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:
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: https://www.mdcalc.com/subtle-anterior-stemi-calculator
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!
Thus, if there is TQRSD, assume LAD occlusion until proven otherwise.
What is a J-wave?
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):
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!
|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):
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:
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.
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)
The formula value then = 20.25.
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.
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:
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?
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.
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