textbook typical" ECG picture of acute pericarditis — ST elevation is seen in all but the right-sided leads (which are leads III,aVR,V1). There should not be suggestion of reciprocal change (as we see in lead aVL of Figure-1) — and there should not be a flat ST segment in lead V2 (as we see in Figure-1).
As stated earlier — the ST-T waves in lead V3 (and to a lesser extent, in lead V4) look hyperacute (BLUE arrow highlighting the disproportionately "fat" T wave peak and "bulkier"-than-expected T wave dimensions in this V3 lead). In contrast — with the "textbook picture" of pure acute pericarditis, otherwise "normal" ST-T waves tend to look as if "lifted" above the ECG baseline instead of producing the hyperacute appearance that we see in lead V3.
NOTE #1: Acute myocarditis could easily have produced the identical ECG picture that we see in Figure-1 — in which case it would be impossible to distinguish between acute myocarditis vs acute MI on the sole basis of this single ECG. But the completely normal cath — negative Troponins — normal Echo without wall motion abnormality — and normal MRI (without evidence of inflammation) ruled out acute myocarditis.
NOTE #2: No mention is made in today's history as to whether a pericardial friction rub was (or was not) present. This is unfortunate (but all-too-common in the cases I routinely see posted on the internet) — because IF a pericardial friction rub is heard, then you have made the diagnosis of acute pericarditis!
NOTE #3: No mention was made regarding any potential positional relationship or pleuritic nature of this patient's CP (the CP was instead described as "constant" and "stabbing", and associated with nausea). While a patient's description of the nature of their CP is by definition subjective, with imperfect correlation to textbook description of pericardial pain — there is a tendency for pericarditis CP to be "pleuritic" (increasing with inspiration due to commonly associated pleural inflammation) — and "positional" (commonly relieved by sitting up and exacerbated by lying supine, which increases "stretch" on the inflammed pericardium).

BOTTOM Lines:

I've always believed it important to be humbled on occasion by cases in which the patient "doesn't read the textbook" before seeking emergency care. Clinical reality is not always predictable. Despite including specific chapters on the ECG findings of pericarditis for each of the ECG books that I've written over the years — I simply did not feel today's initial ECG suggested pericarditis over acute MI (See Figures-2-thru-6 in My Comment at the bottom of the May 16, 2023 post in Dr. Smith's ECG Blog for an example of such chapters).
Today's case is important because: i) It illustrates completely appropriate indication for prompt cardiac cath to exclude the possibility of acute infarction; — ii) It expands our insight regarding potential ECG presentations of pure acute pericarditis (as well as the diagnostic path for confirming this diagnosis); and, iii) It keeps us humble (while reminding us that in the great majority of cases in which a patient presents to the ED with sudden onset of severe, new CP — the diagnosis will be an acute cardiac event instead of acute pericarditis or myocarditis).