Wednesday, October 24, 2018

Is this a STEMI? No, not by definition! Why not? Why is this Important?

A 40-something male presented with dyspnea and left arm numbness, and perhaps some chest tightness, for 1 1/2 hours.

Here is his triage ECG:
There is massive STE in V3-V6, and also STE in II, III, aVF.
This is all but diagnostic of STEMI, probably due to wraparound LAD

The cath lab was activated.

The patient was given sublingual nitroglycerine and his symptoms greatly improved, and another ECG was recorded:
Now there is much less ST Elevation

If you had not seen the prior ECG, you might have called this normal variant STE, or early repolarization --there are well-formed J-waves.

Because there is reciprocal ST depression in aVL, this should not be called early repol.

Suppose you had used the formula?Values: STE60V3 = 2.0, QRS V2 = 10, RAV4 = 15.5, QTc = 377 by computer
4-variable formula value = 16.2, which is very low and suggests early repol

The patient was taken to the cath lab and a Type III (wraparound) LAD with a proximal hazy area was seen. There was good flow.  This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque.  It was stented.

A 0-hour troponin I, drawn 2 hours after symptoms onset, was below the level of detection (LoD, less than 0.010 ng/mL.

A subsequent troponin drawn 6 hours after symptom onset, remained below the LoD.

No further troponins were drawn.

Therefore, this does not meet the definition of myocardial infarction (4th Universal Definition of MI), which requires at least one troponin above the 99% reference range.  It is possible that subsequent troponins would have been elevated had they been drawn.  But maybe not.

You can see the deficiency of the definition of MI.  This was clearly severe subepicardial ischemia causing ST Elevation, but it was not of a long enough duration to result in measurable infarct.

Therefore this is "Transient ST Elevation Unstable Angina."  As there was ruptured plaque, this is NOT Prinzmetal's angina.

Why is this important?

1. First, the name (Myocardial Infarction or Not) is not important.  It is just as dangerous, as there is a ruptured plaque with thrombus (which lysed) in the proximal LAD.

2. Imagine if you had only recorded the 2nd ECG.  The patient would not have been diagnosed with acute coronary syndrome and would not have had an angiogram, would have been discharged (or perhaps had a stress test, which would be negative), and would be at great risk of another event, possibly resulting in death or heart failure.

Here are many other cases of Unstable Angina, in spite of Eugene Braunwald's Requiem for Unstable Angina.

So Unstable Angina still exists [even with high sensitivity (hs) troponins].

This was NOT high sensitivity troponin, but we know from a couple studies that, even using hs-cTnI, Unstable angina still exists:

These two slides come from my recent lecture on high sensitivity troponin:

Slide 23 in the lecture.  
Thelin et al. Eur Ht J, Acute Card Care 2014; 4(5):403-9

• Initial hs-cTnT among 478 patients presenting with chest pain as the primary symptom
• 160 (33.5%) had values below 5 ng/L
• NPV of 100% for NSTEMI (70 NSTEMI; 37 UA)
• NPV of only 94% for any ACS (includes Unstable Angina)
• Sensitivity 91% (80-95)
– Missed 10 of 107 ACS as diagnosed by angiography; 8 PCI

• Clinical judgment and pre-test probability of ACS is critical

Slide 32. 
Mokhtari et al. JACC 2016;67:1531. 
0/1 hour algorithm, with vs. w/o ECG and Gestalt

0/1 hour protocol alone (same as other 0/1 hour hs-TnT protocols)
– Rules out 65% (n = 682)
– 87% sens for ACS if one includes unstable angina as a 30 day MACE
• 0/1 hour protocol + ECG non-ischemic + Gestalt not high risk
– Gestalt risk = very low, low, or intermediate (not high risk)
– Rules out 60% (n = 625)
• 97.5% (92.9-99.5) sensitivity, 99.5% NPV (98.6-99.9).

