Chest pain resolved, and a “Normal” ED ECG

A previously healthy middle-aged male presented shortly after the acute onset of chest pain very shortly before calling 911.

On arrival, he was pain free:

What do you think?

There is a very subtle inferior MI.  Some may quibble that this ECG is not diagnostic of MI (although I would say it is “all but diagnostic.”)

Notice the computer called it normal — but it is clearly not normal.

The computer should at least call this “Nonspecific ST-T abnormalities.”

Jerry Jones commented:
“Any ST depression on the ECG of a patient with chest pain credible for ACS represents a reciprocal change until proved otherwise.” 

And also: 
I have, for many years now, taken exception to the term “non-specific ST-T changes.”” There is a finality to that term that suggests “inconsequential, unimportant, pay-no-attention or let’s-move-on.” I prefer the term “unexplained ST-T changes” –Great comments, thanks Jerry!

I like to say: 
“It is not the ECG that is nonspecific; it is the interpreter who is nonspeciific.”  Many “nonspecific” findings are only non-specific because the physician does not recognize their meaning.

In this case, the diagnosis was much easier because there was a prehospital ECG:

less than 1 mm ST Elevation in II, III, aVF, with minimal ST depression in aVL
This is diagnostic of inferior OMI

No clear evidence of ischemia

Computer interpretation
Impressive!  This algorithm called it a STEMI.
It measured all the ST segments and recorded them (see bottom right)
It only measure one lead (III) as greater than 1 mm, so there are not “2 leads with at least 1 mm”.  Yet it gave a diagnosis of STEMI.
I have not seen this before, and perhaps they are altering their algorithms?

There was prehospital cath lab activation (as always) and the patient was taken to the cath lab with a door to opening time of about 20 minutes (very fast).

Left Circumflex (LCx):
Circumflex is a large caliber co-dominant vessel with mild, diffuse plaque
There is a single large caliber first obtuse marginal (OM-1) branch that supplies the lateral wall and inferolateral wall via a significant lateral branch, which is occluded in the proximal segment, suggestive of plaque rupture.  Distal/AV groove Cx supplies a cascade of small caliber LPL branches.

This branch is 100% occluded in the proximal subsection, with Pre procedure TIMI 0 flow and Post Procedure TIMI III flow. 

Here is the post-PCI ECG:
Reperfusion T-waves (T-wave inversion) is present in inferior leads.

Peak cTnI = 9.9 ng/mL

Next day echo:

Regional wall motion abnormality-inferior.
Regional wall motion abnormality-inferolateral.
Regional wall motion abnormality-lateral.
Normal estimated left ventricular ejection fraction lower limits of normal.
My Conclusion: a large myocardial territory

Even though the ECG findings were very subtle, there was a large myocardial territory at risk.  Rapid reperfusion resulted in a relatively low peak troponin.

Learning points

1. This is, in effect, a transient STEMI
2. Although transient, and the pain resolved, the artery remained occluded.
3. Computer interpretations cannot be trusted.  (They may be helpful.)
4. Subtle findings on the ECG may be associated with a large myocardial territory at risk

This is another case in which the chest pain was resolved but the artery remained occluded, as with this post 2 days ago:

What will you do for this patient transferred to you who is now asymptomatic?

See the learning points in that case

Comment by KEN GRAUER, MD (3/8/2019):
Superb teaching case presented by Dr. Smith regarding this middle-aged man who was transported to the ED after new-onset chest pain. I focus my comments on a number of additional points regarding ECG interpretation.
  • For clarity — I show in Figure-1 the initial ECG obtained in the ED ( = ECG #1— together with the prehospital ECG that I have pieced together = ECG #2).
  • For educational purposes — I think it helpful to initially interpret ECG #1 as if it was the only ECG available in this case, keeping in mind that this patient’s chest pain had resolved at the time ECG #1 was recorded.
Figure-1: The first 2 ECGs shown in this case (See text).
COMMENT: As per Dr. Smith — in a patient with new-onset chest pain, ECG #1 should be interpreted as acute inferior MI until proven otherwise.
  • The rhythm in ECG #1 is sinus arrhythmia. PR, QRS and QT intervals are normal. The frontal plane axis is about +30 degrees. There is no chamber enlargement. Small q waves are seen in multiple leads — including 2 of the 3 inferior leads (ie, leads II and aVF). The diagnosis of acute inferior MI is suggested by subtle-but-real ST elevation in leads III and aVF, with reciprocal change in lead aVL in this patient who shortly before had complained of new-onset chest pain.

