Epigastric pain radiating to the chest for 18 hours. ECG makes the Dx. Troponin makes the Dx. CT makes the Dx!

I was shown this ECG with no other information:

What do you think?
Hint: try to see through the artifact!

I answered immediately: "High lateral MI with posterior MI. OMI." (Occlusion Myocardial Infarction)

I asked, "Did the patient present with chest pain?"

Here is the history: "A middle-aged male complained of about 18 hours of epigastric pain that radiated to the chest.  He also had an apparently new facial droop of equal duration.  A stroke code was called, NIH stroke scale was only 1, and attention was turned to the chest pain."  BP was 148/83.

How did I make this ECG diagnosis?

There is subtle STE in aVL with reciprocal STD in II, III, aVF, and STD in V3 and V4.

While there are ECGs that have STE in aVL with reciprocal STD in II, III, aVF in the absence of OMI, they do not also have STD in right precordial leads.  Furthermore, the morphology here is perfect for OMI.

(See the bottom of the post for 3 ECGs from this week with STE aVL and STD III, for which my answer was "no ischemia.")

They performed a point of care cardiac ultrasound (parasternal short axis):

What do you think?

Notice the upper right (septum) contracts much more vigorously than the lower right and right (lateral wall)

The physician did not appreciate this because he was thinking about the patient's pain combined with the facial droop, and so he appropriately obtained a chest CT aortogram to look for aortic dissection.  It did not show dissection, but did show the following images of his heart:

LV on the right. Lower right wall has dark area where there is no contrast in the myocardium (no perfusion)

These show hypoperfusion of the lateral and posterior walls.
Dark areas have no contrast because they are not perfused.

Our radiology chief, Gopal Punjabi, is a CT genius.  He loves to use Spectral CT, and has a spectral CT blog: https://www.ctspectral.com/

He applied spectral CT:

Anterior is to the left, and posterior is to the right
See the dark parts of the posterior wall.  This means there is no contrast there.  It is transmural infarction.

He diagnosed acute MI from his CT reading room. 

For more cases of CT diagnosis of myocardial ischemia via perfusion defect (all by Dr. Punjabi), see here:

--A middle-aged man with severe syncope, diffuse weakness

--A Picture of Subendocardial Ischemia

Case continued
At the very same time that the radiologist was calling to alert of acute MI, the first troponin I returned at 39.4 ng/mL (very high).  In almost any scenario, a troponin this high (even without the ECG and CT) should be considered diagnostic of OMI until proven otherwise by angiography.  The presence of acute refractory chest pain is an indication for emergent angiography regardless of the ECG or any imaging evidence of ischemia.

Could it be something else?  Possible, but unlikely.  Myocarditis, takotsubo, type 2 MI and others almost never have troponin this high.

IV nitroglycerine was started.  Aspirin and heparin were given.

A 2nd ECG was obtained later while the patient had ongoing pain:

OMI looks more obvious

Cardiology was consulted.

A second troponin returned at 55.6 ng/mL.  Pain continued.  A third troponin returned at 57.1 ng/mL.  Pain continued.

The ED physicians decided to give nitroglycerin.

The BP dropped to 96/54 and the pain did not go away (even though hydromorphone was also given -- this can only do harm by masking the pain).  

A 4th troponin returned at 63.8 ng/mL and the patient was taken to angiogram.

At angiogram, he had a 100% occluded circumflex.

It was opened and stented.

The troponin peaked 2.5 hours after the angiogram, and 12 hours after arrival, at 135.6 ng/mL.  This is very high.

Echo next day:

Normal left ventricular size, mild concentric LV hypertrophy, and normal systolic function.

The estimated left ventricular ejection fraction is 60%.

Regional wall motion abnormality-inferolateral, hypokinetic.

(Fortunately, the patient's EF remained quite good.)

Here is the post PCI ECG:

STE and STD remain

Learning points:
1. Learn to recognize STE elevation in aVL, with reciprocal STD in inferior leads.
2. Learn to differentiate it from look-alikes (see below)
3. Pay attention to perfusion of the heart with contrast on CT scan.
4. Very high troponin is almost always a type 1 MI due to OMI
5. Use echo to help the diagnosis.

