Friday, January 29, 2016

Looking for a wall motion abnormality can lead you astray

A Middle-aged male presented with chest pain of 3 hours duration. He has a history of hyperlipidemia only.  There is pressure to mid-chest, radiating to the right arm, associated with diaphoresis.   He never had this before.  It was not related to eating.  There was no cough or fever, nor trauma.  There was no recent surgery, and no h/o thromboembolism.

Exam and BP were normal.

Here is the first ECG:  0526
There is ST elevation in V1-V4, with concave ST segments.  Is it ischemic, or is it early repol?
It does not meet STEMI "criteria," but we know they are insensitive
First, look for any reciprocal ST depression and you see it in lead III, plus some subtle STD in II and aVF.
There is a bit of ST elevation in I and aVL as well.
When there is reciprocal ST depression, it is likely to be LAD occlusion and the LAD occlusion formula may be falsely negative.
Indeed, if you do make the calculation, with STE60V3 = 4, QTc was 385, and R-wave amplitude in V4 = 20 results in 20.98, which is quite low

There was a previous ECG for comparison:
This is truly normal, without any significant ST elevation
You can see that the T-wave are now much larger than on the previous ECG.
These changes are diagnostic!


But the clinicians were not convinced.

So they did a bedside echo.  Here are 3 parasternal short axis views:








They read the echo as normal, without a wall motion abnormality.

Is it normal?



Comment: I think I see a clear wall motion abnormality of the anterior wall (closest to the transducer), but wall motion abnormalities are hard to see, especially for the non-expert, and especially without contrast or stress echocardiography (speckle tracking -- see these cases).



And then a repeat ECG at 0540
Not much different.


They proceeded to look for other pathology with ultrasound:

A bedside ultrasound showed a normal aortic root and distal aorta.  The gall bladder had no stones and a normal duct.  There was no abdominal free fluid and no hydronephrosis.  Chest X-ray showed no infiltrate and a normal mediastinum.  D Dimer was normal, and lipase was minimally elevated.

Cardiology was consulted by our Pathway B, and Nitroglycerine (NTG) initiated with a plan to maximize it to eliminate pain.

Another ECG was recorded at 0556:


Then the first troponin returned at 0.036 ng/mL (99% reference = 0.030 ng/mL).

Comment: A negative troponin does not help in acute coronary occlusion, because it may be too early to be "positive."  But a positive one in a patient with no baseline pathology (heart failure, renal failure) or reason for demand ischemia (sepsis, resp failure, etc.), but only with ischemic symptoms such as chest pain, tells you that an equivocal ECG is a positive ECG.


With a nitroglycerine dose titrated up to 60 mcg/min and a systolic BP of 90-100, the nitro could not be increased further.

The decision was made to activate the cath lab in the setting of elevated troponin, concerning ECGs, refractory typical pain, and no alternative explanation such as pericarditis or aortic dissection.

Another ECG was recorded at 0629:
Now there is more ST elevation and the change in the ECG itself is clearly diagnostic.


0822



At angiogram, there was a 100% mid-LAD occlusion, without good collateral circulation.  It was stented.

Here is the troponin profile:
Notice how the troponin suddenly rises after reperfusion and  release of troponin from the cardiac circulation.
The levels are quite high, consistent with a very large infarction.



Here is the ECG the next morning:
There is still significant ST elevation, now with T-wave inversion.  The persistent STE suggests that there is continued microvascular obstruction and is not a good sign.


An echo the next day showed:
Normal left ventricular size, thickness and systolic function.
The estimated left ventricular ejection fraction is 56%.
Regional wall motion abnormality-distal septum anterior and apex
hypokinetic.



Learning Points:

1. In a patient with real suspicion of MI and anterior ST elevation that does not meet STEMI "criteria," if there is inferior reciprocal ST depression, it is LAD occlusion until proven otherwise.  This is true even if the "early repol -- LAD occlusion" formula value is less than 23.4 (specific) or even if less than 22 (otherwise, a very sensitive cutpoint).

2. Compare with a previous ECG.  If there is a marked change, then it is likely to be due to ACS/coronary occlusion.    

Unfortunately, early repol is not completely stable: Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

3. Bedside echo has many great uses.  In suspected ACS, visualization of a wall motion abnormality may help to make the diagnosis of coronary occlusion, especially with speckle tracking; the positive predictive value is probably good.  But it is hazardous to try to rule out MI with limited bedside echo.  In this case, its use delayed care.

