Tuesday, February 4, 2020

A man in his sixties with chest pain, tachypnea, and hypertension

Written by Pendell Meyers

A man in his sixties presented with acute chest pain and shortness of breath over the past 1-2 hours. Vitals were remarkable for hypertension 180/104 mm Hg and tachypnea at 24/min.

Here was his initial ED ECG:

What do you think?














I texted this to Dr. Smith without any information at all, and he replied: "Obvious LAD occlusion, at least to you and me."

This ECG is subtle but diagnostic of LAD Occlusion MI (OMI). There is STE in V1-V2 and aVL. The T-waves are hyperacute in V2. There is reciprocal STD in V4-V6, and leads II, III, and aVF. It does not meet STEMI criteria because V2 does not have the requisite 2.0 mm STE it takes in a male over 40 years old.


See these related cases for more examples of this pattern:

A 40 year old man with chest pain since last night


A man in his sixties with chest pain at midnight with undetectable troponin








My colleagues Alex Bracey and Scott Weingart recognized this ECG immediately.

They activated a "Heart Alert" (this is what we call it when we believe a patient has very high risk for Occlusion MI but doesn't meet STEMI criteria - it brings us the cardiology fellow immediately, and gets us a call from the interventionalist to discuss the case and decide whether to proceed with full cath lab activation.)

The consultant arrived and decided to cancel the heart alert because the ECG didn't meet STEMI criteria. They stated that the ECG showed "demand ischemia" instead. They initially refused to take the patient to cath. No troponin was back yet.

The team demonstrated an anterior wall motion abnormality on bedside ultrasound but this did not change their decision. Here are some of the images:




The first image is close to a parasternal long view, and the second is close to an apical view. Both are suboptimal, but they appear to show WMAs of the anterior septum, anterior wall, and apex.


So the team continued medical therapy and recorded repeat ECGs every 10 minutes. Here are the next three ECGs:






These repeat ECGs show evolving STE and hyperacute T-waves in the same leads. The Occlusion is ongoing. Yet the ECG still does not technically meet STEMI criteria due to insufficient STE (not 2.0 mm) in V2.


The team knew that these ECGs were only further proof of what they had already seen. The troponin T returned at 0.11 ng/mL. They re-activated the heart alert and this time they were able to convince the interventionalist to take the patient to the lab, with approximately 40 min delay caused by the initial cancellation.


They found a 99% TIMI 1 flow lesion of the proximal LAD which was stented with resultant TIMI 3 flow.


Pre-intervention



Post-intervention



Here is his ECG the next morning:

Terminal T-wave inversion in previously affected leads, signifying successful reperfusion.


Peak troponin T was 7.50 ng/mL (quite a large MI, larger than most STEMI(+) OMIs in my data from the same institution):


You can see that the STEMI(+) OMIs (yellow bar, confirmed Occlusion MIs with STEMI criteria on ECG) had an average peak troponin T of 5.36 ng/mL. The average STEMI(-) OMI (blue bar, confirmed OMI without STEMI criteria on ECG) had an average peak troponin T of 4.44 ng/mL. The point of this diagram is to show that the STEMI(-) OMIs are similar in peak troponin to STEMI(+) OMIs, when both are compared to NOMIs (MIs without Occlusion).



EF was approximately 35% two days later, with anterior and apical wall motion abnormalities.

The patient did well in the hospital and was discharged several days later.


Learning Points:

Remember this pattern of LAD Occlusion MI with STE and hyperacute T-waves in V1-V2 with reciprocal findings in lateral and inferior leads. See the links above with similar cases.

Other than the ECG findings, this patient had evidence of ongoing ischemia (ischemic ECG findings, ischemic chest pain, and rising troponin) despite medical management, therefore warrants emergent cath lab activation even without expert ECG interpretation.

While the STEMI paradigm is still in place, we must protect patients like this from it using all the skills we have at our disposal: expert ECG interpretation, bedside ultrasound, and knowledge of the guidelines' other reasons for emergent catheterization.



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MY Comment by KEN GRAUER, MD (2/4/2020):
===================================
Important case presented in excellent fashion by Dr. Meyers. I must admit that in cases like this one, I repeatedly find myself asking, What am I missing? By this I mean that I just do not understand why it took 4 serial tracings + a 2nd Heart Alert to finally get agreement from the interventionalist to take this patient to the cath lab.
  • I focus my attention on the first 2 ECGs that were done (Figure-1) — since if the interventionalist hesitated after the 1st ECG — I can think of NO reason why in a 60-ish year old man with new-onset chest pain there should be any hesitation after the 2nd ECG about the diagnosis of acute OMI and the need for prompt intervention.

Figure-1: The first 2 ECGs in this case (See text).



MTHOUGHTS: I see 4 fundamental mistakes that the interventionalist made:
  • Oversight #1: As per Dr. Meyers — the cardiology team failed to recognize the acute LAD occlusion that should be evident (given the history) on ECG #1.
  • Oversight #2: The cardiology team failed to change their decision even after Echo at the bedside demonstrated an anterior wall motion abnormality (which given the ECG findings in ECG #1should be diagnostic of acute anterior OMI).
  • Oversight #3: The cardiology team failed to do lead-by-lead comparison of ECG #1 with ECG #2 in context with the clinical presentation (ie, new chest pain in a 60-something man who demonstrates an anterior wall motion abnormality on bedside Echo).
  • Oversight #4: While I could understand (even though I disagree) with the cardiology team deciding not to cath the patient on the basis of ECG #1 — they failed to appreciate the incremental effect of ongoing clinical information from more than a single source. Regardless if strict “millimeter” criteria are (or are not) met — 2 + 2 = 4. In the context of ECG #1 — there is clear progression (See below) in ECG #2 — that occurs in association with a corresponding wall motion abnormality on bedside Echo.



