Wednesday, February 12, 2025

WillyF-DRAFT (KG- Done)- Pericarditis? -No, OMI (2-12.1-2025)- DRAFT- I_am_DONE





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MY Comment, by KEN GRAUER, MD (2/13/2025):  
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Several aphorisms came to mind as I reviewed today's case. These include:
  • "Junk in = Junk out ... "
  •     — "Common Things are Common."
  •         — "If in doubt — Repeat the ECG" (and do it soon! ).

"Junk in = Junk out ... "
Computers are wonderful instruments. But if the data we feed our computer is "junk" — then the answer the computer will give us will inevitably be "junk".
  • The application of this 1st aphorism to ECG interpretation is that if your ECG is so full of artifact that assessment of ECG waveforms is unclear — then our interpretation of that ECG will be equally unclear.
  • One of the most common errors I've observed over the years — is the tendency of all-too-many providers to accept "junk" on an ECG or rhythm strip when assessing the tracing of an emergency patient. While true that artifact may sometimes be difficult to eliminate (ie, in your shivering or trembling patient) — much (most) of the time the quality of your initial ECG can at least be improved by repeating the ECG with efforts to minimize artifact.
  • Today's initial ECG provides a perfect example of this principle (TOP tracing that I have reproduced in Figure-1). Although we can guess at the ECG changes in ECG #1 — because of the small size of the QRS in multiple leads and the amount of baseline undulation — I found it impossible to be confident of my interpretation of this tracing from this patient with 2 days of midsternal CP (Chest Pain). Why guess when the decision of whether or not to immediately activate the cath lab hangs in the balance? Solution: Immediately repeat the ECG!

"Common Things are Common."
The consulting cardiologist in today's case further delayed the decision to perform cardiac catheterization because this cardiologist interpreted the 2 serial ECGs in today's case as consistent with acute pericarditis — despite an initial Troponin value over 25,000 ng/L. 
  • Acute coronary syndromes are common in patients who present to an ED with new CP. In contrast — acute pericarditis is rare among chest pain patients who present to the ED (a point we have emphasized on numerous occasions in Dr. Smith's ECG Blog — including My Comment in the May 16, 2023 post — and the December 13, 2019 post, among others).
  • KEY Point: Since it is rare to see true acute pericarditis among patients who present with new CP to an ED — that diagnosis should only be made after confidently ruling out an acute OMI (and not after an initial Troponin over 25,000 ng/L and 2 serial ECGs that should be interpreted as strongly suggestive of acute OMI until proven otherwise).
  • Solution: The easiest way to avoid the misdiagnosis of acute pericarditis — is to remind yourself that most of the time the patient presenting to the ED with new CP will either have an acute coronary syndrome or "something else", but not acute pericarditis.
  • P.S.: I saw no mention of having listened for a pericardial friction rub in the description of today's case. Not carefully listening for a rub when contemplating the diagnosis of acute pericarditis is not understanding that a pericardial friction rub is the single finding that could potentially be diagnostic of acute pericarditis. In my experience over 4+ decades of Attending and consulting on cases of other providers — not mentioning (and documenting in the chart) whether or not a rub was listened for in cases of suspected pericarditis is the most common oversight I've encountered. Not mentioning as a positive or negative finding whether a pericardial friction rub was or was not heard in my experience means that the provider did not listen for this.

"IF in Doubt — Repeat the ECG (and Do It Soon! )."
We are not told how much time passed in between the recording of ECG #1 and ECG #2 (beyond knowing that at least enough time passed for Troponin results to return).
  • Regardless of how much time passed between the recording of these 2 tracings — it was too much time — since the artifact-laden initial ECG should have been immediately repeated by the "Junk in = Junk out" principle.

      Figure-1: I've labeled the 2 ECGs in today's case.


