STEMI equivalents

It is another weary on call night, where annoyingly everyone has decided to have chest pain. As you sit down to scrutinise probably your tenth ECG, some ST elevation in lead AVR catches your eye. This jolts you from your torpor. Real pathology? You get your registrar to swing by and have a look. He furrows his brow as he looks down his nose at you, saying;

“ Remember, young padawan, one lead is no lead.” He reminds you of the STEMI criteria (1), which must be present in at least 2 anatomically contiguous leads:

  1. ≥1 mm (0.1 mV) of ST segment elevation in the limb leads
  2. ≥ 2 mm elevation in the precordial leads
  3. New LBBB

It turns out this teaching is not quite complete and will eventually cause you to miss some significant coronary occlusions. For you see, the classification of MIs into STEMI and NSTEMI is not some random division based on the aesthetic s of the ECG waveform. STEMI represents total occlusion of a coronary artery, therefore high risk of cardiogenic shock and death, and therefore benefit of immediate revascularisation. NSTEMI, on the other hand, an incomplete blockage, has failed to show benefit from immediate angiography (2).

The key point is that there are other ECG patterns that are also indicative of coronary occlusion which are simply not taught, mostly because they have only been described in the last decade or two, and unfortunately medicine can be slow to catch up. These “STEMI equivalents” cannot just be sat on, waiting for the troponin.

LBBB

To start with, new LBBB is not even considered a STEMI criterion anymore (3). You can however interpret ST segments in a LBBB, despite what you might have been told, by utilising the ‘Scarbossi Criteria’. These will be covered in a separate post.

De Winter’s Waves

de winter
[Image Credit: wikem.org/wiki/File:Dewinter.jpg]
ST depression indicating NSTEMI? Think again.

A decade ago, De Winter et al described the above ECG pattern consisting of  “1-to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves. In most patients there was a 1- to 2-mm ST-elevation in lead aVR” (4).

This pattern was present in 2% of 1532 patients presenting with anterior MI and signifies a complete occlusion of the proximal LAD. Loss of myocardium was “considerable” despite successful PCI.

Hyperacute T Waves

hyperacute t waves
Image credit: My work colleague

The ECG looks similar to the previous one, however there are no ST segment changes, but there are massively peaked T waves localised to leads V2 – V4. This pattern is seen in the hyperacute phase of STEMI and often precedes the development of ST elevation (5). A 1989 study of 18 patients  presenting with this ECG pattern (6) showed that 14 had total obstruction of the LAD, while the remaining four had “near total obstruction”. All but one patient had retrograde filling of the LAD via collaterals, however these were at risk given that 72% of patients had multivessel disease.

The patient in question above proceeded emergently to angiography where an occluded LAD was found and stented.

Posterior MI

posterior MI
Image credit: https://wikem.org/wiki/File:Posterior_MI.jpg

You might think this is an NSTEMI involving the LAD territory. In order to help dispel this notion, it is important to note that while ST elevation localises to a coronary territory, ST depression due to NSTEMI does not localise. ST depression does however localise when it is reciprocal to ST elevation elsewhere. In this case, the ST elevation is on the posterior wall of the heart, which our ECG cannot capture. The reciprocal ST depression will occur on the opposite wall; the anterior wall, which is interrogated by V2-3.

Therefore ST depression localised to V1-4, often with prominent R waves in those same leads, should be considered to be a posterior STEMI (5). In order to diagnose this you must take leads 4 – 6 and place them across the back of the chest, marking them V7, 8, and 9. You should see ST elevation in leads V7 – 9.

This pattern occurs due to occlusion of the circumflex, which supplies the posterior wall in a not insignificant minority of people. Most people have their posterior wall supplied by the RCA, and in RCA occlusion you should see inferior ST elevation also.

posterior ECG leads
Image credit: http://rebelem.com/five-ecg-patterns-you-must-know/

Diagonal artery occlusion

dx occlusion
Image credit: reference (7)

The above image shows ST elevation in both AVL and 1, which are anatomically contiguous, so they satisfy the STEMI criteria. However, you may sometimes see an ECG without the ST elevation in lead 1, and only in AVL and V2, which is also seen above. AVL and V2 are not contiguous, however ST elevation isolated to these leads, without any ST elevation elsewhere, has a 89% positive predictive value for complete occlusion of the diagonal branch of the LAD (7). Note the associated inferior ST depression, which is reciprocal.

