The computer calls this a “normal ECG”. We'll just keep making this point.

This case was contributed by Brooks Walsh, an emergency physician in Connecticut.

A middle-aged woman had an acute onset of chest pain and dyspnea. The symptoms improved somewhat after the paramedic gave her nitroglycerin. 

The pain had almost resolved by the time an ECG was obtained in the ED:

Here is the computer diagnosis 

What do you think?

Perhaps you might think these changes are too subtle to immediately call for the cath lab. But do you think the ECG is “normal?” Well, the computer thought so!

This was not an OMI, but there is ischemia.

Note leads III and aVF. There is subtle ST segment elevation in those leads. Although it is not high in absolute terms, it is quite high relative to the low QRS voltage in those leads. In combination with the subtle ST depression in aVL, these changes are diagnostic for, or at least nearly so, for acute occlusion of a coronary artery, probably with some reperfusion, as inferior T-waves are inverted and the T-wave in aVL is reciprocally upright.

Despite the computer interpretation, the ED physician was concerned about the ECG, and planned for serial troponins.

The first level was undetectable.  Three hours later, however, the troponin I was elevated at 0.08 ng/ml (99th percentile 0.01 ng/ml). The patient was verified to be symptom-free, and a repeat ECG was performed.

Note that the ST elevation in the inferior leads has basically resolved, especially compared with the restored QRS voltage. The ST depression in aVL is also resolved.

This confirms that there were dynamic signs of ischemia on the initial ECG. It was not normal!

A third troponin I returned at 0.27 ng/ml, a three-fold increase from troponin #2, also confirming acute myocardial infarction.

Epilogue:
Angiography, however, did not reveal significant obstruction of the RCA, LAD, or circumflex. No residual signs of a culprit lesion could be identified.

No echo was done.

Management: dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitior (clopidogrel, ticagrelor or prasugrel)

Smith comment: This is another unusual case in which the T-wave in lead III looks like a reperfusion T-wave but is present during pain and then normalizes later.  
This is similar to this case which I posted last week:

Dynamic, Reversible, Ischemic T-wave inversion mimics Wellens'. All trops negative.

Like that last case, the upright T-wave does NOT represent pseudonormalization due to re-occlusion, but rather true normalization. This upright T-wave is associated with absence of chest pain and an open artery (pseudonormalization is associated with recurrence of chest pain and a closed artery). But in contrast to that last case, this case had a positive troponin. This is particularly unusual, as T-wave normalization is usually unstable angina (negative troponin).

Learning Point:

Do not trust the computer when it interprets the ECG as "normal".

Here are many other cases in which the computer algorithm called the ECG completely normal when it was in fact dangerously abnormal.

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Comment by KEN GRAUER, MD (12/19/2018):

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Illustrative case by Dr. Brooks Walsh regarding a number of important concepts! For clarity — I’ve put the 2 ECGs done on this patient together (Figure-1).

Figure-1: The 2 ECGs in this case (See text).

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As per Dr. Walsh — despite computer interpretation of the initial ECG done in the ED ( = ECG #1) as showing,“Sinus rhythm; Normal ECG” — the ED physician was appropriately concerned by a number of abnormal findings. In the interest of academic discussion — I’ll add the following thoughts:

• The computer interpretation was obviously wrong. That said, this is not the “fault” of the computer. The computer is good at some things — but less good at others. Computerized ECG interpretations are generally very accurate for making measurements (ie, of rate, intervals, axis). However, the computer is not good at assessing rhythms other than sinus — and, it is not good at recognizing subtle ST-T wave changes of acute ischemia or infarction. As a result — We should not expect the computer to be accurate in assessing non-sinus rhythms or subtle ST-T wave abnormalities. Instead, I believe it is the clinician’s fault if he/she accepts the computer interpretation as “normal” without first overreading the tracing. We should not be blaming the computer if it doesn’t pick up on subtle infarctions ...

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NOTE: Optimal use of computerized ECG interpretations depends on a number of factors, including: i) Expertise of the interpreter; ii) Awareness of the strengths and weaknesses of the computer interpretation program being used at your institution; and, iii) Remembering what you are looking for on the ECG of the patient in front of you.

• For “My Take” on optimal use of computerized ECG interpretation — please CLICK HERE —

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While good that the ED physician recognized abnormal findings on the initial ECG — an elevated troponin should not be needed in this case before contacting the cardiologist on call. That’s because ECG #1 shows abnormal ECG findings that have to be assumed acute until you prove otherwise.