Comment by KEN GRAUER, MD (10/24/2018):
Important teaching points are made in this post by Dr. Smith. These include: iappreciation of how problematic the definition of “acute STEMI” can be; andiiillustration of how dependence on this definition may result in overlooking acute coronary occlusion.
  • I focus my comments on some additional fine points regarding ECG interpretation of the 2 tracings shown in this case (Figure-1):
Figure-1: Comparison between the initial triage ECG in this case (TOP) — with ECG #2 (BOTTOM) obtained shortly after sublingual NTG, with much improvement in symptoms  (See text).
ECG #the initial Triage ECG (TOP— As per Dr. Smith, the dramatic ST elevation in leads V3-thru-V6, plus additional ST elevation in each of the inferior leads in a patient with new symptoms is virtually diagnostic of acute LAD occlusion. Appropriately, the cath lab was activated.
  • Lack of ST elevation in V1 and V2 suggests a mid (rather than proximal) LAD location.
  • Note baseline wander in lead aVL of ECG #1. This makes it difficult to assess for reciprocal change in this lead — since there is ST scooping with suggestion of slight depression in the first 2 complexes — but if anything, slight ST elevation in the 3rd complex in this lead. A glance at simultaneously-obtained lead aVF in ECG #1 confirms that artifact is the reason for problematic appearance of ST-T waves in the 3 beats shown in lead aVL — with bottom line, that there is no more than modest (if any) reciprocal ST depression in aVL in ECG #1.
  • Although there is no long lead rhythm strip — it is noteworthy that there is marked sinus arrhythmia in ECG #1. This finding is easy to overlook because of the lack of a long lead II … Perhaps this marked sinus arrhythmia reflects increased vagal tone? In any case, sinus arrhythmia is much less marked in ECG #2 after SL NTG with improvement of symptoms.
  • BEYOND-the-CORE: There are extremely prominent J waves in the 2 leads of ECG #1 that show the most marked ST elevation (ie, leads V4 and V5). Although still present in ECG #2 — note how much less prominent these J waves are after presumed reperfusion. We have previously discussed this phenomenon (Please see the P.S. at the bottom of the page in My Comment, from Dr. Smith’s July 11, 2018 blog post). It appears that on occasion — J waves may be induced by ischemia (thought to reflect an acute injury current from impending myocardial infarction). Whether this is the reason for the very prominent J waves in leads V4 and V5 of ECG #1 would have been more evident IF we had access to a 3rd ECG obtained a bit later showing complete resolution of these J waves.
QUESTION: Let’s follow-up with the question posed above by Dr. Smith:
  • Imagine the only ECG you are given is ECG #2 (BOTTOM tracing in Figure-1). Two troponins have come back negative. As stated, the patient is a previously healthy 40-ish year old male with dyspnea, left arm numbness and chest tightness for ~1.5 hours. Why should you resist calling this early repolarization?
ANSWER: Dr. Smith has already indicated that the presence of reciprocal ST depression in lead aVL alone tells you that ECG #2 is not a benign pattern of early repolarization. Additional ECG findings of note in ECG #2 include:
  • The amount of ST elevation in ECG #2 is maximal in leads V4 and V5. It is minimal (ie, no more than 1mm) in lead V2. This distribution of ST elevation is not the pattern expected with early repolarization.
  • The shape of the ST segment takeoff in lead aVF is straight. It is coved (ie, convex-down or “frowny” configurationin lead III. Neither of these shapes is what you expect with early repolarization.
  • Troponin does not always rise with acute occlusion IF spontaneous reperfusion occurs quickly. Two negative troponins do not exclude the possibility of short-lived acute coronary occlusion.
  • Even if you thought ECG #2 looked like early repolarization — more data would be needed because there is ST elevation in this tracing. This might include Echo obtained during symptoms (looking for wall motion abnormality) — and  serial tracings looking for dynamic change. The diagnosis of early repolarization in a patient with new symptoms should always be a diagnosis of exclusion to be made only after you rule out the possibility of an acute event.
Finally — If ECG #2 was early repolarization — we would expect some ST elevation in lead aVL. Instead (as per Dr. Smith) — there is reciprocal change in this lead. This is subtle — but it is definitely present. To assist enhancing instant recognition of the mirror-image picture “painted” by reciprocal changes — we superimpose the mirror-image of lead III above lead aVL — and the mirror-image of lead aVL above lead III (Figure-2).
  • Note that the shape of the ST-T wave of the mirror-image of lead aVL is virtually the same as the shape of the ST-T wave in upright lead III.
  • Similarly — the shape of the ST-T wave of the mirror-image of lead III is virtually the same as ST-T wave shape of upright lead aVL.
  • The finding of mirror-image reciprocal change in leads III and aVL in a patient with new symptoms is virtually diagnostic of an acute event!
Figure-2: We focus on the 6 limb leads in ECG #2 — with superimposed mirror-images of leads III and aVL shown within the BLUE rectangles  (See text).


  1. The aspect of a very small and distorsed QRS in D2 on the 2nd EKG is very worrisome (but I have a knowledge bias because of the first EKG)

  2. I am not sure I see the ST depression in aVL on the second ECG, but I do see STE in II, III and aVF. You'd have been pretty courageous (or half blind) to call it early repolarisation.

  3. Interesting case and discussion as always. However, whilst this case is high risk I would argue the risk is much less than those with a persistent occlusion (provided there was not an immediate cardiac arrest). Moving into the post event period I would also argue a confirmed MI is at higher risk than a matched unstable angina patient due to potential reduced LV function and ventricular arrhythmias from the infarcted myocardium. I would agree that Unstable Angina definitely still exists and can be a diagnostic dilemma. However, high sensitivity Troponin assays do classify more patients as MI with a reciprocal decrease in unstable angina. I believe there are fewer high risk cases such as this one within a high sensitivity unstable angina cohort and a higher proportion of cases of dubious acuity than seen in previous studies using less sensitive assays.

    1. @ Charles — I also agree with your thoughtful comments. I'd add, that this is where serial ECGs can be so helpful — because in cases like this one, they allow you to identify "dynamic ECG changes" — and that's a marker of higher risk compared to patients who just have a positive Troponin ...

  4. thank you, all.
    and thanks Steve for that detailed review of recent studies/papers on the use of the high sensitivity marker with various scoring modules.

    its quite interesting. the end-points vary as well. sensitivity/specificity for AMI, vs. 30 day MACE , vs other.
    and what if one can't arrange close follow up?
    (which is the majority of my patients).
    quite interesting.

    thank you


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