High Lateral Mimics

Here is a previous post on STE in aVL, and when reflects high lateral OMI and when it does not
True Positive ST elevation in aVL vs. False Positive ST elevation in aVL

These are some other ECGs I was shown this week in patients with chest pain:

There is STE in aVL, with reciprocal STD in III
What do you think?

There is STE in aVL, with reciprocal STD in III. What do you think?

There is STE in aVL, with reciprocal STD in III
What do you think?

My immediate response to all was "normal." And they were normal.  They just do not have the "look" of ischemia.  I'm sure Ken Grauer can tell us exactly what makes these non-ischemic when, in contrast, the one at the top of the post is indeed ischemic and we can recognize it as such.  All I can say is that they are a face I can recognize.

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Comment by KEN GRAUER, MD (3/29/2019):

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Great post by Dr. Smith — which should be entitled, “A Face I Can Recognize”. Dr. Smith’s astute step-by-step analysis of serial ECGs in this case + supplemental material (Echo, CT angiogram, spectral CT) needs no further explanation. But I did want to comment on those 3 other ECGs he was asked to assess this week — for which the diagnosis was not OMI.

• As per Dr. Smith, despite ST elevation in lead aVL with reciprocal ST depression in lead III for each case — all 3 of these tracings were “faces” Dr. Smith instantly recognized as not being due to acute ischemia/OMI.
• I have included 4 ECGs in my Figure-1 below. For clarity — I put as the TOP tracing ECG #3 = the 3rd ECG done in this case, which was obtained post-PCI for treatment of acute LCx occlusion. The 3 ECGs below this top tracing — are the 3 “Mimics” that manifest ST elevation in aVL + reciprocal ST depression in lead III, but which are not the result of acute OMI.

Figure-1: The post-PCI tracing ( = ECG #3) + the 3 Mimics not due to OMI (See text).

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COMMENT: Dr. Smith’s ability to instantly recognize the “face” of acute OMI — and to distinguish this from mimics of acute ischemia, is truly exceptional! It is the result of his years of assessing case-after-case, accompanied by his unsurpassable follow-up of each case. He is almost never wrong.

• I am admittedly not as fast as Dr. Smith in arriving at a definitive diagnosis. In the hope that my approach to each tracing may prove insightful — I offer the following reflections on the 4 tracings shown in Figure-1.

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ECG #3: For illustrative purposes — I chose the best quality tracing of the 3 ECGs performed on the patient in this case. This was the ECG done following PCI of acute LCx occlusion ( = ECG #3). Although the amount of ST segment deviation in any given lead in ECG #3 is modest — this tracing should be immediately identified as potentially new or very recent acute ischemia until proven otherwise:

• Lead aVL manifests an “acute-looking” shape of ST elevation. Despite tiny amplitude of the QRS complex — this shape alone is highly suspicious of acute disease. There is also a definite Q wave in this lead — that is disproportionally deep compared to the tiny R wave.
• Not only does lead III manifest a mirror-image picture of reciprocal ST depression (to the ST elevation seen in aVL) — but both of the other inferior leads (II, aVF) show subtle-but-definitely-abnormal ST flattening and depression!
• While not elevated — the T wave in lead V2 looks taller-and-fatter-than-it-should-be given the tiny amplitude of the QRS complex in this lead.
• There is subtle-but-real ST segment flattening with ST depression in leads V3, V4, V5 and V6.

BOTTOM Line regarding ECG #3: There is abnormally-shaped ST elevation in lead aVL — with subtle-but-real ST-T wave abnormalities in no less than 8 of the remaining 11 leads. In this patient with new-onset chest pain — a tracing like this has to be assumed acute or recent until proven otherwise.

• I wanted to contrast these findings in ECG #3 — with what we don’t see in the other 3 ECGs ...

