Conclusion to Masters Case #01

I apologize for the giant delay and I know it’s a pain when these cases are so spread out. This is the conclusion to Masters Case #01; be sure to check out the original post first if you haven’t yet done so. This was a tough one and I didn’t take the decision to call these the Masters Cases lightly. Expect some really complex tracings in this series, so to do them justice the explanations are a bit longer than our standard fare.

I’ve seen a lot of interpretations of this case both on the blog and on Facebook and none of them quite matched my read, so that means I’m either brilliant or crazy. On my side, however, is the fact that I was able to correctly predict the locations of the two main lesions found on this patient’s cath, their acuity, and his interventional course given no more information than was contained in the original post. I say this not to brag but to tell you that there really is a wealth of information contained in a single ECG. Also, there must have been something about the way I approached this case that gave me some manner of unique insight. There are bound to be folks who have a different read of this tracing and that’s okay. In fact, I’ve already got a second opinion post in the works for this case where we review the other reasons this EKG could look the way it does, so if you have differing thoughts let me know in the comments so I can include them. I’ve already been in correspondence with Dr. Stephen Smith of the eponymous ECG blog, and knowing how my friend Dr. Ken Grauer operates I’ll bet he’ll have a few important points to add as well! The nice part about this being my platform (on Tom’s blog) is that I get to present my side first.

While we still see a great deal of truly non-specific ECG’s every day, something I’ve learned to appreciate over the past couple of years is that there are times when the ECG can appear as kind of a jumble at first glance, but after careful and deliberate dissection it actually tells a complex story. This is one of those cases. What follows is an in-depth analysis based off how I originally read this tracing.

Masters Case: 50yo M - Severe Chest Pain

First off, we must note that this is not a 10-second ECG but rather the same 5-seconds of data duplicated for in both the limb and precordial leads. Some prehospital monitors can print this way in order to present the best possible ST/T-wave complexes at the expense of rhythm interpretation. As a result, there is really only one instance of wide-complex tachycardia shown here, not two.

The narrow-complex rhythm is a bit uncertain. No definite P-waves + irregularity is the simple criteria for atrial fibrillation and I try not to over-think it, so we’ll call it a-fib. I’m a bit tempted to call it subtle atrial flutter and can’t rule that out, but the important thing is that it’s not sinus (or AV-block) despite some P-wave-looking blips. The rate also seems to be pretty well controlled, suggesting, but not nearly diagnostic of this possibly being a chronic issue.

The wide complexes are irregular, vary slightly in morphology, and follow a narrow beat after a long pause, raising the possibility of aberrancy and Ashman’s phenomenon. On the other hand, the slurred, monophasic R-wave in V1 with an S>>R in V6 and monophasic upright complex in aVR (frontal axis roughly 250 degrees) are all indicative of ventricular origin. In this case we have to believe this is ventricular ectopy rather than benign aberrancy, especially since the patient’s heart is likely ischemic and prone to the former anyway. We’ll call it a triplet, technically brief VT, though aberrancy cannot be ruled-out.

Approximate measurements:
– Frontal QRS-axis: -80 degrees (left-axis deviation).
– Frontal ST-axis: 195 degrees. Maximal ST-deviation of 2.5-3.0 mm.
– Precordial ST-axis: To the right, maybe towards V4R. Maximal ST-deviation of at most 0.8 mm.

– Frontal T-axis: 50 degrees.

The QRS-interval is at least 100 ms, maybe 110-115 ms, despite looking narrower in many leads. There is a poor R-wave progression across the precordials with a weird rSr’ in V6. I’m going to call this a non-specific intraventricular conduction delay (NSIVCD), due to old infarction +/- left-anterior fascicular block +/- some truly non-specific abnormalities in the ventricular conduction.

The QS complex in lead III looks legit and suggests old inferior MI (no acute ST/T-wave changes in III).

In comparison to the limb leads, the ST-abnormalities in the precordial leads are impressively unimpressive. There is subtle, concordant, mostly up-sloping ST-depression from V2-V6. While the frontal plane ST-vector suggests diffuse subendocardial ischemia (190 degrees, leading to ST-elevation in aVR), when that is the case the precordial leads usually show pronounced changes equal-to or greater in magnitude than the limb leads.