• As emphasized numerous times on this ECG Blog — troponin values may be initially normal in cases of brief coronary occlusion in which there is prompt spontaneous reperfusion. As a result, even if the first one or two troponin values in this case were to come back normal (and the 1st troponin in this case was undetectable) — nothing is proven. Instead, time is lost ... This patient should be admitted to the hospital — and, at the least — should be cathed at some time during her hospital stay before she goes home. Making cardiology aware sooner (rather than later) that they have a consult in the ED with new-onset chest pain and recent (if not acute) ECG changes on her initial ECG, will hopefully serves to expedite decision-making.
• History is important. The fact that this middle-aged patient had new-onset chest pain that was severe enough to call EMS — in association with the initial ECG shown in Figure-1 — significantly increases the likelihood of an acute event even before you look at the initial ECG. In contrast, the initial ECG in Figure-1 would be less suspicious if the history was unconvincing.

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In a patient with new-onset chest pain — the findings in ECG #1 are of definite concern:

• Acute inferior MIs often manifest no more than low-amplitude ST-T wave changes. As a result — shape rather than amount of ST segment deviation is most important. Hyperacute-looking ST-T waves with slight-but-real ST elevation is seen in all 3 of the inferior leads of ECG #1. Given the tiny height of the R wave in lead aVF — the amount of ST elevation in this lead proportionately is considerable (ie, almost 1/3 the height of the R wave!).
• There is a small-but-real q wave in lead II.
• There is a QS complex in lead III (at least for the first 2 beats in lead III).
• Although T wave inversion in lead III is not necessarily an abnormal finding when the QRS complex in this lead is predominantly negative — the coved shape of the ST segment seen here in lead III is never normal.
• Finally, the slight-but-real coved ST depression in lead aVL is the exact mirror-image opposite shape of the coved ST elevation in lead III. This qualifies as reciprocal ST depression.
• Subtlety — In additional to some baseline artifact, there is some beat-to-beat variation in QRST morphology in lead III of ECG #1. For example, the ST-T wave of the 1st complex in lead III looks the most abnormal. Is this the “real” shape of the ST-T wave in this lead? Given how subtle ST-T wave changes are in ECG #1 — this beat-to-beat variation in one or more leads makes accurate assessment that much more difficult. SUGGESTION: When the initial ECG is equivocal — and especially when there is some beat-to-beat variation in morphology — obtaining one or more follow-up ECGs much sooner than 3 hours should help to clarify if there are acute changes.
• P.S. — Some time ( ? how much) had passed since the onset of symptoms and the time when ECG #1 was recorded in the ED — and, the patient's chest pain was almost gone by the time ECG #1 was recorded. As a result, we might expect ECG findings in ECG #1 to be more subtle than if symptoms were still ongoing ...

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QUESTION: Has there been a change in frontal plane axis between ECG #1 and ECG #2? If so — How might this alter your ability to assess serial change between these 2 tracings?

ANSWER: The frontal plane axis in ECG #1 is about +15 degrees. The axis in ECG #2 is about +45 degrees.

• Lead-to-lead comparison of the 2 ECGs in this case facilitates recognizing this change in frontal plane axis. That is, the QRS complex is predominantly negative in lead III of ECG #1 — but predominantly positive in lead III of ECG #2. While I agree that ST segment deviation has clearly improved in ECG #2 — it should be appreciated that the shift in frontal plane axis makes comparison and detection of serial ST-T wave change in these 2 tracings that much more challenging.

Dynamic, Reversible, Ischemic T-wave inversion mimics Wellens'. All trops negative.

A middle-aged man presented with 7-8/10 non-radiating chest tightness to the left chest wall, associated with nausea but no diaphoresis, that began while walking approximately 40 minutes prior to arrival at the ED. The pain resolved as he arrived to the emergency department. He had 2 episodes over the past 2 days of similar chest tightness. He had a history of hypertension but stopped taking his medication several years ago.  The patient is pretty sure that this discomfort was his reflux.

BP was 200/100.

Here was his triage ECG.   It is uncertain if the patient was pain free at this time or not, or, if pain free, for how long he had been pain free.  He was definitely pain free by the time of arrival at his ED room.

What do you think?