      ECG Findings in Today's CASE:
      Despite the technical problems with ECG #1 — there are a number of insightful findings. As per Dr. Frick — there are subtle hyperacute T waves in multiple leads (upward arrows that I have added in).
      • I enclosed lead V2 within a RED rectangle — because this is the lead that immediately caught my "eye". This lead eliminated acute pericarditis from my differential diagnosis. Among the ECG findings of acute pericarditis that I review in My Comment in the May 16, 2023 post — there should not be ST depression in lead V2 (RED arrow in this lead).
      • Instead, in this patient with persistent CP and a markedly elevated Troponin — the ST depression seen in lead V2 is diagnostic of acute posterior OMI. This diagnosis is supported by the lack of any ST elevation in neighboring lead V3 (since there should normally be a slight amount of gently upward sloping ST elevation in leads V2,V3).
      • The question marks and +/- label that I added in ECG #1 also negate consideration of acute pericardits, which would not show more ST elevation in lead V6 than in leads V3,V4,V5. Instead (and despite the artifact) — the unmistakable ST elevation in lead V6 confirms (until proven otherwise) that there is ongoing acute lateral OMI.
      • Limb lead findings consistent with acute infero-lateral OMI are the subtly elevated ST segments in leads I,II,III,aVF — and especially the T wave inversion in lead aVL (BLUE arrow in this lead). Abnormal straightening of the ST segment takeoff in leads II and aVF is seen through the artifact — but before clinical decisions are made, this tracing should be repeated.
      • Finally — there is low voltage in the limb leads. While many entities may cause low voltage — this is potentially a worrisome sign when seen in association with acute MI, as it may be an indicator of extensive infarction with myocardial "stunning" (See My Comments in the November 12, 2020 post and the January 24, 2020 post).

      The Repeat ECG in Today's CASE:
      Artifact was virtually eliminated in the repeat ECG. As noted — we are not told how much time passed between the recording of ECG #1 and ECG #2. There have been some serial changes between these 2 tracings. These are best appreciated by putting both ECGs side-by-side (as in Figure-1).
      • QRS amplitude remains tiny in the limb leads. Considering the small size of QRS complexes in all 6 limb leads — the ST-T wave shape and the amount of ST elevation relative to the QRS is extreme.
      • Why is there now ST depression in lead III? Presumably the increase in ST elevation in lateral leads I,aVL; V5,V6 from acute LCx/OM-1 occlusion attenuated the ST elevation from associated inferior infarction as it is seen in oppositely-directed lead III (lead III being the most distant of the inferior leads from lateral leads I and aVL).
      • Chest lead findings in ECG #2 that further support acutely evolving posterior OMI include: i) Development of a tall R wave in lead V2; and, ii) Subtle increase in the amount of J-point ST depression in leads V1,V2,V3.

      Conclusion: There is much to be learned from today's case ... 





      XXXX
      XXXXX 
      • XXXXX

      XXXXXX
      (See My Comment in the May 16, 2023 post — and the December 13, 2019 post, among others).


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      My Comment by KEN GRAUER, MD (5/16/2023):
      https://hqmeded-ecg.blogspot.com/2023/05/a-man-in-his-late-30s-with-acute-chest.html
      ==================================
      I was intrigued by today’s case — more by what we do not know — than by what we know.
      • As per Dr. Meyers (and as often occurs when the patient is not managed by one of us) — the information provided to us was limited. That said — I still thought this case to be highly instructive for discussion.
      • For clarity in Figure-1 — I’ve reproduced the only ECG in today’s case.

      Figure-1: Today's ECG. (To improve visualization — I've digitized the original ECG using PMcardio).


