ECG Blog #337 — NSTEMI or OMI?

The ECG in Figure-1 — was obtained from a middle-aged man who presented to the ED (Emergency Department) with severe chest pain of uncertain duration.

• How would YOU interpret his initial tracing?

Figure-1: Initial ECG obtained in the ED from a middle-aged man with severe chest pain of uncertain duration. Is this ECG of concern?

MY Approach to Today's Case:

Even before troponin comes back — the history in today's case and the ECG shown in Figure-1 should raise concern:

• The fact that this patient presents to an ED with new-onset severe chest pain immediately places him in a "higher prevalence" population for having an acute event. The fact that the duration of his symptoms is "uncertain" — means that IF he had an acute event — it could either be acutely ongoing — or — it may have been completed in recent hours (or within the past day or so). Awareness of the uncertainty of this timing is critical for understanding the KEY findings in this initial ECG shown in Figure-1.

Regarding the ECG in Figure-1:

Although resolution of today's initial tracing is poor (and it is admittedly difficult to make out ECG grid lines) — the rhythm appears to be sinus bradycardia and arrhythmia. (NOTE: There is no significant pause in the rhythm — as the 2nd QRS complex is hard to see because it is almost completely hidden by the lead change between leads I,II,III and leads aVR,aVL,aVF).

• All intervals (PR,QRS,QTc) are normal in ECG #1. The frontal plane axis is normal at +20 degrees. Criteria for chamber enlargement are not met.
• Narrow Q waves of uncertain significance are seen in high lateral leads I and aVL. There may be tiny septal q waves in leads V5,V6.
• Regarding R wave progression — Transition occurs early! (ie, The R wave becomes taller than the S wave is deep between leads V1-to-V2).

The most remarkable findings in ECG #1 — relate to subtle-but-real ST-T wave changes in multiple leads:

• The most "eye-catching" finding is the surprisingly deep, symmetric T wave inversion in lead III. Although isolated T wave inversion in lead III (or in lead aVF) in association with a predominantly negative QRS complex in this lead is not necessarily abnormal (See ECG Blog #79) — it is of concern in today's patient because: i) The History is very concerning; ii) There are subtle-but-real ST-T wave abnormalities in multiple other leads; and, iii) The abrupt transition with unexpectedly tall R wave in lead V2 could be consistent with posterior infarction (and posterior MI is so very often associated with inferior MI, that might cause T wave inversion in lead III).
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• Lead III is abnormal because, in addition to the deep T wave inversion — the ST segment is coved (ie, with a "frowny"-configuration) — and the J-point is depressed. The other 2 inferior leads (leads II and aVF) both show ST segment flattening with slight-but-real ST depression.
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• Lead aVL (and to a lesser extent lead I) — shows a mirror-image opposite picture to lead III, in that there is slight ST elevation with a more voluminous T wave than expected.
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• In the Chest Leads — the T wave in lead V2 is taller-than-expected given the height of the R wave in this lead.
• Normally there is slight ST elevation in lead V3 — but the ST segment in this lead appears to be isoelectric, with a straightened (rather than smooth and gently upsloping) ST segment. That these very subtle ST-T wave changes are likely to be "real" — is supported by suggestion of slight ST depression in the lateral chest leads.
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• P.S.: There are U waves of uncertain significance in leads V2,V3,V4 of ECG #1 (I do not know serum K+/Mg++ at the time this tracing was recorded).

Putting It All Together:

To Emphasize — The above findings are subtle! That said:

• The history for today's patient places him in a "high prevalence" group for having an acute or recent cardiac event.
• While frank ST elevation is lacking — the deeper-than-expected symmetric T wave inversion in lead III — in association with subtle-but-real ST depression in all 3 inferior leads — in this patient with severe chest pain of uncertain duration — is clearly consistent with possible reperfusion T waves following recent RCA (Right Coronary Artery) or LCx (Left Circumflex) coronary occlusion.
• Reciprocal ST-T wave changes in high lateral leads I and aVL support this suspicion. The ST elevation in these leads may indicate lateral involvement and/or inferior reperfusion.
• Sinus bradycardia is a common accompaniment of inferior wall infarction.
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• Posterior involvement is commonly seen with inferior infarctions. The ECG picture we see in lead V2 is consistent with a positive "Mirror Test" for recent posterior MI, now with reperfusion (ie, abrupt transition with a tall R wave already seen in lead V2 — and a taller-than-expected T wave in lead V2, which is the mirror-image opposite picture of the symmetric T wave inversion in lead III).
• Finally — the History of severe chest pain of uncertain duration could be consistent with spontaneous reperfusion after acute RCA or LCx occlusion.
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• BOTTOM Line: Especially if this patient's chest pain had just subsided prior to recording this ECG — the story and ECG findings could be perfectly consistent with infero-postero reperfusion changes following spontaneous reopening of the "culprit" vessel. 
• MY Thought: If the above was not enough to convince the consulting cardiology team to promptly perform cardiac catheterization — rapid collection of additional data might help to do so.

