Wednesday, April 2, 2014

A Non STEMI that needs the cath lab now.

A male in his 60's called 911 for chest pain.  He had some cardiac risk factors including hypertension, on meds, but no previous coronary disease.   His pain was intermittent and he was vague about when it was present and when it was resolved.  Here is his prehospital ECG:

Diagnosis? 

He had an immediate ED ECG:
There is artifact, but the findings appear to be largely gone now





















The diagnosis is acute MI, but not STEMI.  There is slight ST elevation in lead III with reciprocal ST depression in aVL.  The T-wave is inverted in III, indicating reperfusion (what I like to call "inferior Wellens' syndrome).  There is no Q-wave, so this is unlikely to be old MI, and more likely to be acute NonSTEMI of the inferior wall.

I saw these ECGs, and since there was no immediate urgency, allowed the resident to manage it without any comment.  However, he did not see the abnormality on the prehospital ECG, so I finally said something like: "What are you going to do about the MI patient?".    When I pointed out the findings, we recorded another ECG:
Now there is increased ischemia, but where is it? My interpretation was that this is an inferior MI with posterior extension, as the ST depression in the precordial leads was maximal in V3 (opposite the posterior wall). There is about  1 mm of STE in aVR  I considered but rejected subendocardial ischemia.  

The ST elevation vector is posterior, inferior, and right, to the right of lead III and also posterior.  Is it subendocardial ischemia, or inferior MI?  See this post on the (Five primary patterns of ischemic ST depression, without ST elevation)

Because of the dynamic ACS, we activated the cath lab in the middle of the night.  Aspririn, Plavix (in spite of STE in aVR, because I thought this was inferior MI), Heparin were given.  The BP was elevated, so we gave metoprolol 5 mg IV x3 + 50 mg po.

His pain resolved and another ECG (but with precordial leads on the right) was recorded:
ST Depression is Resolved in V2 (=V1 R).  No evidence of RV MI.


Then the patient complained of increasing pain again:
There is now profound ST depression and STE in aVR, and the ST depression extends deeply in V5 and V6.  There is little ST elevation in inferior leads.

This time, the ST vector is more rightward, toward aVR and also posterior.

Now I regretted giving Plavix, as the probability of 3 vessel disease or left main insufficiency (not occlusion!) was much higher.  Thus, the chance of needing CABG was higher and Plavix can cause much operative bleeding.

Amazingly, the bedside echo showed very good LV function.

A nitro drip and sublingual nitro was given, the drip rapidly titrated to 80 mcg/min.  The BP came under better control and the patient was moved to the cath lab.

Outcome:

Was it RCA or LCX with inferior MI?  Or was it 3 vessel disease/left main insufficiency?

Both!

The active culprit was an RCA thrombus with 99% occlusion, but there was severe LAD and circumflex disease as well (severe 3 vessel disease).

The RCA was opened with POBA ("plain old balloon angioplasty") and eptifibatide was started.  The patient was referred for CABG and did well.


13 comments:

  1. Is the "ST Depression is Resolved." ECG perhaps right sided + posterior?

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  2. Fascinating case Dr. Smith!
    Couple of questions... In the final ECG that looks more like subendocardial ischemia, lead III still seems a little unusual, and I wondered if the forces of the negative ST vector of subendocardial ischemia cancelled out the ST elevation previously seen, so that the ST elevation is not so much resolved as "hidden"?
    Also, in the same ECG, it seems as though the ST depression in the precordial leads is still maximal in V3. Would that not be unusual for subendocardial ischemia alone?

    Thanks,
    DaveB

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  3. Dave, yes no doubt about it. This is because there is simultaneous subendocardial ischemia and inferior-posterior MI. So you have a fusion of inferior MI findings with subendo ischemia findings. As for subendo cancelling out lead III, it is possible to a small degree, but should not be much because aVR is at a right angle to lead III, not opposite. In other words, the subendo ischemia vector is perpendicular, or nearly so, to the inferior MI vector.
    STeve

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  4. Dr Smith, is the upright T in V1 significant? That was what I saw besides the T inversion in lead III and was thinking of an ACS event.