Since this artery supplies such a large proportion of the anterolateral wall, there is potential for death of a large portion of the LV when it is occluded. This is obviously less than ideal.

Left Main Stem Occlusion

LMCAO
Image credit: Reference (7)

Perhaps this is the ECG you saw on that torrid on call night. The ST elevation in AVR is obvious, however, as advertised, it is confined to one lead. Note however the diffuse ST depression in the majority of the remaining leads.

Such a pattern can be consistent with occlusion of the Left Main Stem Coronary Artery. As might be envisaged prognosis with this type of lesion is poor and in fact many patients don’t even make it to the hospital door.

This ECG pattern is seen in 90% of patients with greater than 70% stenosis of the LMCA. However, a greater than 70% stenosis is not an occlusion, which is what I have been harping on about for most of this article. Additionally, 49% of patients without significant LMCA stenosis also demonstrate this pattern. Lastly, someone with an acutely occluded LMCA will be pretty sick and the clinical features alone may be enough to make the call on emergent angiography (7).

All of this means that the question of whether a patient with the above ECG will be taken immediately to the cath lab is not as definite as with the other examples of “STEMI equivalents”. At the very least however, a discussion with the on call cardiologist should take place ASAP.

Conclusion

We have gone through 5 examples of high risk ECG patterns that do not meet the classic STEMI criteria, yet may require immediate PCI nonetheless.

It is tempting as a house officer to regard these as “small print” stuff which you do not need to know. I guess few people would fault you for not picking up on one of these ECG patterns as a “STEMI equivalent”. If you learn to recognise them though, you could well be the person that saves someone’s life. Recognition of any of these patterns should prompt an immediate reperfusion call rather than your standard chest pain work-up or NSTEMI management. Somewhat controversially, I would add that if the registrar attending the call blows you off, you should speak to the on call cardiologist. It is difficult being so junior to act in such an apparently brazen and arrogant way, but if you are seeing something that looks like one of these patterns, there is no reason not to. No harm will come to anyone from an extra phone call, and if you can state plainly on the phone what you are worried about, no cardiologist will be upset at being woken up.

 

References

  1. ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care — Part 8: Stabilization of the Patient With Acute Coronary Syndromes. Circulation. 2005. 112 (24_suppl):IV–89–IV–110. 2005.
  2. Optimal timing of invasive angiography in stable non-ST-elevation myocardial infarction: the Leipzig Immediate versus early and late PercutaneouS coronary Intervention triAl in NSTEMI (LIPSIA-NSTEMI Trial) . Holger Thiele Justus Rach  Norbert Klein  Dietrich Pfeiffer  Andreas Hartmann Rainer Hambrecht  Peter Sick  Ingo Eitel  Steffen Desch Gerhard Schuler for the LIPSIA-NSTEMI Trial Group. European Heart Journal, Volume 33, Issue 16, 1 August 2012, Pages 2035–2043, https://doi.org/10.1093/eurheartj/ehr418
  3. Jain S, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. Am J Cardiol. 2011; 107:1111-1116.
  4. de Winter R, et al. A new ECG sign of proximal LAD occlusion. NEJM. 2008; 359:2071–2073.
  5. J Electrocardiol. 2012 Sep;45(5):463-75. doi: 10.1016/j.jelectrocard.2012.06.011. Common pitfalls in the interpretation of electrocardiograms from patients with acute coronary syndromes with narrow QRS: a consensus report. Birnbaum Y1, Bayés de Luna A, Fiol M, Nikus K, Macfarlane P, Gorgels A, Sionis A, Cinca J, Barrabes JA, Pahlm O, Sclarovsky S, Wellens H, Gettes L.
  6. SagieA, Sclarovsky S, Strasberg B, et al. Acute anterior wall myocardial infarction presenting with positive T waves and without ST segment shift. Electrocardiographic features and angiographic correlation. Chest. 1989;95:1211–5.
  7. The electrocardiogram in the ACS patient: high-risk electrocardiographic presentations lacking anatomically oriented ST-segment elevation. Mathew Macias, Jordan Peachey, Amal Mattu and William J. Brady. American Journal of Emergency Medicine, 2016-03-01, Volume 34, Issue 3, Pages 611-617.
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