Wednesday, January 29, 2020

A 20-something woman with Chest Pain

A 20-something woman presented with 30 minutes of sudden onset chest pressure that started while in the bathroom. She had no relief from nitro x1. ASA 325 given by EMS.

Here is her prehospital ECG:

What do you think?



Here are limb leads magnified:


Precordial leads magnified:
Notice the hyperacute T-waves in V4





She arrived in the ED with her pain diminishing.

Here is her ED ECG:
What do you think?










The first ECG is diagnostic of inferior OMI, with probable lateral involvement as well (V4-V6).

In the 2nd (ED) ECG, the inferior findings are gone.  The lateral ST segments remain elevated.  The T-waves appear hyperacute.   If there had been no prehospital ECG, one may not have noticed these subtle findings. 

The ED physicians immediately recognized inferior OMI and activated the cath lab.


Angiogram

Culprit is 100% occlusion of the Distal LAD due to athorosclerotic thrombosis (not spontaneous coronary dissection), affecting the inferoapical LAD hence an inferior (II, III, aVF) and apical (V4-V6) MI.

Peak troponin I was 4.7 ng/mL (99th %-ile URL = 0.030 ng/mL).

Echo

Normal left ventricular size, thickness, and systolic function with an estimated EF of 61%.
Very small regional wall motion abnormality--hypokinesis of the apical inferior and apical lateral segments.

Here is the next day ECG:
All ST segments are isoelectric, proving that BOTH the inferior and lateral ST elevation was indeed ischemic ST elevation.

She had extremely rapid reperfusion of this 100% obstructed distal LAD and thus had a lot of myocardium salvaged.

These docs and medics did a great job!


Learning Point:

1. Don't forget that young women have myocardial infarction too!
2. Prehospital ECGs are critical
3. Always look for hyperacute T-waves and for reciprocal ST depression in lead aVL.

See this case:

24 yo woman with chest pain: Is this STEMI? Pericarditis? Beware a negative Bedside ultrasound.







===================================
MY Comment by KEN GRAUER, MD (1/29/2020):
===================================
Illustrative case with the important Learning Points put forth by Dr. Smith. These include:
  • Young women can (and do) have acute MIs.
  • Prehospital ECGs can be invaluable to our interpretation about what is going on.
  • KEY findings on ECG to look for include hyperacute T waves — and, that magical” reciprocal relationship with inferior OMI between leads III and lead aVL (For more on this “magical” relationship — Please see My Comment in these Dr. Smith posts — from 8/9/2018 — andfrom 10/6/2018).

I focus my comments on some additional subtle changes seen in ECG #1, and confirmed by comparison with ECG #2 (Figure-1).

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



MThoughts oECG #1:
Although resolution of this tracing is clearly suboptimal — this Pre-Hospital ECG ( = ECG #1) in a patient with new-onset chest discomfort is clearly of concern.
  • The rhythm is sinus at 60-65/minute. All intervals are normal. The frontal plane QRS axis is normal at about +30 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Small and narrow Q waves are seen in leads I and aVL.
  • R wave progression is appropriate, with Transition (where R wave height exceeds S wave depth) occurring at a normal position, here between leads V3-to-V4.
  • As per Dr. Smith — ST segments are elevated in each of the inferior leads — and in lateral chest leads (V4, V5, V6) — and, possibly also in high lateral lead I.


QUESTION: What distinguishes ECG #1 — from a tracing that might simply reflect a repolarization variant in a 20-something woman?



ANSWER: What distinguishes ECG #1 from a repolarization variant is a number of subtle findings that just should not be there in a normal tracing:
  • Normal variants do not manifest the reciprocal ST depression that we see in lead aVL of ECG #1.
  • T waves that are fatter-than-they-should-be at their peak in the inferior leads, and in leads V3 and V4. In addition — T waves are disproportionately taller-than-they-should-be (considering R wave amplitude) in leads V3 and V4. In the context of new-onset chest discomfort — all of these T waves qualify as hyperacute changes.
  • Lead V2 in ECG #1 is clearly abnormal. Missing is the slightly elevated, upward sloping ST segment — that is replaced in ECG #1 with a relatively flat ST segment in lead V2, with disproportionately taller-than-it-should-be T wave in this lead.
  • Lead V6 shows significantly more ST elevation than-should-be-seen in this most lateral chest lead.
  • BOTTOM Line: Taken together — this makes for 10 out of the 12 leads in ECG #1 that show suspicious changes in this patient with new chest discomfort.