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    1. That is a very good question. It could be a sign of right ventricular infarction, going along with inferior MI. But also an upright T-wave in the one is a normal finding. In our study comparing early repolarization with anterior MI, we found an upright T-wave in the one was very common in normal variant and did not help in the diagnosis. However, in this case, early repolarization is not part of the differential diagnosis. We also did a right-sided ECG in this case, but it was not done while there was ST elevation in the three. So I'm not sure of the absence of right ventricular infarct. And now I don't know if it was a proximal RCA or not.

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  5. A truly interesting case and it really wrestles with a lot of concepts I've been trying to work out over the last year.

    The first is differentiating true PWMI from subendocardial ischemia (SI). I've emailed you before about the proposed "V6 sign" I've been playing with to distinguish the two. This case highlights one of the problems that can crop up, however, in that an acute occlusion in the setting of multi-vessel CAD can create a convincing picture of subendocardial ischemia (ST-D in V3 and V6) even though there is still a lesion amenable to PCI. I don't like that my sign would call the 2nd and 4th ED ECG's subendocardial ischemia. True, that's one of the factors at play creating the pattern we see, but the reason for my interest in the sign is not to pick up SI but rather PWMI. The issue I worry about more is providers over-calling ischemia and missing true PWMI.

    It would have served you well here in helping to identify the multi-vessel disease, but you're not my target audience. I'd be much more worried about someone who sees these tracings, uses the sign as evidence of multi-vessel disease, and thus thinks the patient doesn't need immediate cath.

    The next issue for me has to do with my recent semi-obsession with vector electrocardiography. We know that an ST-vector of 210-240 degrees in the frontal plane is highly suggestive of subendocardial ischemia, while most RCA occlusions create a vector of almost 120 on the money (with some swinging down towards 90). The question is what to do with the mixed picture we have here in the second ED ECG with a frontal vector of almost exactly 180 degrees. I've seen this pattern go both ways (diffuse CAD w/ no acute process and true acute RCA lesion), and as you mention in the comment above, it's because it really is a combination of two different forces at play. For whatever reason it seems like the fourth ED ECG is much more consistent with pure subendocardial ischemia (though there's still a counter-clockwise rotation of the QRS in the precordial leads like we see in PWMI).

    Sorry these comments don't add much to the discussion of this case and kind of mirror what you've already said, I just wanted to get my thoughts down concerning where I am in my understanding of these complicated and rarely discussed cases/patterns.

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  6. Amal Mattu gives good opinions on STE in aVR and I am of the opinion that it is undercalled and underestimated even when spotted. I cant recall the statistic, but the untreated (PCI) mortality is astonishingly high. He would have woken up the cardiologist on the basis of the ambulance ECG alone, for me.

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  7. Dear sir how cold we dismiss sub subendocardial ischemia and what a st vector tells as it is the reciprocal change of st suppression.a little bit confused

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    1. I certainly hope I did not give the impression that I am dismissing subendocardial ischemia. It must be acted upon. But it is important to understand the ECG manifestations of subendocardial and subepicardial ischemia, when the primary ECG manifestation is ST elevation with reciprocal ST depression, and when it is ST depression due to subendocardial ischemia, with reciprocal ST elevation

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  8. , Prehospital ECG shows "slight ST elevation in lead III with reciprocal ST depression in aVL. The T-wave is inverted in III, indicating reperfusion (what I like to call "inferior Wellens' syndrome)" as you mentioned in blog. Sir, is there is subtle ST depression in lead V2 in same ECG along with depressed PR segment in V5 and V6?

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  9. I don't see any ST depression in V2 in the preshospital ECG. There is VERY subtle (within normal limits) ST depressioin in V2 on the 2nd. I don't see the PR depression (????)

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