      MY Thoughts on Today’s Case:
      As per Dr. Meyers — We do not know the “final answer” in today’s case. Instead, all we know are results from a number of tests — and — that this patient did not have acute coronary occlusion. I’d emphasize the following:
      • The patient in today’s case is a man in his late 30s, who presented to the ED with acute CP (Chest Pain) — and — a fast sinus tachycardia (at ~115-120/minute). While important that the correct decision was made not to activate the cath lab in today’s case — it’s equally important that this patient not be discharged from the ED until some explanation is found for his CP and his significant sinus tachycardia. Given that 3 troponins and formal Echo were done prior to discharge — one would think that IF the treating clinicians had arrived at some explanation, that this would have been part of the record.
      • As per Dr. Meyers — the ECG in Figure-1 is not suggestive of acute OMI. This is because ST elevation is so diffuse (ie, present in 9/12 leads!) — the shape of the ST elevation is everywhere similar (ie, gently upsloping) — together with prominent J-point notching (in 4 leads) — but without any reciprocal ST depression. As per the QoH (Queen of Hearts) AI interpretation — this ECG picture simply does not look like an acute OMI. Instead — it looks much more like a patient with a repolarization variant plus sinus tachycardia — or possibly like acute pericarditis. While completely appropriate to verify our impression that ECG #1 is unlikely to be an OMI (as was done by 3 negative troponins and an unremarkable Echo) — it is hard to understand how additional ECGs would not be part of the record.
      • IF ECG #1 was the initial tracing of an acutely evolving cardiac event — given this patient’s new-onset CP, in association with all of the ST elevation we see — within 10-20 minutes (at most), there would probably be at least some evolution of ECG findings that would confirm the diagnosis. On the other hand — lack of such evolution on serial tracings over the next 30-to-90 minutes would support our impression that ECG #1 is unlikely to indicate an acute event.

      • To Consider: It would not be optimal to discharge a patient who presented to the ED for new CP with only a single ECG showing a tachycardia of 115-120/minute.


      Additional Considerations Regarding the Sinus Tachycardia:
      Knowing the clinical presentation of today’s patient and the final disposition (ie, discharge from the ED after ruling out acute OMI) — several additional considerations should come to mind. These include the following:
      • Tachycardia is a potential cause of ST elevation! I’ve been fooled by this clinical reality on a number of occasions — in which seemingly hyperacute ST elevation (sometimes with reciprocal ST depression!) — turns out to resolve as the heart rate slows down without any evidence of acute infarction. As a result, although I definitely consider the possibility of a new event in ECGs such as today's tracing — I’ve learned to reserve final judgment regarding both ST elevation and/or ST depression until I see worrisome ST-T wave changes persisting at a slower heart rate.
      • Anxiety is a common cause of chest pain with tachycardia. If such a patient had some baseline repolarization ST elevation — an ECG similar to that in Figure-1 might be seen (with the amount of ST elevation potentially increased by the tachycardia).
      • Hyperthyroidism may present to the ED with chest pain and tachycardia (which could produce an ECG similar to that in Figure-1 if there was some baseline early repolarization ST elevation).
      • Recreational drug use and/or alcohol overuse — might do the same ...

      • Finally — Today’s patient could have acute Pericarditis …


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      Could Today's Patient Have Acute Pericarditis?
      Perhaps my favorite among the many clinical truisms coined by Dr. Smith, is the following statement — "You diagnose acute Pericarditis at your peril!" The clinical reality that we’ve emphasized many times in Dr. Smith’s ECG Blog — is that the diagnosis of acute pericarditis is rare among chest pain patients presenting to the ED. 
      • This is not to say that acute pericarditis never occurs — but rather to emphasize that the diagnosis of acute pericarditis should only be made after you've ruled out an acute coronary syndrome.
      • On the other hand, what I have all-too-commonly observed — is clinicians making a diagnosis of acute pericarditis without documentation of having listened for a pericardial friction rub — and without specifying whether historical/exam features that could be suggestive of the diagnosis are present (ie, recent viral infection in a younger adult — and — a pleuritic or positional type of chest pain, aggravated by inspiration and/or lying supine). In the absence of a rub and these historical/exam features — acute pericarditis is unlikely.
      • The normal troponin values in today's case rules out myocarditis. There may or may not be some troponin elevation (usually modest, if present) with acute pericarditis.
      • The unremarkable Echo in today's case does not rule out pericarditis (Echo is often normal with acute pericarditis; Most patients with acute viral pericarditis do not have pericardial effusion).


