Chest pain in a 30-something: Is it Normal variant STE or OMI? Get the prior ECG, and don't trust Point of Care troponin assays!

Submitted by Benjamin Garbus, MD with edits by Bracey, Meyers, and Smith 

A man in his early 30s presented to the ED with chest pain described as an “explosion" of left chest pressure.

Triage EKG:

What do you think?

There is STE present in leads V2-V5. The STE and the amplitude of the T wave seems to be proportional relative to the QRS complex. There is J point notching present in lead V5. Application of the 4 factor subtle LAD calculator yields 14.9, which is consistent with benign early repolarization. The formula comes with a warning that it is best used to alert you to an LAD occlusion that you thought was benign, not to dissuade you from a diagnosis of LAD occlusion.

See this for more information on the calculator (formula):

12 Example Cases of Use of 3- and 4-variable formulas, plus Simplified Formula, to differentiate normal STE from subtle LAD occlusion

The case continued with additional clinical information:

The patient presented with acute onset crushing left chest pain with some radiation to his left shoulder.  Occurred while driving to a doctor’s appointment. Has had several, less severe episodes over the last several weeks, typically associated with exertion.  He had been seen several weeks ago at an outside hospital for a similar issue and had been discharged home, presumably after unremarkable workup.  Today’s pain lasted around 20 mins, but was severe enough that the patient called EMS.  Pain largely resolved prior to EMS arrival but completely subsided after prehospital NTG and aspirin.  At the time of arrival to the ED, the patient reported 1/10 chest pain with normal vital signs. He had no apparent risk factors for cardiovascular disease. A prior ECG was available for comparison.

Prior EKG from 2 months ago was available:

Let's put the precordial leads from the 2 ECGs side by side:

Now you can really see the difference.

This proves that the first one was, surprisingly, due to ischemia!!

Fifteen minutes after the patient arrived he again developed worsening pain and another ECG was performed (There was no interval ECG recorded after the patient had become fully pain free).

EKG 2 (15 mins after first):

Re-demonstration and slight increase in STE in V2-V5
In the context of the baseline ECG this is highly concerning for OMI

Compare to baseline again

Comparison of the precordial leads of today's presentation compared with the patient's baseline

It is unclear if the initial and subsequent ECGs were prospectively perceived to have hyperacute T waves; however, given the high suspicion for OMI, the emergency physician immediately consulted cardiology in order to expedite coronary angiography.

Immediately after the second ECG was performed, the patient's pain resolved completely. 

After reviewing the case, cardiology requested that the patient be admitted to observation for stress testing the next morning.

The first troponin I was less than 0.30 ng/mL (undetectable).

Smith comment: the only troponin assay (I or T) that has such a high limit of detection is a point of care (POC) assay. Although new high sensitivity POC assays are coming in the future, the present point of care assays should never be used in emergency medicine. They are extremely insensitive. Most contemporary (in contrast to high sensitivity) trops have Limit of detection (LoD) in the range of 0.010 ng/mL. The iStat POC assay is 0.08 ng/mL and it is not sensitive and also should not be used; this one has an LoD of 0.3 ng/mL!!.

Because the patient's pain had resolved completely and cardiology had declined immediate intervention, the patient was admitted but continued to board in the emergency department. Approximately 4 hours after arrival, the patient was re-examined by the emergency physician. A second troponin had been drawn 3 hours after arrival and was again less than 0.30ng/mL. After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality.

We assume that at some point the patient's pain returned, but it is not documented, so exactly when this happened is uncertain.

Apical four chamber view with apical wall motion abnormality

Parasternal short view with anterior wall motion abnormality

 

The Regional Wall Motion Abnormality (RWMA) prompted the emergency physician to consult cardiology again. After reviewing the EKGs and POCUS, cardiology agreed to take the patient emergently to the cath lab where the patient was found to have a 100% occlusion of his proximal LAD. He was successfully treated with one drug eluting stent.

Post cath EKG:

Reperfusion of anteroseptal territory

Interestingly, the first two troponins obtained at the time of arrival and 4 hours after arrival were negative (less than 0.30ng/mL).

Smith comment: this patient might have been sent home because of the poor sensitivity of this Point of Care (POC) assay. Do NOT use them. We do not know whether a better assay would have given better information, but it is very likely.

He underwent formal echocardiogram several days later, which confirmed the findings of anterior, and apical wall motion abnormalities. The cardiology service continued to trend troponins, which did convert to positive on the third measurement, and was still rising at 5.9 ng/mL when they stopped ordering further troponins. Peak troponin level unknown.

He was ultimately discharged after a brief, uncomplicated hospital course. 

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Teaching points:

This case highlights the importance of comparing an ECG to a prior if it is available, particularly in equivocal cases. If a prior ECG is unavailable and concern for OMI exists, performing serial ECGs may help to identify dynamic change. Dr. Smith's comments to me on this case: "Without a previous ECG and/or clinical suspicion there is no way that this would have been diagnosed!"  In fact, with 2 troponins below 0.30 ng/mL by this terrible assay, the patient would probably have been sent home and might have even died.

Do NOT rely solely on the troponin to make the diagnosis of OMI, especially if it is a point of care assay!! Both conventional and high sensitivity[1] assays can be "negative" if the time of occlusion onset to troponin measurement is fast enough. In this case, there was two negative troponins despite a cath proven 100% LAD OMI. This likeliest possibility is that the patient had spontaneous reperfusion that occurred after arrival, likely coinciding with the resolution of pain. Ideally, a subsequent EKG would have been performed to demonstrate reperfusion and might have hastened time to intervention. Remember that, when the troponin is negative in the early stages of OMI, the benefit of emergent reperfusion is maximal! 

In equivocal cases, point-of-care ultrasound may be the difference between taking the patient to the lab or not. Practice putting the probe on the chest of someone with an obvious STEMI(+) OMI in order to look for regional wall motion abnormalities.

The subtle LAD OMI calculator, like any other diagnostic tool should not be followed blindly. Clinical concern and gestalt should ultimately guide management.

There is no age cut-off for ACS. Failure to consider the disease based on a patient's age will lead to missed diagnoses and worse outcomes.

In this study, Smith and others show that the initial high sensitivity troponin is often below the 99th percentile in true STEMI (+) OMI (and sometime even below a very low threshold).

[1] Wereski, R., Chapman, A. R., Lee, K. K., Smith, S. W., Lowe, D. J., Gray, A., & Mills, N. L. (2020). High-Sensitivity Cardiac Troponin Concentrations at Presentation in Patients With ST-Segment Elevation Myocardial Infarction. JAMA Cardiology, 5(11), 1302–1304.