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Tracing A: Despite ST elevation in lead aVL with reciprocal ST depression in lead III — this tracing looks far less likely to be acute. Reasons for having a low index of suspicion for acute OMI in Tracing A include:

• There is marked LVH! The finding of very deep anterior S waves (~23mm in V2; ~20mm in V3) + a surprisingly tall R wave in V6 (despite the late transition) clearly satisfies voltage for LVH. Although ST-T wave changes of LV “strain” are most often seen in lateral leads — sometimes LV “strain” may manifest itself as ST elevation in anterior leads, especially in association with unusually deep anterior S waves. The magnified insert to the right of Tracing A shows that the mirror-image of the ST-T wave in lead V2 conveys an ST-T wave shape identical to that expected with marked LV “strain”.
• The isolated finding of T wave inversion in lead III (even when deep and symmetric, as seen in Tracing A) — is not necessarily abnormal. This is especially true when the QRS complex in this lead is predominantly negative, as seen here.
• The shape of the upright T wave and slightly elevated ST segment in lead aVL looks similar to the ST-T wave appearance in 5 of the 6 chest leads — and this shape in those chest leads with deep S waves seems most likely to be due to LVH.
• BOTTOM Line: The predominant finding in Tracing A is marked LVH + LV “strain” in the anterior leads. LVH is a common mimic of acute ischemia. While I would not be 100% certain from Tracing A alone that nothing acute is going on (ie, the T wave in lead V5 seems a bit-taller-than-expected given the relatively small r wave in this lead) — almost all of the findings described above are explainable by the marked LVH.

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Tracing B: The QTc is prolonged in Tracing B (I estimate it to be ~460-470msec). Although the ST segment is coved and slightly elevated in leads I, aVL and V2 — the arc of the ST segment looks very gradual in these leads (in contrast to the ST-T wave in leads aVL and V2 of ECG #3). This does not look acute. In support of low likelihood that this ST coving is acute — the mirror-image downward arcing of the ST segment in leads III and aVF is equally gradual — and ST-T waves are simply “flat” (not depressed) in 5 other leads (leads II, V3-V6).

• This tracing just doesn’t look acute ...

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Tracing C: The finding of T wave inversion in either lead III and/or in lead aVF is not necessarily abnormal. For this reason — I place great weight in decision-making on the ST-T wave appearance in the 3rd inferior lead = lead II. Although in Tracing C, the ST-T wave in lead II is somewhat flattened — there is no hint of T wave inversion. Given that the QRS complex is predominantly negative in these 2 leads with T wave inversion and, the lack of J-point ST depression in these 2 leads — I don’t think any conclusion can be reached as to whether or not T wave inversion in leads III and aVF of Tracing C is acute.

• The slight ST elevation in lead aVL is concave-up (ie, “smiley” configuration) — and totally consistent with a repolarization abnormality. The q wave in lead aVL is consistent with a normal “septal” q wave. And, the shape of the ST segment in lead III is the mirror-image opposite of the elevated ST segment in aVL that looks like a repolarization variant.
• The overall picture in the limb leads does not look acute.
• In support of low likelihood that these limb lead findings are acute — the chest leads are inconclusive. While one might wonder about the size of the T wave in lead V2 relative to the small r wave in this lead — neither neighboring lead (V1 or V3) gives even a hint of abnormality — and, the ST-T waves in V4-6 are unimpressively flat. So, while I might not be 100% certain from Tracing C alone that nothing acute is going on (depending on how suspicious the history was) — my index of suspicion for acute coronary disease would clearly be low.

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Additional Learning Points:

• Pay attention to ST-T wave shape. Shape is often more important than the amount of ST-T wave deviation.
• The more leads that show subtle-but-real ST-T wave abnormalities consistent with the overall picture — the more likely these changes are to be acute.
• You don’t have to make a definitive decision on the basis of a single tracing. Clinical correlation with history, serial tracings and additional diagnostic modalities can usually provide a more confident answer in a time-efficient fashion.

Our THANKS to Dr. Smith for this highly insightful case!