      Is Today's ECG Consistent with Acute Pericarditis?
      Today's tracing does show many ECG findings that are consistent with a diagnosis of acute pericarditis. These include:
      • Diffuse ST elevation that is present in all of the 9 leads that may be expected to manifest ST elevation with acute pericarditis. The 3 leads that most consistently do not show ST elevation in acute pericarditis — are right-sided leads III, aVR and V1 — and those are the only leads not showing ST elevation in Figure-1.
      • The gently upsloping shape of ST elevation in today's tracing is consistent with that seen in acute pericarditis.
      • The shape of the ST-T wave in lead II much more closely resembles the shape of the ST-T wave in lead I. In contrast, with acute MI — ST-T wave shape in lead II much more closely resembles ST-T wave shape in lead III.
      • There is marked PR segment depression in multiple leads (most marked in lead II — but also seen in 8 other leads). The PR segment is elevated in lead aVR.
      • There is no reciprocal ST depression (whereas with acute infarction — reciprocal ST depression is typically seen, with possible exception of a less proximal LAD occlusion).
      • Infarction Q waves are not seen. (To emphasize that many leads do show q waves — but these are narrow and most consistent with septal q waves in a patient with a relatively vertical axis).
      • The ST-T wave ratio in lead V6 looks elevated (though this is admittedly difficult to assess given PR segment depression in this lead).

      • BOTTOM Line: As per Dr. Meyers — We lack clinical information in today's case. However — IF clinical features were suggestive of acute pericarditis (and if the diffuse ST elevation in ECG #1 persisted after some slowing of the heart rate) — the ECG in Figure-1 could clearly be consistent with this diagnosis.

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      ADDENDUM (5/16/2023): 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-2-thru-6.
      • 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 see My Comment at the BOTTOM of the page in the December 13, 2019 post of Dr. Smith's ECG Blog).



      Figure-2: How to make the diagnosis of acute Pericarditis (ie, use of the History and Physical Exam).



      Figure-3: ECG findings (4 Stages of acute pericarditis — with attention on diagnostic Stage I). How helpful is PR depression?


       

      Figure-4: PR depression (Continued). Spodick’s sign. Acute MI vs Pericarditis vs Repolarization variants?


       

      Figure-5: Acute MI vs Pericarditis. ECG findings with acute Myocarditis. Pericarditis vs Early Repolarization?


       

      Figure-6: Pericarditis vs Early Repolarization? (Continued).






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      Comment by KEN GRAUER, MD (6/20/2018):
      https://hqmeded-ecg.blogspot.com/2018/06/you-diagnose-pericarditis-at-your-peril.html
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      Great case & supporting comments by Drs. Smith & Meyers. I’d add the following:
      • Dr. Smith’s concept of terminal QRS distortion is worth repeat emphasis (link to his paper given above in the text). A picture is worth 1,000 words — and lead V3 illustrates this concept to perfection. Like visual recognition of what a Brugada-1 ECG pattern looks like — the picture of terminal QRS distortion in a patient with new chest pain (as seen in lead V3 of this 1st ECG) is a pattern to be memorized by all emergency care providers.
      • I love Dr. Smith’s quote, “You Diagnose Pericarditis at Your Peril (and at the Patient’s Peril!)”. I use this quote often when questions regarding this diagnosis arise. But not only is acute pericarditis a diagnosis of exclusion — the clinician should also be knowledgeable about how acute pericarditis (on those occasions when it does occur) presents. The most common form of acute pericarditis is associated with recent viral infection — and, the nature of the chest pain is typically positional (worse in supine position) and pleuritic (aggravated by deep inspiration). Although a pericardial friction rub is not always present — it should always be carefully listened for, because if you do hear a rub in the right clinical setting — then you have made the diagnosis. Why then in the literally hundreds of suspected cases that I’ve seen ECGs posted on the internet in recent years with a query about pericarditis — is it so very rare for anyone to ever describe the nature of the patient’s chest pain? — and rarer still to even mention having thought about listening with a stethoscope to see if a rub might be present? 


