Wednesday, May 13, 2020

What do you think the echocardiogram shows in this case?

A 60-something man presented by EMS with 5 hours of fairly typical sounding substernal chest pain. 

Here is the EMS ECG:

Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR

Of course this pattern is most often seen from etoliogies other than ACS.   The ECG only tells you there is ischemia, not the etiology of it.
Nevertheless, the clinical situation made other etiologies unlikely.


EMS gave 324 mg aspirin and 3 sublingual NTG, which the patient stated reduced the substernal chest pain from an 8/10 to 4/10.

Here is the ED ECG on arrival:
Less STE/STD

Provider's Clinical Impression: "findings concerning for myocardial infarction, likely proximal LAD or Left main."

Cath lab activated

Dual antiplatelet therapy and heparin given.  NTG drip started. Pain better still.

What do you think the echocardiogram shows?

First trop I returns at 1.5.














POCUS Echo:

POCUS Echo with no wall motion abnormality and normal ejection fraction.

This was a point of care ultrasound, not a bubble contrast echo.  Sensitivity of POCUS even for definite wall motion abnormalities is far from perfect.

But there are frequently no wall motion abnormalities when there is diffuse subendocardial ischemia.  This is an anecdotal observation that I and others I know have made, and I cannot find any formal literature on the topic.  I have posted previous such cases, but in searching my own blog, I could not find them.

It would be a good topic for study.


Angiogram:

Severe diffuse left main disease, up to 80% at the ostial left main.  Stented.

Post cath ECG:
Normal or near normal


Peak troponin I was 15 ng/mL.

The post cath contrast echo also showed no Regional wall motion abnormality.  One would not expect wall motion to recover so quickly after stenting, so this is good evidence that the POCUS echo was indeed accurate.

Why would there be no Regional wall motion abnormality? 

It is because the epicardium remains functional; it is only the endocardium that is ischemic, and it is ischemic everywhere.  So both are true: no decrease in EF and no WMA.

Is this OMI?  Not strictly speaking, but cath lab activation is usually required.

There is a subtle but important difference between OMI and subendocardial ischemia: OMI (that is not STEMI) is due to TIMI 0/1 flow and has any combination of subtle STE, hyperacute T-waves, reciprocal ST depression, decreased QRS amplitude, terminal QRS distortion and other findings.  It is distinguised from subendocardial ischemia (SI) in that SI has diffuse ST depression with reciprocal ST Elevation in aVR.  The artery is open, but flow is insufficient to perfuse the entire myocardial thickness (subendocardial AND subepicardial).

On echo, OMI has a wall motion abnormality, but SI usually does not.  





===================================
MY Comment by KEN GRAUER, MD (5/13/2020):
===================================
It’s good to periodically review the differential diagnosis of the diffuse subendocardial ischemia. Recognition of this ECG pattern should be an automatic REFLEX for the emergency care provider — As soon as one sees diffuse ST segment depression (usually present in at least 7-8 leads) + ST elevation in lead aVR — one should consider:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; shock/profound hypotension; GI bleeding; anemia; etc.).

The initial tracing in this case illustrates an extreme example of this phenomenon — in which all leads except for aVR and V1 manifest profound ST segment depression (Figure-1).
  • ST depression attains up to 5 mm in several leads!
  • A comparable amount of reciprocal ST elevation is seen in lead aVR.
  • As is seen in ECG #1 — a lesser amount of ST elevation is sometimes seen in lead V1.

Figure-1: The initial ECG in this case, done in the field by the EMS team (See text).



In the March 9, 2020 post of Dr. Smith’s ECG Blog — Dr. Smith presented results from a 2019 article by Harhash et al, that confirm how the ECG pattern shown in Figure-1 does not represent acute LMain occlusion — but rather the differential diagnosis that I show above.
  • The case I presented in My Comment to that March 9, 2020 post showed a patient with this pattern — who on cath had no more than minimal coronary disease.
  • Dr. Smith also referenced an article by Knotts et al, showing that even when diffuse subendocardial ischemia is due to coronary disease — that only a minority of patients had severe LMain coronary disease as the cause.

