- The cardiologist on call noted ST elevation in multiple leads — and diagnosed the patient as having acute pericarditis, primarily on the basis of this ECG.
- Do YOU agree with the diagnosis of acute pericarditis?
- If so — Why?
- If not — Why not?
- KEY Point: How to increase the certainty of your diagnosis?
- Q Waves — Small and narrow Q waves are seen in multiple leads (ie, in leads II,III,aVF; and in leads V3-thru-V6). Although this is a lot of leads to have Q waves in — the finding that each of these Q waves is small and narrow renders them non-diagnostic.
- R Wave Progression — There is early transition, with the R wave becoming predominant already by lead V2. That said, the clinical significance of this early transition in the context of this tracing is uncertain and non-diagnostic.
- ST-T Wave Changes — There is diffuse ST elevation! In addition to seeing ST elevation in each of the 7 above-noted leads that manifest Q waves — there is also ST elevation in leads I and V2 (ie, which makes for 9/12 leads that show ST elevation).
- QUESTION: What do YOU think?
- Reason #1 = Statistics! — Acute pericarditis is not common. In my experience — acute pericarditis is rare in the clinical setting presented in today’s case (ie, in a previously healthy middle-aged adult — who presents to an ED with new-onset CP). Instead, ACS (an Acute Coronary Syndrome) is a much more common cause of new CP when a middle-aged or older adult presents to the ED with this complaint. As a result, to help me resist the temptation to reflexively diagnose acute pericarditis whenever ST elevation is seen in multiple leads — I embrace (and frequently repeat to myself) the mantra put forth by Dr. Stephen Smith — “You diagnose acute pericarditis at your peril”.
- Today’s case was sent to me with no mention of pertinent positives and pertinent negatives regarding the nature of this patient’s CP. While exceptions exist — the CP of acute pericarditis is typically pleuritic (increasing with inspiration) —and typically positional (exacerbated by lying supine — and reduced by sitting up and leaning forward). The physiologic basis for this positional effect is that lying supine places stretch on the inflamed pericardium — whereas sitting up and leaning forward reduces that stretch.
- There was also no mention of potential predisposing factors that might suggest a diagnosis of acute pericarditis (ie, no known ongoing medical illnesses that may be associated with pericarditis — and no mention of recent viral infection). Although there are many potential causes of pericarditis — the most common clinical setting for acute pericarditis in a previously healthy individual, is in a young adult who presents with an acute viral illness (See the ADDENDUM below).
- Finally — today’s case was sent to me with no mention of having listened for a pericardial friction rub (which IF heard, would confirm the diagnosis of acute pericarditis — albeit not ruling out the diagnosis if not heard).
- Simply stated — IF the clinician note does not specifically state, "No pericardial friction rub" — this tells me with 99% accuracy that the clinician either did not auscultate the chest specifically listening for a rub and/or simply doesn't appreciate that the BEST (and fastest) way to confirm acute pericarditis is to detect a friction rub.
- NOTE: See the ADDENDUM below — for more on the clinical and ECG diagnosis of acute pericarditis.
- I introduced the concept of T-QRS-D in ECG Blog #318. I fully acknowledge that prior to my active participation as an Associate Editor in Dr. Smith's ECG Blog — I had not been aware of this ECG finding. In the years since then, I've seen numerous examples of patient cases that validate the clinical utility of this unique ECG sign promoted by Dr. Stephen Smith.
- When present — T-QRS-D may provide an invaluable way to distinguish between a repolarization variant vs acute pericarditis vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI = Occlusion-based Myocardial Infarction).
- T-QRS-D — is defined as the absence of both a J-wave and an S-wave in leads V2, V3 and/or lead V4.
- Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.
- TOP in Panel A — Despite marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
- BOTTOM in Panel A — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).
- In Lead V2: The ST elevation is not consistent with T-QRS-D — because there is prominent J-point notching (BLUE arrow).
- In Lead V3: There is T-QRS-D — because there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).
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| Figure-3: What is (and is not) T-QRS-D. |
- T-QRS-D — is definitely present in leads V3 and V4 in Figure-2, as there is no J-point notching and there is no S wave (because the last QRS deflection clearly does not descend below the baseline).
- I believe T-QRS-D is also present in lead V2 — although I acknowledge that one might question whether the last QRS deflection reaches the baseline.
- Given definite T-QRS-D in leads V3 and V4 (and probably also in lead V2) — I'd include lead V5 by association. NOTE: Data is lacking to support the validity of T-QRS-D as indication of acute OMI if this finding is only seen in lead V5.
- PEARL #4: I added a BLUE arrow in Figure-2 to highlight the ST-T wave in lead aVL. Although very subtle — in the context of seeing T-QRS-D in multiple leads (and considering the tiny size of the QRS in lead aVL) — I believe there is the suggestion of reciprocal ST depression in this lead.
- To emphasize that by itself — I would not think much of the ST-T wave in lead aVL. But in the context of this patient with new CP and T-QRS-D in multiple leads — I interpreted the appearance of lead aVL as showing supportive reciprocal ST depression.
- For example, in today's case — I found that although PMcardio digitalization improved overall resolution of ECG #1 — it rendered the presence of T-QRS-D less evident in several leads by slightly alterating J-point and S wave appearance.
- Bottom Line: As much as I regularly use PMcardio to improve visualization of many imperfect resolution tracings — for fine details in complex arrhythmias and for intricate patterns (such as recognition of T-QRS-D) — it is important that YOU verify the accuracy of the digitalization before blindly accepting the PMcardio version.