      SSmith - My Comment - criteria for acute pericarditis
      December 13, 2019

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      Comment by KEN GRAUER, MD (6/11/2022):
      https://hqmeded-ecg.blogspot.com/2022/06/is-this-myo-pericarditis-or-omi-with.html
      ===================================
      The topic of acute traumatic pericarditis was just discussed in the June 8, 2022 post by Drs. Nicholson and Meyers. In My Comment on that post (at the bottom of the page) — I contrasted the ECG findings of typical acute pericarditis with those of the patient in that case, who survived among other injuries a penetrating wound to the heart.

      Today's case by Dr. Smith illustrates another facet regarding the ECG diagnosis of acute pericarditis. To emphasize — there are multiple potential causes of acute pericarditis. These include:
      • Acute viral pericarditis (probably the most common cause in a general population).
      • Other infectious conditions (ie, bacterial infections, fungal, TB).
      • Inflammatory disorders (ie, RA, SLE, rheumatic fever, other forms of vasculitis).
      • Metabolic disorders (ie, uremia from renal failure, hypothyroidism).
      • Miscellaneous conditions (ie, cancer, certain drugs, radiation therapy, sarcoidosis, trauma).
      • Idiopathic (ie, cause unknown — although many of these are probably undiagnosed viral infections).
      • Cardiac causes (ie, post-infarction regional pericarditis, Dressler Syndrome [ie, an autoimmune-mediated response to myocardial antigens, usually seen 2-3 weeks after an MI], post-cardiac surgery).

      Also to emphasize is: i) That for all the discussion about pericarditis — this disorder is not a common diagnosis in an emergency setting; ii) When pericarditis occurs — its manifestations may vary depending on which of the above factors are causative; and, iii) The uncommon cardiac causes of Dressler Syndrome and post-infarction regional pericarditis have become even less common in recent years, felt to be a positive result of the increase in reperfusion therapy.

      Today's case is interesting in that the patient is felt to have had both an acute OMI and post-infarction regional pericarditis. This 57-year old man presented to the ED with a 2-day history of chest pain, including a pleuritic component (CP worse on taking a deep breath) — and positional change (CP worse on lying supine, and improved on sitting up).
      • What pertinent negative was missing from the history provided?
      • For clarity — I've reproduced the initial ED from today's case in Figure-1. What ECG findings in today's initial tracing are consistent with acute pericarditis?
      • Which ECG findings are against acute pericarditis?

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


      ANSWERS:
      • The pertinent negative missing from the history in today's case, is that, "No pericardial friction rub was heard". In my experience of reviewing literally hundreds of internet cases in which the diagnosis of acute pericarditis was suspected — the overwhelming majority of clinicians FAIL to ever mention that they listened for a pericardial friction rub. If Not Mentioned as a positive or negative finding — this usually means that the clinician did not listen for a rub. Failure to listen for a rub is a critical oversight — because IF you hear a pericardial friction rub — then you have made the diagnosis of acute pericarditis! 

      • ECG findings in Figure-1 consistent with acute pericarditis include: i) Upward sloping ST elevation in multiple leads; ii) The shape of ST-T wave elevation in lead II looks more like lead I than lead III (whereas with acute inferior MI — the ST-T wave shape in lead II looks more like lead III); and, iii) The ST-T wave ratio in lead V6 is >0.25 (whereas it tends to be less than this with repolarization variants) — See My Comment in the June 8, 2022 post for review of these and other ECG findings typical for acute pericarditis.

      • Of no diagnostic help in Figure-1 are the findings of: i) PR depression — which I found difficult to assess in the inferior leads of this tracing (due to baseline wander). I don't see diffuse PR depression — and even if I did, the specificity of this finding for acute pericarditis is lacking; and, ii) Multiple leads in this tracing show Q waves — however, the q waves in leads I,II,III,aVF and V4-6 are small and narrow (and most likely insignificant).

