Conclusion to Snapshot Case: 85 Year Old Male With Chest Pain

This is the conclusion to the Snapshot Case from a couple of days ago. If you haven’t already done so, I suggest reviewing the very brief initial case description.

Here again is the EKG from Tuesday’s case.

01 - 85yo M

This tracing is nearly pathognomonic for true occlusion of the left main coronary artery (LMCA), resulting in a “left main STEMI.”

Since this a Snapshot case with no follow-up this diagnosis cannot be confirmed, but it is a rather unique pattern I have yet to see mimicked by any other form of ACS. I’m not surprised that few, if any, readers were familiar with this presentation. It is not commonly taught, and in fact I only came across it from seeing a few cases and reading case reports. Let’s review the pattern of ST-deviation that we are seeing…

First, consider the limb leads.

There is massive ST-elevation in leads I and aVL with massive reciprocal ST-depression in leads II, III, and aVF. This pattern is consistent with STEMI of either the left main (LMCA), left anterior descending (LAD), or circumflex (LCx) coronary artery. Though there is really no way to differentiate them using the limb leads alone, the magnitude of the ST-elevation enough to produce a true “tombstone” pattern in I and aVL certainly suggests a large area of ischemic myocardium consistent with the LAD or LMCA.

For those following my 360 Degree Heart series, here’s what the leads look like displayed in that fashion (though it adds nothing to the diagnosis here).

360 Degree Layout

Though informed by the limb leads, the probable diagnosis here resides in the precordial leads. The ST-elevation is maximal in V2 and extends out to V4-V6 with reciprocal ST-depression in V1.

This pattern could be somewhat consistent with an isolated lesion in the LAD but there is a problem: a typical LAD occlusion should not have ST-depression in V3, especially if there is ST-elevation extending all the way out to V6. Seeing no ST-elevation in V3, maybe even a little ST-depression, when there is a large amount of ST-elevation in the rest of the classic “anterior” leads is a big issue. It’s right to consider that perhaps V2 and V3 have been swapped, but based on how the rest of the tracing plays out I can tell you that is not the case here.

The pattern could also be considered consistent with an LCx culprit, and the large amount of ST-elevation in V2 certainly suggests that (V2 is a “high-lateral” lead, believe it or not), but there is a bit too much elevation in V4-V6. Though this latter territory is often considered part of the lateral wall (a pun?), it’s actually pretty low [caudal] on the heart compared to the area the LCx and its branches typically serve and is really part of the antero-apical region supplied by the LAD.

In this case the real lynchpin for me is V3. A lot of findings are pointing towards an LAD culprit but that sudden loss of elevation in V3 sticks out like a sore thumb. I’m left to conclude that there should be anterior ST-elevation in V3 with our LAD occlusion but some other force is acting to cancel it out; that force is posterior STEMI from a LCx occlusion as well. Combine the anterior ST-elevation of an anterior STEMI with the posterior elevation of a large posterior STEMI and they can cancel one-another out, leaving a net of almost no ST-deviation.

So what we have here is a mixed STEMI picture with features consistent with both LAD and LCx occlusion, and that’s exactly what is causing it. The LMCA supplies both the LAD and the LCx, so a true occlusion of the left main essentially creates a STEMI of both those territories. [You could also have a dual-culprit STEMI with culprits in both the LAD and LCx but that is rather rare, even when compared to LMCA STEMI.]

Also consistent with LMCA STEMI is the presence of right bundle branch block (RBBB) and left anterior fascicular block (LAFB) in a pattern of bifascicular block. Given the marked STEMI this is probably an acute finding and fits the picture of ischemia involving a massive area of the myocardium (and is also associated with a markedly increased mortality).

“But LMCA occlusion presents with diffuse ST-depression and ST-elevation in aVR and V1!”

Despite the extremely prevalent teaching, that finding is actually what you see with diffuse NSTEMI, sometimes involving the LMCA, and usually with a less-than-total culprit lesion; whereas what we see here is LMCA STEMI with a complete or near-complete occlusion of the LMCA. For more on the diffuse subendocardial ischemia seen in LMCA NSTEMI see my prior post here.

“I still don’t believe you.”

That’s fine, but I highly suggest checking out these other cases with very similar patterns of ST-deviation.

Image from Panel A of the NEJM article linked here.1

Invasive Cardiology

Image reproduced from Figure 1 of the Invasive Cardiology article linked here.2 There is significant ST-elevation in V3, likely due to a non-obstructed RCA supplying the posterior wall instead of the LCx.

Image reproduced from Figure 1 of the Invasive Cardiology article linked here.

Image reproduced from Figure 1 of the Invasive Cardiology article linked here.3 Similar to the prior tracing there is massive ST-elevation in V3.

Image reproduced from this linked case at Dr. Smith's ECG Blog.