This appears to be a classic Wellens' ECG, Pattern A, with terminal T-wave inversion in V2-V4, preserved R-waves, and it appears to be Wellens' syndrome, as it occurred after resolution of typical angina pain.

We assumed this was Wellens' syndrome and treated as such.

Wellens' syndrome represents the aftermath of an unrecorded occlusion (STEMI) with spontaneous reperfusion.  Wellens' waves are "reperfusion T-waves" and are identical to the T-waves seen after therapeutic reperfusion.  If true Wellens', they always are associated with slightly elevated troponin and always evolve over the next 12-72 hours into Pattern B waves (deep, symmetric).  If they do not evolve in this manner, it is not true Wellens'.

Wellens syndrome requires that the pain be resolved and the R-waves are preserved.  (In other words, the artery was occluded but has sponteneously reperfused, resulting in pain relief)

It is important to monitor patients with Wellens' syndrome for re-occlusion, which is usually, but not always, associated with recurrent chest pain.  Re-occlusion results in the T-wave becoming upright again (T-wave pseudonormalization).

We treated him with aspirin and heparin and metoprolol. 

The patient remained pain free.   Repeat BP was 140/80.  90 minutes later, another ECG was recorded:

What do you think?

With a newly upright T-wave, one must consider pseudonormalization and re-occlusion.  In fact, that would be most likely.  Even if the patient is pain free, as this patient was (he felt fine).

See this case: Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome

But this ECG does not look like an LAD occlusion.  Moreover, an echo showed no wall motion abnormality. 

This was my interpretation: although most ischemic T-wave inversion is post-ischemic like Wellens, sometime active ischemia results in isolated T-wave inversion.  In such cases, if there is no infarction (necrosis), when the ischemia resolves, the T-wave may normalize (in contrast to Pseudo-normalize).  When this happens, troponins are negative, there is no wall motion abnormality, and it is true unstable angina.  (Wall motion abnormalities may also occasionally quickly resolve in Wellens syndrome if the infarct is very small and the ischemia brief).

Case continued

All troponins were negative.  The patient underwent a stress echo, which was MARKEDLY positive.  The angiogram showed a 95% LAD stenosis and a 70% stenosis of the first diagonal off the LAD (LADD1).

Here is the post-PCI ECG, 2 days later:

There is again terminal T-wave inversion. This time it is associated with a post PCI troponin of 0.055 ng/mL (elevated).  The 4th Universal Definition of MI calls this Cardiac Procedural Myocardial Injury.

Comment

Imagine this scenario:

The patient did not get his ECG at triage. Rather, it was not recorded until he arrived at his room.  The ECG could have been completely normal.  He has negative troponins.  He thinks it is his reflux.  His HEART score would have been 3 (low) and he would be discharged.  His EDACS score would have been 14 (low risk).

Learning Points:

1. Unstable Angina still exists
2. Chest pain scores can result in discharge of a high risk patient.
3. The ECG is essential, and recording it at triage can avoid missing a diagnostic moment.
4. T-wave inversion can be due to acute non-infarct ischemia, in which case it can reverse and normalize.  Troponins are negative and it is thus "unstable angina."
5. T-wave inversion can be post-ischemic.  If it is, the troponins are positive and the T-wave inversion evolves to become deeper and deeper.

Classic Evolution of Wellens' T-waves over 26 hours

Other posts

Dynamic T-wave inversion (apparent Wellens' waves), all troponins negative: Unstable Angina

Subtle Dynamic T-waves, Followed by LAD Occlusion and Arrest

Subtle LAD Occlusion with Pseudonormalization of Wellens' Waves.

Pseudonormalization of Wellens' Waves

Pseudonormalization of T-waves

Anterior pseudonormalization

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Comment by KEN GRAUER, MD (12/14/2018):

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Interesting case that brings up a number of important concepts regarding Wellens’ Syndrome. For clarity — I’ve reproduced the first 2 ECGs in this case in Figure-1.

 

Figure-1: The first 2 ECGs in this case (See text). 