For a couple of examples of cases of true diffuse subendocardial ischemia, check out these links:
68 Year Old Male: Chest Tightness Part 2
Conclusion: 81 YOM with Chest Heaviness

Here’s a visual representation of the ST-vector here in comparison to what we usually see with run-of-the-mill diffuse subendocaridal ischemia and acute epicardial ischemia in the LAD distribution (aka STEMI).

Frontal ST-Vectors\

Transverse ST-Vectors

I don’t think the wide-complex beats offer us any additional insight into the ST-changes as they sometimes can, though the morphology in V6 is a bit worrisome. What I mean by that is that the T-waves there are a bit large and feature a rather convex shape. While not diagnostic of anything it’s worth keeping in mind.

At this point in my analysis I think it’s safe to say this patient has severe coronary artery disease of some manner. Even before this particular event, from his history alone (obese 50yo M w/ HTN and DM) we probably would have been safe to assume he had coronary artery disease lacking a formal diagnosis. With today’s presentation he sounds very sick and it is clear we should be very concerned about acute coronary syndrome, but what kind? We have to suspect the patient has an acute lesion, but does the EKG support that case and what signs can help us?

Well, my first prediction is that the patient is going to have an RCA occlusion on cath. This, however, is not our culprit! Rather, it is an old occlusion from a silent MI some time in the past as evidenced by the Q-wave in lead III with no evidence of ST or T-wave changes there, it must be at least a couple of months to years old. Recall that this patient carries no prior diagnosis of MI or CAD, so it is very likely going to be chronically occluded.

So now we have the challenge of identifying a culprit lesion in the setting of at least two-vessel, maybe even three vessel disease.

The next consideration, and really the crux of my whole argument, is the interplay of the ST-elevation and depression between the limb and precordial leads. As stated before, given the large amount of ST-deviation in the limb leads (maximum of 2.5-3.0mm, with maybe 2.0mm of elevation in aVR), the precordial leads just aren’t showing as much ST-depression as we should expect. In most cases of diffuse subendocardial ischemia we see significant, often striking amounts of ST-depression in leads V3-V6, but that finding is really lacking here. So is this really subendocardial ischemia just because there is ST-elevation in aVR, or is it something else?

My next prediction is that we will find an LAD culprit. I’m slightly guessing at the location of the lesion within the LAD, but my hunch is that it will be in the mid-LAD (distal to the first-diagonal artery).

How can I say with confidence that we’re looking at an LAD culprit? It all comes down to the ST-vectors. Using some of the same vectors I roughly displayed in the images above, here they are overlaid on one-another. It’s clear that our cases’ vectors are quite literally halfway between what we classically see with mid-LAD STEMI and diffuse subendocardial ischemia!

Frontal ST-Vectors Overlay

Transverse ST-Vectors Overlay

What I suggest is that what we’re seeing on the ECG could be a combination of diffuse subendocardial ischemia (due to multi-vessel disease) and anterior epicardial ischemia (due to mid-LAD occlusion). In the transverse (precordial) plane the two vectors nearly cancel out, but in the frontal (limb lead) plane the mid-LAD vector hardly affects the subendocardial ischemia vector, leaving the latter almost perfectly intact.

That vector argument is a bit tenuous by itself, but another key finding (picked up on by Dr. Ken Grauer in the comments on the first post) is the morphology of the precordial T-waves, most obvious in V6. Unlike the typical horizontal or down-sloping ST-depression we see in pure subendocardial ischemia, the T-waves here are slightly up-sloping. While clearly not de Winter’s T-waves (though V6 comes closest), one can imagine that they have the appearance of wanting to be upright except that their J-points are being pulled down. I suggest that this is due to the interplay of the precordial ST-elevation due to the acute LAD lesion with the diffuse ST-depression caused by the concomitant multi-vessel disease. The diffuse ischemia is pulling the J-point down while the acute injury is causing the initial part of the T-wave to slope upward.