Ahmed Adel — FB Messenger (11/23/2025)
— Await permission from Ahmed (from Baghdad, Iraq) —
AHMED — Please feel free to use the case for your blog. It would mean a lot, and I'm excited to read it!
Yes, it's Ahmed Adel from Baghdad, Iraq.
Yes, that clears everything up.
Thank you so much, Dr. Ken. I really appreciate you taking the time to review the case & share your insights.
ME— THANKS Ahmed. I may be a month or so until I get to it, as I have other cases before — but I think it is a very important case! — :)
THE CASE:
Hello Dr. Ken, hope you’re doing well. I wanted to share this interesting and educational case with you, and I’d really appreciate any insights you might have whenever you have the time.
A 55-year-old male with a negative past medical history presented with chest pain.
The senior cardiologist diagnosed this as pericarditis based on the diffuse concave ST elevations and the “PR depression with a Spodick sign in lead II.” He wanted to start the patient on an NSAID & colchicine.
But my colleague who recieved this patient in the ED wasn't convinced & called me for a second opinion regarding this case. My opinion was: "lead II is entirely slanted (wandering baseline) giving the FALSE appearance of PR depression & Spodick sign. V3 shows terminal QRS distortion (TQRSD), which is a HUGE RED FLAG for a potential LAD occlusion. I think it would be wise to withhold the NSAID for now & order serial ECCs & trops before calling this a pericarditis".
Shortly after, the patient went into VFib & shocked back into sinus rhythm... twice!
A repeat ECG showed dynamic changes with a new ST depression in lead II, which I think confirms LAD (wraparound?) occlusion.
I have a few questions:
• Would you have activated the cath lab based on clinical suspicion + the initial ECG (which only had TQRSD in V3 as the only clue for OMI that I could find)?
• Were there any other "red flags" in the initial ECG that were missed?
• Do you know of any literature on the value of TQRSD in differentiating LADO from pericarditis? I only know of its use in LADO vs BER. Thank you in advance!
================
MY REPLY:
Hello Ahmed. I completely agree with you!
I would like to use this case for an ECG Blog — because it is indeed challenging, with the very important lesson of calling this an acute STEMI (not just an "OMI" — but there is enough ST elev. to call this a STEMI)-in progress until proven otherwise.
I'd be happy to acknowledge you if you like (Is it Ahmed Adel from Baghdad, Irag? ) — or if this case is too "sensitive" — I could make it anonymous. Just let me know if you would allow me to write this case up — :)
So — Statistically, it's important to remember that in a patient with new CP (Chest Pain) — acute MI is much, much more common than acute pericarditis — which is why Dr. Smith says, "You diagnose acute pericarditis at your peril!"
There clearly are features that could be consistent with acute pericarditis = diffuse ST elevation — and a positive ST-T wave ratio in lead V6 (See my ECG Blog #365 and my ECG Blog #208). But #1) There is NO mention of the nature of CP (pleuritic? positional? as it should be with pericaridits) — lead II looks more like lead III (should be that lead II looks more like lead I with pericarditis) — and there is T-QRS-D in the 4 leads that I have circled (See my ECG Blog #318). So this ECG is unique in that I don't know that I've seen a case in which it is mainly the T-QRS-D that removed my doubt about an acute MI!
As to PR interval depression — I think it probably is seen in leads II, aVF, V3,4,5 — with some PR elevation in aVR — BUT — in my experience, PR depression is NOT a specific sign (I've seen this in normal ECGs and in acute MI).
As to Spodick's Sign — I sometimes think that ony Dr. Spodick can reliably identify this. It does look like Spodick's Sign may be present in V3-thru-V6 ... but I find the reproducibility of this sign by anyone other than Dr. Spodick (who is a true pericarditis expert) is very poor — so I never depend on Spodick's sign.
Finally, very subtle — is what looks like reciprocal ST dep in aVL (which does not occur with acute pericarditis!).
So YES — this ECG should have been repeated within 15 minutes and at the very least, one should have gotten Troponin to help.
I hope the above answers your questions. Your concerns are perfectly valid!
https://ecg-interpretation.blogspot.com/2023/02/ecg-blog-365-30yo-with-pericarditis.html
https://ecg-interpretation.blogspot.com/2021/03/ecg-blog-208-ecg-mp-25-st-elevation-but.html
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- The material that follows below on the ECG diagnosis of acute Pericarditis — is from ECG Blog #365.
In the following 5 Figures — I post written summary from my ECG-2014-ePub on the ECG diagnosis of Acute Pericarditis.
- CLICK HERE — for a PDF of this 9-page file on Pericarditis that appears in Figures-4-thru-8.
- An additional criterion that has sometimes been cited as helpful for making the diagnosis of acute Pericarditis — is the ST/T Wave Ratio in Lead V6 (Please Check out ECG Blog #365).
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| Figure-5: How to make the diagnosis of acute Pericarditis (ie, use of the History and Physical Exam). |
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| Figure-6: ECG findings (4 Stages of acute pericarditis — with attention on diagnostic Stage I). How helpful is PR depression? |
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| Figure-7: PR depression (Continued). Spodick’s sign. Acute MI vs Pericarditis vs Repolarization variants? |
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| Figure-8: Acute MI vs Pericarditis. ECG findings with acute Myocarditis. Pericarditis vs Early Repolarization? |
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| Figure-9: Pericarditis vs Early Repolarization? (Continued). |
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