      • ECG findings in Figure-1 against the diagnosis of acute pericarditis include: i) There is J-point ST depression in lead V2 (Other than right-sided leads III, aVR and V1 — there should not be ST depression in other leads with acute pericarditis); ii) The T wave in lead V2 is surprisingly tall and peaked (Normally there is a similar shape to the diffusely elevated ST-T waves); and, iii) It looks like there is already a hint of beginning T wave inversion in a number of the leads that show ST elevation (whereas T wave inversion with acute pericarditis typically does not begin until ST elevation has resolved).


      Conclusion: Although at 1st glance, it looked like the ECG picture in Figure-1 might be suggestive of acute pericarditis — on further inspection, there are significant ECG features against the diagnosis of acute uncomplicated pericarditis.

      • As per the superb discussion above by Dr. Smith — evolution of this case (including the ECG picture on serial tracings) — are consistent with what probably occurred in today's case, namely the combination of acute OMI from LCx occlusion, followed by development of post-infarction regional pericarditis.



      =



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      Comment by KEN GRAUER, MD (6/8/2022):
      https://hqmeded-ecg.blogspot.com/2022/06/st-elevation-after-gunshot-to-chest.html
      ===================================
      The young man in today's case was lucky to have survived multiple gunshot wounds — including a penetrating wound to the heart. In addition to his traumatic injuries — he was discharged from the hospital with a diagnosis of traumatic uncomplicated pericarditis. Realizing that the circumstances of today's case are very different from the usual setting that prompts consideration of a diagnosis of acute pericarditis — I still thought the topic of the ECG Diagnosis of Acute Pericarditis to be a worthy one for our periodic review.
      • I found it difficult to locate literature on specific ECG findings with traumatic pericarditis from penetrating cardiac trauma. As alluded to in the above discussion by Drs. Nicholson and Meyers — you might find almost anything on ECG, depending on the specific nature of cardiac injury (ie, there may be direct damage to coronary arteries resulting in acute thrombotic occlusion or dissection — pericardial effusion, possibly with tamponade — pneumopericardium — neighboring pneumothorax, including tension pneumothorax altering the relationship of anatomic structures — and/or cardiac contusion of varying severity).
      • In contrast — a specific set of ECG findings has been described for non-traumatic acute pericarditis (See below). By way of perspective — despite being one of the most common considerations in international ECG forums — acute pericarditis is extremely uncommon in clinical practice.
      • As has been emphasized many times on Dr. Smith’s ECG Blog — acute pericarditis is far less common than acute MI or a repolarization variant among patients who present to an emergency setting. As per Dr. Smith, “You diagnose acute pericarditis at your peril!" That said — it is good to keep in mind what the ECG criteria for this diagnosis are.

      The Initial ECG in Today's Case:
      For clarity — I've reproduced in Figure-1 the initial ECG in today's case. From a purely educational perspective — I thought it interesting to assess this initial ECG for findings consistent with a diagnosis of acute pericarditis — as well as for findings against that diagnosis.

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



      ANSWERS:
      • ECG findings in Figure-1 consistent with acute pericarditis include: i) Upward sloping ST elevation in multiple leads; ii) Spodick's sign (most obvious in lead II — as per Drs. Nicholson and Meyers); and, iii) The ST-T wave ratio in lead V6 is >0.25 (whereas it tends to be less than this with repolarization variants).

      • Of no diagnostic help in Figure-1 is the finding of PR depression — which is seen in some but not other leads (ie, it is present in leads II, V4,5,6). Even if PR depression was more diffuse — the specificity of this finding for acute pericarditis is modest at best.