Before dissecting the first 2 tracings — I wanted to highlight the clinical utility of using lead aVL as an invaluable clue to the location of the acutely occluded coronary artery. I believe Figure-2 below speaks for itself.

Figure-2: The clue to the “culprit artery” provided by lead aVL in acute OMI.



Looking More Closely at ECG #1 and ECG #2: Let’s return to the first 2 tracings shown in this case. I’ve added a few labels to Figure-1 to clarify the points I wish to emphasize (Figure-3):

Figure-3: I've labeled KEY findings from Figure-1 (See text).



As per Dr. Meyers — ECG #1 shows ST elevation in leads V1, V2 and aVL. There is reciprocal ST depression in the inferior leads (ie, leads II, III, aVF) — and in the lateral chest leads (V4, V5, V6).
  • To me — the appearance of lead aVL in ECG #1 is not subtle. There is a large Q wave (quite deep and wide, considering how small the R wave in lead aVL is). In addition — there is both coved ST elevation (that is at least 1/3 the amplitude of the R wave in aVL) with clear T wave inversion. In association with worrisome ST depression in each of the inferior leads (ie, reciprocal ST depression) — these findings alone should be diagnostic of acute OMI until proven otherwise in this patient with new chest pain.
  • The SHAPE of the ST elevation in leads V1 and V2 is concerning. The ST coving (ie, “frowny”-configurationin lead V1 (curved BLUE line in this lead) is definitely not normal in a lead V1. In lead V2 — there is clear ST segment straightening (slanted BLUE line in this lead+ about 1.5 mm of J-point ST elevation + the hyperacute T wave mentioned by Dr. Meyers.
  • It should be noted that in lead V3 of ECG #1 — not only is there no ST elevation — but the shape of the ST segment in this lead is gently upsloping (as per the upward curving BLUE line in this lead). Lead V3 does not look abnormal in ECG #1.
  • The reason I presented Figure-2 above on ST Elevation in Lead aVL — is that while I was convinced (as were Drs. Meyers & Smith) that ECG #1 represented acute OMI — I thought it possible that the “culprit artery” might be the 1st or 2nd Diagonal Branch of the LAD — since there was ST elevation in leads aVLV1 and V2 — but not in any other anterior leads. In my experience — it is sometimes difficult early on to distinguish between acute proximal LAD occlusion vs acute occlusion of the 1st or 2nd branch of the Diagonal. Typically, with acute Diagonal occlusion — ST elevation is limited to leads aVL and V2 (and is not seen in lead V1 — See THIS CASE) — but I just wasn’t certain about the “culprit” artery at the time I saw ECG #1. BOTTOM LINE  what counts is that ECG #1 has to be assumed indicative of acute OMI until proven otherwise! (Subsequent tracings clarified that ST elevation was indeed present also in lead V3 — so clearly suggestive of acute proximal LAD occlusion!).
  • HOW MANY LEADS with Abnormal ST-T Waves does this make in ECG #1ANSWER: With the exception of leads I and V3 — we have just described definite ST-T wave abnormalities in at least 9 of the 12 leads in ECG #1 (10 if you count the marked ST elevation in lead aVR, that is a reciprocal change to the 6 leads in this tracing with ST depression).

Looking More Closely at ECG #2: Lead-by-lead comparison between ECG #2 and ECG #1 is essential to pick up KEY differences:
  • There is minimal (insignificant) shift in the frontal plane axis. Transition occurs a bit later in ECG #2 (ie, the R becomes taller than the S wave is deep by V4-to-V5, compared to between V3-to-V4 in ECG #1). What is important — is that QRS morphology in leads V1, V2 and V3 is quite similar in the 2 tracings (albeit with slight voltage differences). Therefore — lead-to-lead comparison is valid in these 2 tracings!
  • I do not know why the Q wave, ST elevation and T wave inversion that we saw in lead aVL of ECG #1 was not present in any of the 3 serial tracings done every 10 minutes after this 1st ECG.
  • That said — there are serial ECG changes in ECG #2 compared to ECG #1. I now measure ≥2 mm of ST elevation in both lead V2 and lead V3 in ECG #2 (PURPLE arrow depicting where I place the J-point — with the RED horizontal line depicting the baseline in these leads). Note how the takeoff of the ST segment in lead V3 of ECG #2 is now straight — whereas it was upward sloping (curved BLUE line) in lead V3 of ECG #1. So, there now is more ST elevation in lead V2 than there was in ECG #1 — and, there is new hyperacute ST elevation in lead V3. I find it hard to say this isn’t indication for acute cath in this patient with new chest pain and new anterior wall motion abnormality on bedside Echo.

Our THANKS to Dr. Meyers for presenting this case!


2 comments:

  1. Lead aVL represents high lateral LV wall, providing useful information but it is often the overlooked lead. The high lateral LV wall is perfused by the first diagonal branch of LAD.
    Therefore,
    1) Anteroseptal MI involving aVL= prximal LAD occlusion
    2) Anteroseptal MI not involving aVL= LAD not proximal
    3) STEMI of aVL without V leads= only the diagonal branch occlusion, not involving LAD
    Thus, we can often predict the culprit lesion from the ECG findings. This is very important because there may be other worrisome-looking lesion(s) in other vessel(s), and the angiographer may open up that lesion and declare "mission accomplished" while the culprit lesion is still there untouched!!
    K. Wang.

    ReplyDelete
    Replies
    1. I agree completely K. I summarized the data on these points from the Birnbaum study in my Figure-2 (above). The link to THIS CASE that I give is precisely that — it was the ECG that told the angiographer to look for acute Diagonal occlusion, that otherwise might have been missed. Thanks as always for your comments! — :)

      Delete

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