Saturday, May 13, 2017

An intoxicated, agitated, 29 year old with chest pain

Here is a one hour lecture on the topic of subtle coronary occlusion, especially on the left anterior descending coronary artery

Case 1:

The outcome of this case is at the far bottom.

A thin, athletic young African American male presented by private transportation to the ED after use of "ecstasy" and alcohol and other drugs.  He complained of severe chest pain and was extremely agitated, so much so that he was throwing chairs in triage.  He had an ECG recorded and was brought to a room.  Here is the ECG:

Figure 1:
Sinus rhythm.
What do you think?

Figure 1 shows marked ST Elevation (STE) at the J-point relative to the PQ junction:
1.5 mm in V2
3.0 - 3.5 mm in V3
2.0 mm in V4

The size of the T-wave relative to the QRS in lead V2 is concerning; it is due to very low QRS voltage.

Technically, the STE meets STEMI criteria because there is greater than 2.5 mm STE in V3 and greater than 1 mm in an the adjacent lead V4 (even though V2 does not meet criteria of 2.5 mm).

But this is a thin athletic 20-something and since such STE can occur in this population, it is easy to dismiss it.  The normal upper limit for ST Elevation in lead V2 (as measured at the J-point, relative to the PQ junction) in males under 30 years is 3.0 mm and 3.5 mm in 20 year old males.

How about using the LAD-early repol formula to help differentiate normal variant ST elevation from the ischemic ST elevation of LAD occlusion?

The formula comes from this paper:

In this complex paper, we compare Subtle LAD occlusion to early repolarization (now known as "normal variant ST elevation"").  All early repolarization ECGs had to have at least 1 mm of ST elevation in V2 and V3 (of 242 cases of early repol, 71 were excluded due to absence of sufficient STE), at the J-point, relative to the PQ junction.

Among LAD occlusions, "Subtle" meant we excluded those ECGs we defined as obvious:
1) greater than 5 mm ST elevation in at lead one lead
2) just a single lead of V2-V5 with a straight or convex ST segment
3) any ST depression (inferior or anterior)
4) any Q-waves in V2-V4.
5) T-wave inversion in any of V2-V6

These ECGs were excluded from the study as "obvious" LAD occlusion, and the formula was not derived or validated on those patients, and therefore should not be applied.

On this blog, the warning is this:
It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. Thus, there must be ST Elevation of at least 1 mm. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI.

The formula is also at MDCALC:

iPhone app
There is a free iPhone app called "SubtleSTEMI".  (Sorry, no Android)  When you open the app, this caution comes up:

If you click on "show warning," this comes up:

You must click this in order to proceed.

Then you must answer all these questions.  If the answer to any is "Yes", you cannot trust the formula.

Then you must answer all these questions.
If the answer to any is "Yes," you cannot trust the formula.

If the answer to all these is "NO," then the formula can be applied.
But still the formula was not perfect: it was about 90% sensitive (86% actually, at the most accurate cutoff of 23.4) and 90% specific.

Because normal variant ST elevation is far more common that LAD occlusion, especially among 20-somethings, the negative predictive value in this population is indeed very high.

The NPV is even higher for a young athletic male who presents with drug use and agitation!
The Fourth Question: Terminal QRS distortion:

Notice the 4th Question: "Is there terminal QRS distortion?".  This is confusing to people, but is very important: 20% of our exclusions were due primarily to terminal QRS distortion.  

Terminal QRS distortion (TQRSD) is something I noticed long ago in LAD occlusions, and did not see in normal variant ST elevation.  That is why we excluded patients with this finding. 

Definition of TQRSD: Absence of S-wave and J-wave in either of leads V2 and V3.

Last year, we studied it among the 171 patients with proven Normal Variant ST Elevation:
We found that, indeed, none of 171 cases of Normal Variant ST Elevation had TQRSD.
90% had an S-wave in both of leads V2 and V3
Of the 10% without an S-wave in both leads, all had a J-wave of at least 0.5 mm.

An S-wave was defined by a deflection that is negative relative to the PQ junction
J-wave was any deflection of at least 0.5 mm at the J-point
Thus, if there is TQRSD, assume LAD occlusion until proven otherwise.

What is a J-wave?

Figure 2.
These are J-waves (V3-V6).
Notice that there is a very well-formed S-wave in V2, but no true S-wave in V3.
However, there is a marked J-wave at the J-point in V2.
There are of course very well-formed J-waves in V4-V6 also, but these are not sufficient to satisfy the rule.
To use the formula, there must be an S-wave or J-wave in BOTH V2 and V3.
The J-wave in V3 satisfies the criterion, and the formula may be used.The presence of S-waves and J-waves (absence of QRS distortion) does NOT preclude LAD occlusion.  In our study, most cases of LAD occlusion did NOT have terminal QRS distortion, and many had J-waves
(J-waves do not make early repol definite!!) 