      • ECG findings in Figure-1 against the diagnosis of acute pericarditis include: i) There is a fairly large Q wave with ST elevation and T wave inversion in lead III that resembles the picture of acute MI (whereas with acute pericarditis — Q waves should not be seen — and T wave inversion typically does not begin until ST elevation has resolved); and, ii) ST elevation is lacking in leads aVL, V2 and V3 (The ST segment straightening in leads aVL and V3 is much more characteristic of coronary disease than acute pericarditis).

      Conclusion: The ECG in Figure-1 would not be typical for non-traumatic acute pericarditis. However, it could be consistent with traumatic pericarditis (because ECG findings are so variable in traumatic pericarditis).
      • NOTE: The ECG features of acute myocarditis may differ substantially from those of a "pure" pericarditis. There may be a resemblance between these 2 entities — but ST segment deviations (elevation and depression) with myocarditis may not follow the timing seen with pericarditis. In addition, Q waves may develop — so at times it may be difficult to distinguish myocarditis from infarction on ECG.

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

      ECG Findings of Acute Pericarditis:
      By way of Review — I’ve excerpted in Figure-2, relevant paragraphs from a 2017 ESC (European Society of Cardiology) article on this subject by Xanthopoulos & Skoularigis (ESC: Vol. 15, No.15-9/6/2017).
      • CLICK HERE — for a 9-page PDF of "My Take" on the ECG diagnosis of acute pericarditis.

      Figure-2: Excerpt from ESC review on acute pericarditis (See text).


      Among the KEY points regarding ECG diagnosis of acute pericarditis from Figure-2 (to which I’ve added some of my own points) — are the following:
      • Typical ECG findings of acute pericarditis are not always present! The ECG is far from a perfect diagnostic tool.
      • 4 Stages are described in the ECG evolution of Acute Pericarditis findings. These can be summarized as: i) Stage I — in which there is generalized ST elevation in most leads (except perhaps in the “right-sided” leads = leads III, aVR and V1); ii) Stage II — in which this generalized ST elevation returns to baseline (ie, “pseudo-normalization” phase); iii) Stage III — in which there is diffuse T wave inversion; and, iv) Stage IV — in which the overall tracing normalizes.
      • Of these 4 stages — only Stage I is readily recognizable as potentially due to acute pericarditis. You would never guess “pericarditis” if given an isolated tracing from Stage II, III or IV.
      • The time course of these 4 ECG Stages (in those pericarditis cases in which they occur) — is highly variable. The ESC summary in Figure-2 states that Stage I may last “between hours to days” — before evolving into Stage II.
      • The shape of the ST elevation is typically concave-up (ie, a “smiley” configuration).
      • ECG signs usually associated with acute MI (ie, abnormally large or wide Q waves — reciprocal ST depression) are absent!

      • PEARL: The appearance of the ST-T wave in lead II tends to resemble that in lead I with acute pericarditis. In contrast, with acute MI — ST-T wave appearance in lead II resembles lead III (and not lead I).
      • There may be PR depression in many leads — with “reciprocal” PR elevation in lead aVR.

      • The RATIO of the amount of ST elevation to T wave amplitude in lead V6 should be more than 0.25 (ie, height of the ST elevation, as measured from the end of the PR segment to the J-point — should be more than 1/4 of the height of the T wave in lead V6 — as shown below in Figure-3).

      Figure-3: Illustration of how the ST segment to T wave ratio is calculated — adapted from Life-In-The-Fast-Lane (and taken from My Comment in the December 13, 2019 post of Dr. Smith's ECG Blog).



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

      WILLY Draft (2/12/2025):

      Written by Willy Frick

      The answer is at the bottom, and illustrated by this case.


      Written by Willy Frick

      A man in his mid 30s with type 1 diabetes presented with two days of midsternal and epigastric pain, described as both "sharp" and squeezing." There was associated nausea, vomiting, and dyspnea. He said the pain was worse with supination and improved with upright posture.

      What do you think?




      Despite the noisy baseline, this ECG is easily diagnostic for OMI. The Queen of Hearts diagnoses OMI with 0.99 confidence (near perfect). Here is her explainability.


