Spot the STEMI #1

You have a 50/50 shot at getting this one right. Are you feeling smart… or lucky?

Two 50-year-old men present complaining of chest pain x 1 hour. One patient is suffering from a very subtle acute STEMI while the other has a non-cardiac cause for his chest pain.

Which patient is experiencing the subtle STEMI?

0054-1032 Combined

The answer is below but take some time to analyze the ECG’s and come to a decision before scrolling down.

 

 

 

 

 

 

 

 

 

 

 

 

Answer and Discussion

Patient A is experiencing a subtle lateral STEMI while Patient B has a normal ECG.

Both tracings exhibit slight J-point elevation in V2 with a tall T-wave. In fact, Patient B shows an even taller T-wave than Patient A and also has a similar morphology in V3 that Patient A lacks. Taken in isolation these findings are mildly concerning for a subtle “hyperacute” T-wave morphology indicative of ischemia.

Given only the precordial leads I’d actually be more worried about Patient B.

0054-1032 Combined Precordials

But there’s a reason we look at all twelve leads—and in this case the limb leads are absolutely key to the diagnosis.

0054-1032 Combined Limbs

The first thing worth noting is that Patient A shows 0.5 mm of ST-elevation in leads I and aVL while Patient B shows no elevation in aVL (we can’t scrutinize lead I closely due to artifact). This elevation is only minor in amplitude, however, and features a concave (“smiley”) morphology often associated with (but not diagnostic of!) early repolarization, so the ST-elevation alone is non-specific.

As Dr. Amal Mattu often mentions in his lectures and ECG videos (and which he learned from Dr. Henry Marriott), any time you see concerning findings in aVL you should look down to see what lead III is doing (and vice-versa).

0054-1032 Combined Inferior

Both patients have a frank T-wave inversion in III—but an inverted T-wave in that lead can be a normal finding. Patient A‘s abnormalities, however, extend into aVF.

An inverted T-wave in both III and aVF is a less common normal variant than an isolated inversion in III, but it’s not uncommon and often insignificant. Importantly though, Patient A doesn’t show a true T-wave inversion in aVF. Instead, his ECG features a downsloping ST-segment with an upright terminal T-wave. Compare that with Patient B‘s normal aVF.

We discussed the significance of downsloping ST-segment into an terminally upright T-wave last week, and yet again that pattern has proven to be diagnostic of reciprocal changes. Last time it was reciprocal to a subtle anterior STEMI and this time it is due to a subtle lateral STEMI.

For further illustration of the difference between these two ECG’s we can examine what leads III and aVF would look like when flipped upside-down.

0054-1032 Combined Inferior Flip

First note the size of the T-waves in comparison to the QRS complexes. With Patient A the T-wave in lead III towers over the diminutive QRS while in Patient B‘s ECG the T-wave appears appropriate for the QRS size. In absolute terms B‘s QRS in III isn’t large but the T-wave is still appropriately smaller.

0054-1032 Combined III Flip

Also scrutinize the shape of the ST-segments and T-waves in III. While still technically slightly “concave” in Patient A, it is also apparent that the upslope is steeper and straighter when compared to Patient B‘s. This is the same morphology we actually see with subtle STEMI’s—but in this case it is just happening upside-down because we are looking at reciprocal changes.

It is common for the reciprocal changes of a lateral STEMI to be more pronounced than the actual ST-elevation.

In this case the significance of Patient A‘s ECG abnormalities went unrecognized and he was admitted to the hospital for an ACS rule-out with the belief that his ECG was essentially normal. Serial troponin-I levels (ref. <= 0.04 ng/mL) approximately q6 hours trended as:

  • 0.03 ng/mL (“negative”)
  • 5.56 ng/mL
  • 14.72 ng/mL
  • 16.95 ng/mL

Echocardiography showed an EF of 40–45% with hypokinesis of the mid- and apical-lateral segments. Serial ECG’s showed changes consistent with an evolving infarction of the lateral wall (vs. questionable reperfusion). Telemetry showed multiple 4–12 beat runs of non-sustained VT and the patient was transferred for catheterization 48 hrs after first presenting.

ECG approximately 48 hrs after the patient's initial presentation. T-wave inversions in I and aVL are consistent with either evolving MI or possibly spontaneous reperfusion. No also the non-hyperacute appearance of the T-wave in V2 and extraordinarily subtle terminal T-wave inversion.