In the Figure 2 ECG, there is also

1) Upward concavity in all of V2-V6
2) No inferior ST depression (it is important to note that inferior ST depression is absent in 50% of acute LAD occlusion).
      Reference: [Walsh BM.  Smith SW.  Differences in electrocardiographic Findings Between Acute Isolated Right Ventricular Myocardial Infarction and Acute Anterior Myocardial Infarction.  JAMA Internal Med 2016 Dec 1.; 176(12)1875-1876.]
3) no STE of at least 5 mm
4) no T-wave inversion
5) No Q-waves in V2-V4

Thus, the formula may be used in the Figure 2 ECG.
This is a graphic from the paper (Figure 3):
The complex in V3 on the left:
The end of the R-wave does not descend below the PQ junction, therefore no S-wave
There is no J-wave.
No case out of 171 proven early repolarization cases had this morphology.
It is LAD occlusion until proven otherwise.

On the right:
There is both an S-wave and a minimal J-wave (although this is barely 0.5 mm)
Although this was indeed a case of early repolarization, it could be STEMI.

TQRSD rules out early repol.
Absence of TQRSD does not establish early repol!!

Case 2

Here is a case of a patient with chest pain:
See magnification below

Here is V1-V6 magnified:
There is a well-formed S-wave in V2, but this is not sufficient to rule out TQRSD
There is clearly no S-wave and no J-wave in V3.Hence, there is TQRSD.
LAD occlusion until proven otherwise; do not use the formula!

This case was immediately recognized as LAD occlusion and went to angiography.  A 100% LAD occlusion was opened.  The post cath ECG is here:
Notice that the S-wave has been re-constituted with reperfusion of the LAD.

Some time later, reperfusion T-waves developed (analogous to Wellens' waves):

Case 3

Here is a case of a 30-something otherwise healthy male with chest pain:
There is neither an S-wave nor J-wave in lead V3.
This was a proven LAD occlusion.

Case 1 progression

Let us return to the case at hand:
There is a tiny S-wave (tiny QRS!) in V2
There is no S-wave in V3 (remember, only 10% of early repol do not have this!)
Is there TQRSD?

Here are V1-V6 magnified:

And here magnified even more:
There are indeed tiny deflections, but with all the noise there and the lead-to-lead variability, these are unlikely to be J-waves.
In only 1 of 3 complexes (middle) could you say that the noise reaches 0.5 mm (0.05 mV).
So this is TQRSD: no S-wave or J-wave in one of leads V2 and V3 (in this case, V3)

When in doubt, assume LAD Occlusion until proven otherwise!!
So, this noise should not be considered TQRSD, and then the formula should not be used.

In any case, the patient needs at a minimum serial ECGs and perhaps a formal echocardiogram.

Case progression:

The providers interpreted this as early repolarization.  Not recognizing the exclusion, they used the "SubtleSTEMI" formula and the value was low:

= (1.196 x STE60V3) + (0.059 x QTc) - (0.326 x RAV4)

--QTc = computerized QTc  
                     (here it was 391 ms)
--RAV4 = R-wave amplitude, in mm, in lead V4.  
                     (here it is 21.5 mm)
--STE60V3 = ST elevation measured at 60 milliseconds after the J-point in lead V3, relative to the PQ junction, in millimeters.
                     (here it is ~3.5 mm)
The formula value then = 20.25.  

This value is very low and is well below 23.4, which is the most accurate cutoff.  But 20 out of 143 had a value less than 23.4.  It is also below the safer value of 22.0.  

Only 6 of 143 LAD occlusions had a value below 22.0 (sensitivity, 96%).  But still, six had values below 22.0!  No test is perfect, and this test has been particularly valuable in changing the diagnosis from early repolarization to MI.  It's greatest value is in warning you that a case you thought was benign is not benign.


The patient was given sedatives for agitation and he did calm down.  His chest pain resolved.  Another ECG was recorded:
This is now unequivocally diagnostic of LAD occlusion!
That is to say: this ECG proves that the first one was indeed LAD occlusion.

The ECG was seen only a bit later by the provider.  As he was alarmed by it, he went to the patient who now was having recurrent pain, then suddenly went into cardiac arrest (ventricular fibrillation).  A prolonged resuscitation ensued but the patient could not be resuscitated.  ECMO and cath lab were not available.

Autopsy showed proximal LAD thrombus with 100% occlusion.