Today’s Post by Dr. Smith adds to our knowledge of this syndrome. For as helpful as POCUS Echo can be in the diagnosis of acute coronary occlusion — we need to remember that there are frequently no wall motion abnormalities when there is diffuse subendocardial ischemia — because (as emphasized by Dr. Smith): iThe epicardium remains functional, since it is only the endocardium that is ischemic; andii) Subendocardial ischemia is diffuse — and therefore does not localize to any particular myocardial region.

P.S.: Much of the time — the amount of ST depression (and the amount of reciprocal ST elevation in lead aVR) will not be as extreme as it is in Figure-1. Nevertheless, this ECG pattern of subendocardial ischemia needs to be instantly recognized — so that optimal decision-making based on the clinical scenario can promptly begin (See the October 31, 2018 post on Dr. Smith’s Blog).



7 comments:

  1. Aortic dissection is another differential for this EKG. Important to remember because it directly affect the management (anti platelets and hnf/lmwh could lead to a disaster)

    Excellent blog ! Thanks doctors

    ReplyDelete
  2. Dr Smith Can you list the OMI signs in addition to the following ones?
    subtle STE, hyperacute T-waves, ST depression V1-V4, decreased QRS amplitude, terminal QRS distortion

    This blog is really inspirational to me and it changed my approach to EKG radically.
    Thank you.

    Giacomo from Italy

    ReplyDelete
    Replies
    1. Grazie Giacomo per le belle parole! Siamo felici che questo ECG Blog sia utile per te! (Thanks for the nice words! We’re happy this ECG Blog is useful for you!). Among the ECG findings that in the “right” clinical setting (ie, new-onset chest pain) may suggest acute OMI are: i) Hyperacute T waves; ii) Reciprocal ST-T wave changes (especially when a “mirror-image” picture of ST-T waves is seen between leads III and aVL); iii) ST elevation of ANY amount (even less than 1 mm) of a shape that suggests acute injury (especially when present in more than a single lead of a given lead area); iv) ST depression of the “right shape” post posterior involvement (ie, positive “mirror test”) in one or more anterior leads (especially if seen in association with suspicious-for-acute inferior lead changes); v) Terminal QRS distortion (terminal QRS does not extend down to the baseline, with absence of both a J-wave and an S wave in leads V2 or V3); vi) New development of infarction-Q-waves; vii) An overall “Gestalt picture” that might be difficult to “put into words”, in which a patient with worrisome new symptoms shows abnormal ST-T wave changes in multiple leads — that taken TOGETHER suggest acute OMI in progress; and viii) The finding of “dynamic” ST-T wave changes (on either serial tracings OR compared to a prior baseline ECG) — that in the setting of new worrisome symptoms suggest an ongoing acute process. Added to this might be findings from other testing (ie, positive troponin; stat Echo during chest pain showing localized wall motion abnormality). NOTE — As is probably apparent from the above — it may be hard to “put into words” all criteria without seeing a specific tracing — but hopefully the above will be helpful! P.S. — I’ve referred your excellent Question to Drs. Smith & Meyers for their additional input! — :)

      Delete
    2. Giacomo, we are nearly done with a manuscript that will list the 7 findings of OMI that is not STEMI.

      Here they are:


      Hyperacute T-waves
      Pathologic Q-waves
      Terminal QRS distortion (terminal QRS does not extend down to the baseline, with absence of both a J-wave and an S-wave)
      Reciprocal STD and/or T-wave inversion
      Subtle STE not meeting criteria
      STD maximal in V2-V4
      Any STE in inferior leads with any STD/T-wave inversion in aVL

      Delete
    3. Thank you Dr Steve and Dr Ken!

      Delete

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