A man in his late 30s with acute chest pain and ST elevation

Sent by Dan Singer MD, written by Meyers, edits by Smith

A man in his late 30s presented with acute chest pain and normal vitals except tachycardia at about 115 bpm. Here is his triage ECG:

What do you think?

Dr. Singer sent this to me with just the information: "~40 year old with acute chest pain". I immediately responded: "cool fake! Not OMI. Do you have a prior? There is a reasonable chance of pericarditis in this case, or this could be a baseline." 

It could easily be mistaken for a South African flag pattern anterolateral OMI, with STE in I, aVL, V2. But importantly there is no reciprocal STD in III (which would usually be expected if the STE in aVL were indicative of acute transmural infarction). Additionally, there are prominent remarkable J waves in I and aVL. The significant STD in aVR belies a significantly diffuse STE vector which is maximal in the leftward and downward directions.

No prior ECG was available.

Here is the Queen of Heart's interpretation:

The cath lab had been activated for concern of STEMI.

I do not have much clinical detail available, but cardiology cancelled the cath lab activation for some combination of reasons.

Three serial high sensitivity troponins were all below the limit of detection. 

Formal echo showed normal function, no WMA, and no effusion.

No angiogram was performed.

AMI was ruled out, therefore OMI is ruled out.

Other outcome information is not available. Sadly, I did not receive enough information to adjudicate whether this patient has pericarditis or not. 

I sent this to Dr. Smith and this was his response: 

"Likely pericarditis, but that is perilous.  Lots of PR depression and elevation in aVR.  ST vector not typical of OMI.  But I would cath unless there is some clear clinical feature that points to pericarditis.  Any more data than just “cp”.  Pleuritic? Positional? Rub? Fever? Acute pain?"  

-------(Dr. Smith has a saying: "You diagnose pericarditis at your peril -- or your patient's peril" -- see Ken Grauer comments below).   And this is because OMI is frequently misdiagnosed as pericarditis.  Always, the most important factor AGAINST pericarditis is its relative rarity compared to OMI. Pretest probability is crucial in ECG diagnosis of OMI or ECG diagnosis of OMI mimic.

As Ken says below, tachycardia is not common in OMI and distorts the ST segment, so managing the tachycardia and repeating the ECG is a good strategy.

Learning Points:

This is one of many examples of false positive STEMI criteria, which is distinguishable by expert humans, and now by AI such as QOH.

In the OMI paradigm, we seek not only to improve detection of STEMI(-) OMI, but also to reduce false positives.

Emergent CT coronary angio also likely has a role in such cases. Imagine: the providers in the case above are not sufficiently sure that the patient above doesn't have OMI. Like they would for any other acute arterial occlusion syndrome (such as suspicion of acute large vessel stroke), they take the patient across the hall and perform an immediate CT (coronary) angiogram, showing patent coronaries. An emergent echo also confirms no regional wall motion abnormality. This way, they don't have to choose between: A) waiting for trops to rapidly rise, thereby missing crucial time-based benefit for OMI, or B) wasting a trip to the cath lab. 

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My Comment by KEN GRAUER, MD (5/16/2023):

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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).