The final part of my interpretation, the prediction of the patient’s future management, relies on putting all of the previous findings together. I think the patient has a mid-LAD culprit, so that will probably be amenable to stenting. Importantly, however, he also has an old RCA lesion that will be chronic and difficult (or even unnecessary) to re-open along with probably multi-vessel non-culprit lesions. As a result, even following successful cath, I think this patient will end up receiving planned CABG on a non-urgent basis.

Now, I wouldn’t blame you for thinking this interpretation is a bit tenuous. In fact, I’d hope that you would question anyone trying to say so much with so little to go on. What did the cath show though?

1) 100% chronic mid-RCA (right coronary artery) occlusion with good collateral development.
2) >50% LCx (left circumflex artery) stenosis, non-culprit.
3) Non-culprit lesions of the proximal LAD (left anterior descending artery, stenosis % not noted).
4) 95% culprit lesion of the mid-LAD.

So, as my method of interpretation predicted, this patient displayed a mid-LAD culprit lesion in the setting of an old RCA occlusion and multi-vessel disease. How was he managed? The LAD lesion received one stent and he later went on for bypass surgery. He had to be defibrillated twice during his hospitalization but he was later discharged home with a good outcome!

Not too shabby for one ECG and a brief HPI

Let me know your thoughts in the comments and look forward to some more equally difficult (and probably controversial) yet still diagnosable tracings in the near future. Also, I want to send a huge thanks to Dr. Bojana Uzelac for sharing this excellent tracing all the way from Serbia. She really has a great eye for spotting these unique kinds of tracings and has very graciously shared a number of them with us. The next Masters Case will also be one of her ECG’s.

Addendum (2014/05/28):
If you want to see another case of diffuse chronic CAD plus an acute culprit, check out this post by Dr. Smith. He actually shared his case maybe a day or two before I saw this tracing, which is certainly what allowed me to consider the possibility of mixed-lesions in this patient’s presentation.


1 Comment

  • Nice case – THANKS for presenting. I think there are features suggestive of both proximal vs more-mid LAD disease. ST elevation in lead aVR is really quite marked – and I didn’t expect to see that in a less proximal LAD lesion. Fully agree that the amount of anterior ST depression is less than expected – and those hyperacute T waves in lateral precordial leads was one more unexpected finding. Bottom line is that I expected interplay between chronic and acute disease with some canceling out. Credit to YOU for your theory on mid-LAD occlusion from the start.

    GOOD POINT about this really being one 5-second (rather than a 10-second) rhythm strip!

    LAST COMMENT: While hard to “prove” the in the absence of sinus rhythm that the one salvo we see is VT and not aberrantly conducted supraventricular impulses – I think the evidence we do have is pretty overwhelming (and supports 99.9% certainty in the absence of “absolute” proof). I think this is an important point because of frequent ongoing debates regarding whether or not the Ashman phenomenon in valid in AFib. Those who believe it is state the presence of a long-short cycle as seen here “proves” these are aberrantly conducted beats. In my opinion- that line of reasoning is flawed. Aberrancy vs ventricular is never an “all-or-none” decision. Some patients in AFib do seem to obey Ashman sequencing. The reason I support Marriott’s contention that Ashman is unreliable in AFib is that there is LOTS of concealed conduction penetrating (at least partially penetrating) from the 400-600 fib impulses bombarding the AV nodes – such that the usual constant relationship between long preceding cycle prolonging the subsequent refractory period becomes unreliable when you have AFib.

    So – Reasons this salvo of wide beats is almost certainly VT and NOT aberrant are: i) There is acute coronary occlusion – ergo VT is far more likely; ii) QRS morphology in lead aVR is a monophasic R wave (virtually 100% specific for VT by Sasaki); iii) Extreme axis deviation during the salvo; iv) almost entirely negative QRS complex in lead V6; v) Monophasic slurred complex in V1 with VERY different initial deflection compared to the normal beats in this lead; vi) the R-R interval during the salvo is not regular (so it keeps with the underlying irregularity of the underlying AFib rhythm); and vii) VT should be assumed until proven otherwise (and not the other way around). Other than the long-short – there is really NOTHING suggestive of aberrant conduction on this tracing.

    THANK YOU again Vince for presenting this case!

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