NOTE: Technically — ECG #1 is a challenging tracing to interpret. This is especially true for leads III and aVL— for which we are trying to establish that “magical” reciprocal relationship.
  • For example — there is significant variation in QRST morphology for the 3 complexes that we see in these 2 leads (RED numbers 1, 2, 3). Which of these 3 beats in these 2 leads should we use to assess for ST-T wave morphology? Clearly the 2nd beat in lead III, and the 2nd beat in lead aVL look the most worrisome.
  • PEARL  Many tracings manifest far less than perfect quality. It’s important to “take this in” as you assess any ECG — and then render an overall Gestalt impression on the theme of the ECG findings you see. In ECG #1 — that theme includes inferior lead ST elevation with reciprocal ST depression in aVL.


MThoughts oECG #2:
We are looking for dynamic ST-T wave changes. How is ECG #2 different from ECG #1?
  • As per Dr. Smith — the inferior lead ST elevation is essentially gone (albeit harder to assess this in lead II of ECG #2, due to so much baseline wander).
  • Did YOU notice the change in Axis between the 2 tracings? That is — the QRS in Lead III was all positive in ECG #1 — but in ECG #2, the QRS in lead III is predominantly negative. That said — the reduction in inferior ST elevation between the 2 tracings looks real despite this change in frontal plane axis.
  • Given that QRS morphology in lead aVL is very similar (a qR complex) in the 2 tracings — the change from a depressed ST segment to a flat ST segment is real.
  • Overall QRS morphology in the chest leads of both tracings looks similar (albeit with slight change in amplitudes). This strongly suggests that the change in lead V2 appearance (which now shows a coved ST segment in ECG #2) is a real change.
  • As per Dr. Smith — the hyperacute T waves and ST elevation in lateral chest leads persist.
  • BOTTOM Line: There are subtle-but-real ECG findings on these serial tracings. There has been dynamic change + persistent lateral chest lead abnormalities in the follow-up tracing ( = ECG #2) — which taken together, strongly support the premise of an acute ongoing event.



10 comments:

  1. Great case, Steve and Ken...

    I'm always amazed at the number of participants in my classes who have never heard of a Type 3 (wrap-around) LAD (they aren't beginners!). They are usually quite surprised to learn that the LAD can also cause inferior MIs. Then I ask them what percentage of LADs are Type 3. I typically get responses of 5% - 10%. They are shocked when I tell them that 75% - 80% of LADs are Type 3.

    Regarding Type 3 (wrap-around) LADs...

    When the occlusion is DISTAL to D1, the basal lateral area is unaffected which allows aVL to react reciprocally to ST changes in Lead III. Thus, in the first tracing we see reciprocal ST depression in aVL. Reciprocal changes are produced only when normal, non-ischemic myocardium is located under the lead electrode recording the reciprocal change.

    However, when the occlusion is PROXIMAL to D1, There will be STE in Leads I and aVL and also in II, III and aVF. Since the ischemic vectors are pointing in opposite directions, they will cancel each other and what results may be an ECG that is non-diagnostic for acute MI or - in some cases - an ECG that is completely normal. This may very well be a contributor to "non-STEMIs."

    With almost 80% of LADs being Type 3, think about how often this may occur.

    Great case and I congratulate the physicians involved on their excellent management of this young lady!

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    1. THANKS as always for your wonderful comments Jerry! I’ll add to your insightful explanation the caveats that — anatomic variations — prior events — multivessel disease — and unpredictable patterns of collateral vessels that may develop — may ALL complicate the resultant ECG picture. And then, some patients simply “don’t read the textbook” before they have their MI. That said — I’ve found the points you raise regarding the appearance of lead aVL to be especially helpful to me in determining whether LAD occlusion is likely to be more proximal or distal. THANKS again for your comment! — :)

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  2. Great post like always !

    Can we have a look on the r waves in the precordial leads ?

    - ECG 1 : the height of r is clearly decreasing from V1 to V2 and not growing from V2 to V3 as it should
    - ECG 2 : the height of r is now decreasing from V2 to V3 and from V3 to V4
    - Dynamic changes between ECG 1 and ECG 2 : r waves in V1, V4, V5 and V6 are exactly alike, BUT much taller in V2 and V3

    Thanks to Dr Smith for presenting this case !