What happened?
That first ECG represents 100% occlusion.  As with many thrombi, it autolysed and the artery spontaneously reperfused, resulting in pain resolution.  The thrombus is "hot," however, and can propagate.  It propagated again resulting in 100% occlusion with recurrent pain and then ventricular fibrillation.

Transient STEMI should always have the cath lab activated, or patient transferred to PCI capable facility.  Antiplatelet and antithrombotic therapy is essential:
I have mentioned this case many times:

Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

How about the new 4-variable formula?

We recently published a new formula based on the same data as the first study.  This was done because I noticed that false positives would happen when there was high voltage in lead V2 and negatives when there is low voltage in lead V2.

The new formula was significantly more accurate, with an area under the curve of 0.9686.

The same exclusions apply, but this case had very low voltage in lead V2, and maybe it would have performed better in spite of the exclusion?

--QTc = computerized QTc  
                     (here it was 391 ms)
--RAV4 = R-wave amplitude, in mm, in lead V4.  
                     (here it is 21.5 mm)
--STE60V3 = ST elevation measured at 60 milliseconds after the J-point in lead V3, relative to the PQ junction, in millimeters.
                     (here it is 3.5 mm)
--QRS V2 = 
                     (here it is 4 mm)

Formula0.052*QTc-B - 0.151*QRSV2 - 0.268*RV4 + 1.062*STE60V3

Value: = 17.68

At a cutoff of 17.75, the formula was 90% sensitive, missing 14 of 143.  This value is slightly below 17.75, so it has

 Learning Points:

1.  I think this is the most difficult diagnosis in emergency medicine.

2.  The vast majority of the time, ST elevation in leads V2-V4, especially in young men, is NOT due to LAD occlusion.  You have to find this needle in a haystack.

3.  The formula should only be used if the exclusions are met.  Terminal QRS distortion is one of the exclusions.

4.  Even if the exclusions are met, and the formula used, like all tests it has false negatives and false positives, and all results must be viewed with skepticism.

5.  Resolution of ST elevation with resolution of chest pain makes the diagnosis.

6.  Even if ischemic ST elevation is resolved (Transient STEMI), activate the cath lab or transfer to PCI capable facility. The artery can close again with very bad outcomes.  Antiplatelet and antithrombotic therapy is essential.


  1. Hello doctor.... Where were this thrombi coming from?

  2. Dr. Smith - can you comment on how the last ekg is diagnostic of LAD occlusion? although it definitely looks different than the previous ekg i don't see any STE or hyperacute t waves. is this perhaps the wrong ekg?

    1. The idea is that this relatively normal ECG tells you that the other one is diagnostic of LAD occlusion. This one is due to reperfusion. Sorry for the confusion.

  3. Superb post with an important message! Otherwise, I don't yet see your new 4-variable formula under your Rules + Equations Tab at the top of your blog — so awaiting a way to quickly find your new equation. THANKS for synthesizing this important topic!

  4. how do you think this case could have played out differently? Think very few providers would get their cardiologists to bite on young, intoxicated male c/o chest pain with that initial ekg. I'm sure most would write it off to early repol. maybe with serial ekgs or echo, but even then it'd be a tough sell. Even more concerning is that we all see quite a few intoxicated and agitated young males/females in the department daily. Similar presentations. Feel as though we are so prone to write it off as demand ischemia, coronary vasospasm, trop leak etc.. in this population.

    Terrible outcome for the patient. Really tough case. Thoughts????

    1. It is definitely a very tough case. However, there are ways to make the diagnosis definite, as described above. By learning these, knowing them, you can convince/educate the interventionalists-cardiologists. At our shop, if the cath lab is activated, they much come in without questioning. That of course only works if you have great skills and confidence in them.

  5. Thank you! This may be complex, but it fills a huge gap, and has been much-needed for a long time.

  6. - 1. ECG (patient extremely agitated): why not tachycard ? (Toxycology ?)

    - "Without Autopsie" could be only a "simple spasm" (or ?)

    toujours merci (for the excellence)


    1. Al,
      good question about the tachycardia.
      Partly, by the time he was able to have an ECG recorded, he must have been more calm and under control.
      Also, there are some new drugs out there that cause agitation but have paradoxical effects on heart rate.

  7. Steve, with the standard 12 lead having real problems detecting anterior MI as in the excellent cases you have described above, is there a place for researching the use of additional lead placements? Would the placement of posterior leads have helped by demonstrating reciprocal change for example?

    1. Tom,
      I doubt it. It would only show reciprocal ST depression. You would still have to determine the CAUSE of the ST depression.
      I think the principles above are the key.


  8. "Amazing Post!
    I love it. Will come back again - taking your feeds also.

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DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

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