QUESTION: If you focus your attention on simultaneously-recorded leads aVR, aVL and aVF — you’ll see 2 complete QRST complexes. Don’t the ST-T wave complexes in leads aVL and aVF for these 2 beats look quite different?
  • Which complex (Aor B) in these 2 leads is the “correct” complex?
  • Why is this question important?
  • Would your interpretation of ECG #1 change if both of the complexes in leads aVL and aVF looked like A, instead of like B?

ANSWER: Unfortunately, artifact has been introduced into the recording of complexes A and B in leads aVL and aVF.
  • IF the “correct” complex was — then I would have absolutely NO doubt about the occurrence of acute inferior MI in this patient. That’s because straightening of the ST segment takeoff and, ST elevation itself in lead aVF for complex is much more evident than it is for complex B. In addition — the scooped ST depression for complex in lead aVL looks to be the exact mirror-image opposite of the subtle ST elevation seen in lead III. One of the best clues to acute inferior MI is this finding of a near-magical mirror-image picture between ST elevation in lead III with reciprocal ST depression in lead aVL.
  • On the other hand — I would be less certain about acute inferior MI if the “correct” complex in leads aVL and aVF was complex B. Considering how reduced QRS amplitude in lead aVF is — I’d still interpret the T wave in lead aVF as taller-than-expected, and probably hyperacute — but, complex B is less convincing than complex A in lead aVF. Similarly — the ST segment in lead aVL of complex B is inappropriately FLAT, which is clearly abnormal. However, complex B in aVL does not provide the mirror-image reflection of what we see for the ST segment in lead III.
  • The SOLUTION: Especially when ECG changes are subtle (as they are in ECG #1) — Have a low threshold for immediately repeating the ECG when critical leads (ie, like leads aVL and aVF in ECG #1) are technically inadequate. We need to know if complex A or complex B is the “correct” one!

There are other ECG findings suggesting that regardless of whether complex A or B is the “correct” one — that ECG #1 is strongly suggestive of acute inferior MI.What are they?
  • HINT: What abnormal findings do you see in the anterior chest leads?

ANSWER: intentionally omitted assessment for R wave progression in my initial interpretation of ECG #1 above. This parameter is often forgotten — but it is important in this case.
  • Height of the R wave in lead V2 of ECG #1 = depth of the S wave in this lead. Therefore, transition occurs early (ie, between V1-to-V2). In addition — the R wave in lead V3 looks unexpectedly tall.
  • The ST segments in leads V2 and V3 of ECG #1 are straighter-than-they-should be, if not slightly depressed (There is usually slight concave-up ST elevation in these leads).
  • Anterior leads V1, V2 and V3 provide a mirror-image of electrical activity in the posterior wall of the left ventricle. Note the positive mirror-test” shown in the insert in lead V2.
  • BOTTOM LINE regarding ECG #1: Even if it is complex B in leads aVL and aVF that is correct — in a patient with new-onset chest pain — but whose chest pain has resolved by the time ECG #1 was recorded — the combination of residual abnormal findings in leads III, aVL, aVF + leads V2 and V3 strongly suggest acute MI has occurred (likely infero-postero MI ).

As per Dr. Smith — diagnosis of acute MI was made much easier in this case — because a prehospital ECG ( = ECG #2was found. I’ll add a few thoughts regarding interpretation of this prehospital ECG:
  • Although once again, small q waves are seen in multiple leads of ECG #2 — a large and wide Q wave was seen in lead III that was not seen in lead III of ECG #1. What is strange — is that QRS morphology of the other 5 limb leads is not appreciably different in ECGs #1 and #2. We therefore can’t explain disappearance of this large Q wave in lead III from the prehospital tracing on the basis of axis shift. Change in patient positioning might be a factor (ie, acutely ill patients may have difficulty lying completely flat for the recording of an ECG) — but unless specific note was made of a change in patient position, this would be impossible to verify.
  • In any event — the ST segment in lead III of ECG #2 is coved and more clearly elevated — this time, with undisputable mirror-image reciprocal ST depression in lead aVL. Together with inferior Q waves, and frank ST elevation also in lead aVF — ECG #2 is diagnostic of acute inferior MI.
  • Although subtle — note again the hint of ST segment flattening (if not slight depression) in leads V2 and V3 of ECG #2 — once again accompanied by unexpectedly early transition.
  • For more on the magical mirror-image” relationship between leads III and aVL with acute MI — CLICK HERE (Please See My Comment at the bottom of the page.)
  • For “My Take” on use of the Mirror Test for Diagnosis of Acute Posterior M CLICK HERE (Please See My Comment at the bottom of the page.)
  • For “My Take” on use of the Systematic Approach to ECG Interpretation  CLICK HERE.

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