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    Replies
    1. @ Gilles — THANKS for your astute observation — which is exactly the type of CAREFUL scrutiny that should be given when comparing tracings. So while you are correct that the subtle difference you mention ARE present — the next step is to determine what is “real” due to true dynamic ischemic change — vs what might be due to technical factors, including lead placement, patient movement, and the random variable in amplitudes that just occurs in “real life” between one tracing and the next (usually this is minimal, but does occur). This is NOT always easy to do — and the reason for the PEARL I give above, in which one has to “take it all in” — and then render an overall GESTALT impression to the best of our ability as to what is likely to be real vs not “real” (ie, not due to dynamic ischemic change). Remember — ECG #1 was prehospital — and ECG #2 was done IN the hospital ED — so definitely 2 DIFFERENT teams did the ECG. This greatly increases the chance of at least slightly different lead placement. My “gut” ( = my opinion) is that R wave progression in ECG #1 is appropriate. I don’t have explanation for why S waves in V1,V2 in ECG #2 are significantly deeper than they are in ECG #1 — but I don’t think ( = my opinion) that this change in amplitude alters my overall impression ( = Gestalt) that the ST-T wave appearance in lead V2 of ECG #2 is significantly DIFFERENT (now coved) compared to what it was in ECG #1 — but that the shape and amount of lateral chest lead ST elevation is about the same. ON the other hand — DESPITE the change in frontal plane axis, I have NO doubt that inferior lead ST elevation in the inferior leads has for the most part resolved in ECG #2, as has the reciprocal ST depression we initially saw in lead aVL. BOTTOM LINE — This meticulous lead-to-lead comparison IS challenging, it is NOT a “perfect” science — but in my experience, you CAN usually come up with a “synthesis” of where any differences you detect are (or are not) likely to be due to dynamic ischemic change vs non-relevant technical factors. I hope this makes sense to you! THANKS again for your comment! — :

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  3. Great case. As per KEN GRAUER, "T waves are disproportionately taller-than-they-should-be". But how much? Is there some threshold? Thanks a lot again.

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    Replies
    1. Thanks for your comment. I’ll answer by relating something I long ago learned from my radiology colleagues = “It’s an Aunt Minnie”. What they mean is that you could spend ALL day trying to describe how Aunt Minnie looks — and you might still not be able to distinguish her from other elderly women her age in a crowd. But once you SEE Aunt Minnie — then chances are you will NOT forget what she looks like! SAME HERE. I have NO “formula” for saying “how much” is “too much”. It’s that “Gestalt impression” I refer to above — based on too many components to specify (overall appearance of the tracing; relative amplitude within each lead of QRS-to-ST-to-T, etc.) — but after a while your comfort level increases in recognizing ECG findings that just should NOT be there. And when the clinical setting is right (ie, new-onset chest pain) — and when you see things that should NOT be there in MULTIPLE leads — then after a while you KNOW what is and what isn’t within reasonable expectations of “normal”. Hope that helps — :)

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    2. Ken...

      If I could add my own story re: hyperacute T waves... I have a neighbor who owns a chain of men's "Big and Tall" clothing stores. I asked him what percentage of his customers were over 7 feet tall. He smiled and said "Everyone focuses on our tall customers while our income is mostly from the short and big." And that's how I view hyperacute T waves - the width is where most of your observation should focus - not the height. Take a couple of weeks and focus on T waves in the mid-precordial leads. How many T waves are greater than 50% of the height of the R wave? How does the width of the T wave compare to the length of the ST segment? Then pull up some ECGs on the internet and look at some actual MIs and their T waves. Before you have a "feel" for the abnormal, you must have an even better feel for the normal. And I certainly agree with you that there is no threshold or template for recognition. It takes practice and experience.

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    3. We will be trying to do this in a current study. The solution to the problem is to teach a neural network what is and what is not a hyperacute T-wave. After thousands of cases, it will be able to do so as well as an expert, or perhaps even better.

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    4. @ JERRY — Thanks for your own story. When I say, "T waves that are bigger-than-they-should-be" — this actually includes my own "internal Gestalt" of not only too tall, but too "fat" at the peak of the T wave, and too broad at its base (ie, I agree with you that height per se is NOT the key finding ... ). @ STEVE — Why am I NOT surprised that you are also studying this issue regarding whether T waves are or are not "hyperacute"? CREDIT TO YOU for always being at the forefront of ECG research!!! I have no doubt that deriving formulas on this issue WILL help (just as your 4-parameter formula HELPS MANY in assessing the difference between a repolarization variant vs early acute anterior OMI) — though as a "qualitative interpreter" — I suspect I will still prefer to assess T waves by my "internal Gestalt" (though I have NO DOUBT that providing less experienced interpreters formula assistance WILL help them A LOT!). I'll look forward to seeing the results of your study! — :)

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    5. This is what I believe, and what we are studying:

      Primary hypothesis: the ratio of total AUC of the ST- T-wave to total QRS amplitude (total of R-wave +S-wave and/or Q-wave) is the best differentiator of hyperacute T-waves from non-hyperacute T-waves.

      Secondary hypothesis: the ratio of total AUC of the ST-T-wave to R-wave amplitude or S-wave amplitude (whichever is greater)

      So this will include both height and width, as both determine the total area under the curve. And even very small T-waves can be hyperacute, if the AUC to QRS ratio is still large (i.e., QRS is small)

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