CASE Follow-Up:

This patient's initial troponin came back mildly elevated. He was diagnosed as having a NSTEMI ( = Non ST Elevation MI) — and was managed accordingly. But before transfer to a teriary care facility — a 2nd ECG was obtained 30 minutes after ECG #1. For clarity — I've put these 2 ECGs together in Figure-2.

QUESTIONS:

• Does ECG #2 assist in your assessment of what is going on with this patient?
• Do YOU agree with the diagnosis of a NSTEMI?
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• HINT: I've added the following 2 PEARLS to assist in your comparison of ECG #2 with the initial ECG recorded 30 minutes earlier. (Unfortunately — I don't know the status of this patient's chest pain at the time these 2 ECGs were obtained).

PEARL #1: I have often emphasized the importance of appreciating that insistence on millimeter-based criteria for an acute STEMI misses a significant percentage (if not the majority) of cases of acute coronary occlusion. By way of review — I include material on this issue in the ADDENDUM below.

• As per Figure-3 (in the Addendum below) — a combination of ECG findings (such as those that I describe for ECG #1 above) — in association with new cardiac symptoms — can be diagnostic of acute OMI (Occlusion-based MI) — despite the absence of significant ST elevation.
• The problem arises because many acute coronary occlusions spontaneously reopen — only to spontaneously reclose again. At times, the "culprit" vessel may spontaneously reopen and reclose a number of times — until ultimately it reaches its final state. The goal of recognizing acute OMI on ECG in the absence of frank ST elevation — is that doing so at an earlier stage allows the opportunity for prompt intervention in the hope of preventing subsequent permanent reocclusion with significant myocardial damage.

PEARL #2: Missing from today's case is a more detailed history that correlates serial ECGs to the presence and severity of the patient's symptoms. When this correlation has been established — you can know if the "culprit" vessel is open or closed because:

• Recurrence of chest pain in association with recurrent ST elevation tells you the "culprit" vessel has reoccluded.
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• Reduction (or resolution) of chest pain — in association with reduced (or resolved) ST elevation, especially if associated with T wave inversion (and/or ST depression) in areas that previously showed ST elevation — tells you that the "culprit" vessel has reperfused, and is probably now open.
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• Because anterior chest leads provide a mirror-image view of ST-T wave changes occurring in the posterior wall of the left ventricle — development of tall, peaked T waves in anterior chest leads (that previously showed ST depression) — in association with reduced symptoms — indicates posterior wall reperfusion.
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• BOTTOM LINE: The importance of serial ECGs that are closely correlated to the persistence and severity of chest pain (and/or to chest pain resolution) — can not be overstated for its diagnostic value in recognition of the stages of acute OMI.

Figure-2: I've put the initial ECG (from Figure-1) — together with the follow-up ECG obtained 30 minutes later. Has there been any significant change?

Comparison of ECG #1 and ECG #2:

Unfortunately — both of the tracings in Figure-2 lack a long lead rhythm strip. That said — it appears that there is more bradycardia in ECG #2. This may be relevant given concern about potential recent infero-postero infarction. Regarding the difference in ST-T wave changes between the 2 tracings — Lead-by-Lead Comparison of ECG #1 and ECG #2 shows the following:

• The most striking change to me is the indisputable increased size of the inverted T wave in lead III of ECG #2. In addition — T wave inversion is now clearly seen in the other 2 inferior leads ( = leads II and aVF) — whereas it was not seen previously.
• The mirror-image opposite (reciprocal) relationship between lead III and the 2 high-lateral leads ( = leads I and aVL) continues — as the size (and volume) of the T waves in lead I and lead aVL has clearly increased in ECG #2, so as to match the increased size of the T wave inversion in lead III. In addition — there is more ST elevation now in lead aVL (to match the J-point ST depression we see in lead III).
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• In the Chest Leads — although the changes are more subtle, there has clearly been an increase in T wave size (and T wave volume) in leads V2-thru-V6 of ECG #2.
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• P.S. The U waves that were seen 30 minutes earlier in ECG #1 are no longer prominent. If anything, bradycardia accentuates U waves — so I do not know the reason for this change (I'm not privilege to lab work corresponding to ECGs #1 and #2).
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• BOTTOM Line: Lead-to-lead comparison between the 2 tracings in Figure-2 — reveals an increase in reperfusion changes in 10/12 leads. Given the clinical history of severe chest pain of uncertain duration in this middle-aged man — the inescapable conclusion to me on reviewing this case, is that there has been recent infero-postero infarction (from either RCA or LCx occlusion) — and that the increase in ST-T wave abnormalities described above in 10/12 leads most probably reflects reperfusion of the "culprit" artery.
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• P.P.S.: The fact that there is no significant change in either frontal plane axis or QRS morphology in all leads — suggests that all changes seen in ST-T wave morphology between these 2 tracings are "real" (and not a result of axis shift or lead placement differences).  

WHAT Happened . . .

As alluded to above — the patient was diagnosed as having had an NSTEMI, and was treated accordingly. Of note, is that over the course of the initial hospital day — serial troponin values became markedly elevated.

• For personal reasons — the patient chose not undergo cardiac catheterization prior to hospital discharge. He did return for elective cardiac catheterization ~2 weeks later — and was found to have multi-vessel disease. This included mild proximal disease of the LAD (Left Anterior Descending) coronary artery — an 80% ostial lesion of a large 2nd Diagonal vessel — and a dominant 90% midsegmental lesion in the RCA that retrospectively was felt to be the "culprit" artery for this patient's infarction. The Left Main and Left Circumflex vessels were without significant disease.
• PCI (Percutaneous Coronary Intervention) was performed to the RCA — with improvement of coronary flow.

The LESSONS To Be Learned:

Acute OMI ( = acute coronary Occlusion-based MI) — is frequently missed in current practice. All too many clinicians remain "stuck" in the "STEMI" paradigm without appreciation of the clinical reality that many acute coronary occlusions simply do not manifest STEMI criteria (Please see the ADDENDUM below for additional material on this subject).

• Attention to a combination of other ECG criteria — when closely correlated to the clinical history (with serial chest pain severity scores, serial troponin values, detection of wall motion abnormality on Echo) — allows much faster recognition of acute OMI (and therefore much faster initiation of reperfusion therapy that improves prognosis). In contrast — reliance on millimeter-based STEMI criteria results in delay (or missing entirely) all-too-many acute coronary occlusions that could have benefited from prompt intervention.
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• Failure to consider the above factors (and the additional ECG findings I highlight in Figure-3 of the Addendum) — results in the mislabeling of all-too-many acute infarctions that do not satisfy millimeter-based ST elevation criteria — as non-STEMIs (whereas in reality — many of these "NSTEMIs" were actually acute OMIs that should have benefited from prompt intervention).
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• The ECG findings in the initial tracing of today's case — especially after dynamic increase in the abnormal ECG findings noted in the 2nd tracing — were diagnostic of the fact that an acute OMI had taken place (and that prompt cath with PCI was indicated). Subsequent marked troponin elevation of this patient was evidence of significant myocardial damage. How much myocardial loss could have been prevented by prompt intervention is unknown.
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• It should be clear that the final diagnosis in today's case was not a "NSTEMI". This was proven on cardiac cath. Instead — the ECGs correlated with the clinical history in today's case were diagnostic of an OMI that presented with reperfusion T waves which were not recognized as such. The lessons-to-be-learned should be clear.

 

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Acknowledgment: My appreciation to an anonymous sender (from Malaysia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery — as well as the importance of the term, "OMI" ( = Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
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• ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
• ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.
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• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
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• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.

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ADDENDUM (October 9, 2022):

• Included below are a series of links and other material relevant to detection of the “culprit” artery — and my thoughts for making the case to replace the term “STEMI” with “OMI” (in the hope of substantially increasing detection of acute coronary occlusion). 

 

Free PDF Downloads from relevant Sections in my ECG-2014-ePub:

• PDF File: Overview on the Cardiac Circulation and the “Culprit” Artery in Acute MI —
• PDF File: Posterior MI and the “Mirror Test” —  

Figure-3: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post. 

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NOTE: This Editorial just published by Drs. Steven Smith and Pendell Meyers details use of Hyperacute T-Waves in the diagnosis of acute OMI — "Hyperacute T-waves Can Be a Useful Sign of Occlusion MI IF Appropriately Defined" (Ann Emerg Med — March 3, 2023).

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Today’s ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.

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Today’s ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.