Image reproduced from the case linked at Dr. Smith’s ECG Blog.4

Image reproduced from Figure 2 of the Journal of Electrocardiology article linked here.5

14 - Circulation

Left main STEMI in a patient with a traumatic dissection of the LMCA. Image reproduced from the Circulation article at this link.6


  1. Dwyer N, Kanani R. Images in clinical medicine. Left main coronary artery thrombosis. N Engl J Med [Internet]. 2012 Apr 5 [cited 2014 Dec 12]; 366:e21. Available from:
  2. Joumaa MA, Davis T, Rosman H. Acute left main coronary artery occlusion: a catastrophic problem with poor prognosis. J Invasive Cardiol [Internet]. 2006 Jun [cited 2014 Dec 12]; 18(6):E179-80. Available from
  3. Goktekin O, Unalir A, Gorenek B, Kudaiberdieva G, Cavusoglu Y, Melek M, Aslan R, Timuralp B. Traumatic Total Occlusion of Left Main Coronary Artery Caused by Blunt Chest Trauma. J Invasive Cardiol [Internet]. 2002 Aug [cited 2014 Dec 12]; 14(8):463-5. Available from
  4. Smith, SW. Dr. Smith’s ECG Blog [Internet]. Minneapolis; 2008-2014. The difference between Left Main occlusion and Left Main insufficiency. 2014 Aug 2 [cited 2014 Dec 12]. Available from
  5. Fiol M, Carrillo A, Rodri­guez A, Pascual M, Bethencourt A, Bays de Luna A. Electrocardiographic changes of ST-elevation myocardial infarction in patients with complete occlusion of the left main trunk without collateral circulation: differential diagnosis and clinical considerations. J Electrocardiol. 2012 Sep; 45(5):487-90.
  6. Granda Nistal C, Rubio Alonso B, Mejía Martínez E, Blazquez Arroyo L, Coto Morales B, Parra Fuertes JJ, Garci­a Tejada J, Hernandez Hernández F, Velázquez Martín MT, Gonzalez-Trevilla AA. Left Main Dissection and Pseudoaneurysm Formation After a Road Traffic Accident. Circulation. 2015 Sep 15;132(11):e143-5.


  • Ken Grauer says:

    VERY interesting commentary. I’m seeing different things for acute LMain occlusion regarding the picture in aVR & V1. I did note the reference the Fiol article on the short case study of 7 acute LMain occlusions in which lack of ST elevation in aVR & V1 was attributed to simultaneous involvement of the LAD + LCx (which is what happens with acute LMain occlusion) – but some of your figures do have ST elevation esp. in aVR – and that had been my impression for what one may see with LMain occlusion (in addition to RBBB/LAHB and marked anterior ST elevation + ST elevation in aVL with often dramatic reciprocal ST depression in the inferior leads). My guess is that not all LMain occlusions produce the same ECG picture in leads like aVR and V1 where the balance between ST elevation vs reciprocal ST depression from acute LCx involvement may be difficult to predict. Again – NICE article! – 🙂

    • Was pulling some links from this discussion for another article and your comment got me thinking a bit. Here’s my take on aVR and LMCA lesions (which is pretty much just a re-phrasing of yours)…

      If you have an LMCA NSTEMI (meaning diffuse subendocardial ischemia with diffuse ST-depression) you’re always going to get ST-elevation in aVR. It’s just how the vectors work out. 95% of the time it’s also the reason why aVR comes up in discussions of LMCA stenosis. That ‘rule’ doesn’t apply to LMCA STEMI though, and I think that is the important point.

      When you have a true STEMI of the LMCA it parallels what we see with proximal LAD lesions (and the two are often indiscernible, though that’s off-topic). In some cases of anterior STEMI with a proximal LAD culprit we see anterior elevation with maximal limb lead elevation in aVR, while in other cases you can have a very similar proximal LAD lesion but maximal limb lead elevation in aVL (and none in aVR). Other times the ST-vector points directly upwards at -90 degrees, resulting in equal elevation in both aVR and aVL. In all three situations there is a proximal LAD culprit but what determines the pattern of ST-deviations we see in the limb leads is the balance between the septal and diagonal branches coming off the LAD.

      If the patient has a prominent 1st septal (S1) and only minor 1st diagonal (D1), there balance of the injury is going to be rightward and lead to more elevation in aVR. On the other hand, if the LAD feeds large diagonal arteries that cover a significant portion of the lateral wall, then that larger territory of injury is going to angle the ST-vector to the left and towards aVL.

      As you say, it works out the same way with LMCA STEMI where the balance of the anatomy between the LAD, LCx, and RCA dictate just where that limb lead elevation will show up with the left main is occluded.

      What I’m saying (and what the authors of some of the cited papers try to highlight) is that the absence of aVR elevation is of little predictive value during LMCA STEMI. Unlike LMCA NSTEMI, whose ECG pattern is essentially defined by ST-elevation in aVR, LMCA STEMI can do whatever it wants. If there’s elevation in aVR, great, that anterior STEMI is either a proximal LAD or LMCA lesion, but if there’s no elevation in aVR, a large anterior STEMI still might be due to a LMCA culprit.

  • Sam says:

    Very nice article. Thanks!

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