ECG approximately 48 hrs after the patient’s initial presentation. T-wave inversions in I and aVL are consistent with either evolving MI or possibly spontaneous reperfusion. Note also the more normal height of the T-wave in V2 and extraordinarily subtle terminal T-wave inversion.

 

Further discussion on the definition of STEMI

The STEMI that Patient A shows on his ECG is extraordinarily subtle. Some folks will argue that it doesn’t even qualify as a STEMI because “it doesn’t show enough ST-elevation.” In fact, these cases are almost always formally labelled as “NSTEMI’s” in patient records (which is also what happened here).

I think that’s nonsense.

Patient A was experiencing active ischemia. That ischemia was due to an acute (probably thrombotic) obstruction of one of his major coronary arteries. The blockage was such that it produced transmural ischemia and electrocardiographic injury in a pattern corresponding to the lateral wall characterized by:

  • 0.5 mm of ST-elevation in leads I and aVL
  • Diagnostic reciprocal changes in III and aVF
  • A slightly hyperacute T-wave in V2 [For an explanation of why V2 shows changes during “lateral” STEMI check out our in-depth examination of what makes that lead so special at this link.]
  • Serial changes consistent with ACS of the lateral territory.

Echocardiography showed wall motion abnormality affecting segments of the lateral wall. Troponin levels trended upward showing significant myocardial infarction. The patient showed arrhythmias we’d expect with an acute coronary syndrome.

All of those findings are consistent with a STEMI—except for the absolute height of the patient’s ST-elevation.

We know that all things in medicine present on a continuum. We also know that the millimeter-criteria used in formal definitions of STEMI were arbitrarily defined and gained their notoriety during the early trials of thrombolytics for myocardial infarction (due to ease of use). The modern implementation of mechanical reperfusion carries a very different risk/benefit profile compared with the thrombolytic-only era of two or three decades ago. It is likely that we are able to invasively manage patients with more subtle myocardial infarctions and far less risk than giving them streptokinase twenty years ago.

Our therapy of STEMI has evolved, so our definition of STEMI should as well.

Yet…

I think the millimeter criteria still have a role.

And I do not think Patient A‘s ECG should result in an automatic activation of the cath lab from the field.

When we talk of EMS systems, we are dealing with large numbers of providers with all levels of training, experience, and expertise. We also have the goal of creating the most benefit to our patients with the least amount of harm and without creating undue monetary costs.

The factors at play are often very different from what consider on an individual-patient level.

With that in mind, millimeter criteria are still useful for determining which patient qualify for prehospital activation of the cath lab. They are cheap to implement, they are proven to have an acceptable rate of false-positives (when applied properly by educated providers), and they tend to pick up patients experiencing larger myocardial infarctions.

While not particularly sensitive (meaning they do miss subtle presentations), when applied to the right cases (meaning not in instances of LBBB, LVH, WPW, etc…) they do isolate a decent population of the higher-risk myocardial infarctions that stand to benefit the most from early intervention. Those are the patients who certainly need the cath lab opened from the field to save time and significant myocardium.

That’s not saying prehospital expertise in the recognition of subtle STEMI is wasted training though:

  • Accurate interpretation triages patients to the right receiving facility (PCI vs. non-PCI hospitals) more often.
  • Providers who recognize subtle ischemia can relay that information to the hospital for a second-opinion or consideration of prehospital cath lab activation. Unlike millimeter-meeting cases the patient does not automatically qualify, but an exception can still be made on a case-by-case basis.
  • Most importantly: A prehospital provider trained and confident in the recognition of subtle ischemia can advocate for the patient and prioritize their ischemia.

That last point is the one I consider most important. So many of these patients suffer complications not because their ECG’s weren’t recognized as abnormal—providers do often successfully note the subtle ST-elevations and/or depressions—but because no one advocated for the importance of that finding as a sign of active ischemia.

Patients with subtle STEMI’s, though they are statistically better off than those showing giant “tombstone” ST-elevation, can still suffer life-changing and even life-ending complications from their unimpressive-appearing ischemia. It is the job of emergency care providers—both pre-hospital and in-hospital—to be able to identify these patients so that their care can be prioritized.

They need to be watched closely, assessed frequently, and treated aggressively (even if only medically in certain cases).

Our goal by sharing these cases is to raise awareness that these ECG’s are still on the STEMI continuum. These patients are experiencing the same exact disease, just with a less impressive presentation, and while they may not qualify for field activation of the cath lab, they still need to be handled with care and gravitas.

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