 

 

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It is certainly possible that IF the timing had been such that this patient’s initial ECG was normal (as it was for ECG #2 in Figure-1) — that the severity of this patient’s underlying coronary disease could have been overlooked. I’d add the following points:

• I’ve always thought of Wellens' Syndrome as a way to predict high likelihood of a tight, proximal LAD lesion. True, Wellens' Syndrome is seen before a large anterior infarction has occurred — thus, there should be preservation of anterior R waves. Therefore, the classic Wellens’ ECG Pattern A seen in ECG #1, with steep terminal downsloping T waves and terminal T wave negativity in one or more anterior leads, given the history in this case of intermittent (now resolved) worrisome chest pain — IS highly predictive of proximal LAD narrowing. That’s why the team diagnosed Wellens’ Syndrome, and began treating accordingly.
• In contrast, the isolated ECG finding of deep, symmetric chest lead T wave inversion doesn’t fit my definition ( = My Opinion) of what true Wellens’ Syndrome is — because there are other potential causes of deep, symmetric T wave inversion (ie, cardiomyopathy; ischemia not related to proximal, high-grade LAD narrowing; prior infarction; etc.). Of course, if this Pattern B of deep, symmetric T wave inversion occurs in a patient with the expected history AND follows an initial ECG showing the typical Pattern A — then, this would be consistent with the typical evolution of true Wellens’ Syndrome.
•  
• In this particular case, the history of new-onset, worrisome chest pain (that then resolved) + classic Wellens' Pattern A terminal T wave inversion with preserved anterior R waves in the initial (triage) ECG is definitive for a need to assume severe LAD disease until proven otherwise — almost regardless of what the next ECG might show.
• Normalization of terminal T wave activity in the ECG #2 in this case constitutes a dynamic ST-T wave change. Even if troponins are negative and infarction is not documented — dynamic ECG changes in association with new chest discomfort is indication for investigation.
• Chest Pain scores can be misleading. Such scores all include subjective assessment of the patient's history, as well as at least some subjectivity in ECG assessment. As has been emphasized on numerous blog posts on this site — more than a single tracing will usually be needed for optimal diagnosis whenever the slightest of doubt regarding acuity exists. The onus of proof that chest discomfort in a patient who presents to the ED is not cardiac rests on the clinician (What brought this patient to the ED at this particular moment?). Especially when a single initial ECG is not obviously abnormal, and an initial troponin is negative — the accuracy of a chest pain score depends more than ever on the accuracy of assessing the subjective component of the patient’s symptoms.

Reversible T-wave inversion -- it reverses, then evolves, then reverses when ischemia is gone. Normalization of T-waves, NOT pseudonormalization.

A 62 yo male has had chest pain with exertion for 2 weeks.  He began having chest pain at rest at 2AM, and presented at 7 AM.

Here is his initial ECG:

Sinus rhythm.  There is a QS-wave in V2 (old MI?) and very subtle terminal T-wave inversion in V3, and ST depression in V4-V6, highly suspicous for LAD NonSTEMI.  I believe the extra wave in V1-V3 is artifact. 





This was recorded 2 hours later, after troponin I confirmed acute MI at 0.485 ng/mL:



There is a PVC, but now the terminal T-wave inversion is gone. Some ST depression in V5 and V6 remains.



An angiogram revealed 3-vessel disease and a 90% LAD stenosis, 99% RCA, and 70% ostial right Posterior Descending Artery.  No intervention was done because of consideration of CABG.

This was recorded 9 AM the next day.  A simultaneous echo had very subtle WMA in the LAD territory.

Now there is classic biphasic terminal T-wave inversion (strictly speaking, it is not Wellens' because Wellens' requires preservation of R-waves). There is also subtle new Terminal T-wave inversion in aVF ("inferior Wellens").



On day 2, PCI of the rPDA and RCA was done.  The troponins continued to trend down.  

This ECG was recorded the next AM (day 3):

There is evolution of anterior T-waves, with T-wave inversion in V4 more pronounced now.  T-wave in aVF is now upright.

On day 3, he had the LAD stented.  Troponins bumped to 3.0 mcg/L after the PCI.   This was recorded the next AM:

Now, the anterior T-waves have completely normalized.

Such reversal is usually due to reocclusion (pseudonormalization) and associated with chest pain.  Wellens in the setting of significant troponin elevation usually evolves to deep and symmetric T-waves, then normalizes over weeks to months.  This is an unusual case of T-wave normalization without re-occlusion that occurred in 24 hours.

In unstable angina, with no myocardial cell death, T-waves are more likely to normalize when ischemia is resolved.

Contrast this normalization of T-waves to the pseudonormalization of the last post.