      Here are some of the diagnostic findings:
      • Very subtle hyperacute T waves (HATW) in lead I
      • STE and HATW in II > aVF
      • Subtle STD in V1 and V2
      • STE and HATW in V5 and V6
      Therefore, we have an inferior, posterior, lateral OMI. In fact, even the GE algorithm got this one (partially) right.

      The emergency medicine physician documented, "His initial EKG is riddled with artifact and difficult to interpret but does not look like a STEMI." This is a very bold statement in a type 1 diabetic with very concerning sounding chest pain. One wonders why repeat ECG was not immediately performed, if artifact was felt to be a problem. The patient was treated with aspirin and a GI cocktail, which did not help the pain.

      Initial hsTnI resulted at 25,994 ng/L (ref. <35 ng/L). At this point, the physician started heparin and gave nitroglycerin, which improved the pain from 7/10 to 3/10. He also obtained repeat ECG.


      Once again, easily diagnostic for inferior, posterior, lateral OMI. Getting rid of the artifact increased the Queen's confidence from 0.99 to 1.0 (perfect). The ECG remains positive for STEMI by GE. The emergency physician consulted cardiology. Despite apparently hearing the above history together with two diagnostic ECGs and a troponin compatible with OMI, the cardiologist thought the ECG represented pericarditis and recommended echocardiogram.

      Several hours passed with no documentation as to the reason for delay. Echocardiogram was finally performed five hours after the first diagnostic ECG. The report indicates LVEF 35-40% with "globally reduced wall motion with regional abnormalities." The cardiologist then recommended emergent transfer to a PCI center.

      Upon arrival at the PCI center, he was immediately taken to cath lab. Angiogram showed thrombotic subtotal occlusion of LCx/OM1. Here is an AP caudal view before and after PCI. 



      The true AV groove LCx was "jailed" by the stent and appears occluded in the post PCI image. The OM is a much larger vessel.



      With the delays and recognition and transit, time from first diagnostic ECG to balloon was 15 hours and 47 minutes. This far out, the benefit of PCI is very attenuated. Troponin peaked above the upper limit of quantitation 60,000 ng/L. Echocardiogram showed LVEF 33% with akinesis of the lateral wall.


      Here is the wall motion diagram. The view above is enclosed in a red box.


      Final diagnosis written in the chart: NSTEMI

      Discussion:

      It is hard to understand how this can happen, but unfortunately the blog has innumerable similar cases. If I had to guess, I think some of the cognitive errors that may have contributed to this case are:
      • The patient was young, in his mid 30s. But you are never too young to have an OMI. Even if it is not atherosclerotic, young people can have embolic OMIs.
      • The ECG was perceived as having diffuse ST elevations. But it is not really diffuse -- it is inferior, posterior, and lateral. The anterior leads clearly show reciprocal change.
      • The absolute degree of ST elevation (although enough to meet STEMI criteria), was still relatively small.
      We also see that in the end the patient was labeled as NSTEMI, despite meeting STEMI criteria and having acute coronary occlusion. So the diagnosis does not reflect the ECG or the pathology. Instead, the diagnosis reflects how urgently he was treated.

      Now, when the data are sent to the National Cardiovascular Data Registry, it will appear that the patient was treated appropriately as an NSTEMI! There is no external auditing of diagnoses selected by treating cardiologists, so missed door-to-balloon time metrics can easily be avoided by simply calling cases NSTEMI.

      Smith: We usually talk about OMI that are missed because they do not meet "STEMI criteria".  But in this case, the 2nd ECG definitely meets STEMI criteria, but is nevertheless both missed AND ultimately called "NSTEMI".  We are submitting a paper showing that the most important factor in final diagnosis of STEMI vs. NSTEMI is not whether there is or is not diagnostic ST Elevation, nor whether there is or is not acute coronary occlusion, but rather whether the patient was treated in less than, vs. greater than, 90 minutes.  This makes it easier to have favorable statistics of course.


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