4.  Finally, the clinicians did a superb job by remaining vigilant, continuing to search for alternative causes and to monitor for ACS through serial ECGs, troponin, Nitroglycerine use and more.  This patient could easily have been just admitted for "rule out MI" and been left with a crippling cardiac injury.

5. Many NonSTEMI are due to coronary occlusion.  Early angiography with PCI saves myocardium.

21 comments:

  1. Great learning case, Steve!

    In the setting of typical ACS symptoms, one should always remember that reciprocal changes in the inferior leads due to acute ischemia of the high lateral wall - whether caused by an LCx occlusion or an occlusion involving the first diagonal branch of the LAD - may present well before the primary changes (i.e., STE) of the infarcting area.

    Thanks for a great blog!

    ReplyDelete
    Replies
    1. Jerry,
      They are USUALLY reciprocal to high lateral wall, but not always. The superior part of the anterior wall can produce a superior ST vector which will result in inferior ST depression. However, these are hard to differentiate, because high anterior wall and high lateral wall STE are both due to proximal occlusion.
      Steve

      Delete
  2. Thanks for the great case Dr. Smith, it's good to know the role of US in ACS. After looking through a bunch of BER cases yesterday, this looked classic BER, and I didn't catch that subtle ST depression! A good lesson to look closely.

    A couple questions/comments:
    1. The S-wave in V3 gets smaller as time progresses (and from his baseline) but you can also see a J-wave start to poke its head out concurrently, which makes me think that this likely wouldn't reach terminal QRS distortion because of that J-wave coming out. Is there a case where you've seen BER progress to terminal QRS distortion? Sorry, I can't seem to find one on the blog.

    2. Do you know what time the PCI happened? Was it between 0629 and 0822? Because that EKG at 0822 reminds of reperfusion Wellens' Waves beginning to form and I'm wondering if that was post PCI.

    Dan Lee

    ReplyDelete
    Replies
    1. Dan,
      the PCI was about 0730. There was no QRS distortion in this case.
      Case 1 in this post is a case in which the patient's baseline ECG did NOT have terminal QRS distortion. But when he presented with LAD occlusion it was present. Then after PCI, it was restored. That is the best I have for the dynamic nature of terminal QRS distortion.
      Good questions!!
      Steve

      Delete
  3. Dr. Smith

    thanks for another instructive case.

    The clinicians could not use “early repol-LAD occl” formula since there is inferior ST depression (in the present case honestly not very significant, at least in II e AVF)--by the way what about significant? Greater than --0,5mm?
    I do think the clinicians were rightly worried about the first ECG (STE at J point is 2mm in V2 and 3 mm in V3, almost fitting the guidelines cut-off), besides the other clinical features, not to mention III depression and quite fat V2-V4 T waves.
    Question: what about the patient after PCI? Did he undergo another angiography given the persistence of STE (see the last ECG)? Many thanks.

    Mario Parrinello

    ReplyDelete
    Replies
    1. Mario,
      I think even 0.25 mm ST depression in lead III is pretty specific. Early repol usually has a touch of ST elevation in lead III.
      He did not undergo another PCI. the artery was open. Unfortunately, sometimes when the artery is open, there remain significant downstream small vessel platelet fibrin aggregates that obstruct the microvasculature. This results in what is called "no reflow" (http://hqmeded-ecg.blogspot.com/search/label/No%20Reflow).
      Steve

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  4. Hey Steve,

    Great case! Regarding the use of Bedside Echo for evaluation of RWMA in assessment for ACS, a few comments:

    1. I agree - there is subtle anterior wall hypokinesis on the parasternal short clips here, but this is tough.
    2. If one is going to use Echo in the evaluation, I would always recommend multiple views as RWMA may be more salient on other views.
    3. Lastly, the use of serial ECGs in the assessment of ACS has become a well-known & widespread practice. (rightfully so - as this practice is invaluable!) Why? Bc the ECG evolves with time in acute coronary occlusion. The same is true for RWMA assessment. In this case, I assume the Echo was performed initially and not repeated. If one is going to perform an initial echo, I strongly recommend performing serial Echos along with the ECGs. Just as the initial ECG can be extremely subtle, then will involve into more obvious dynamic change consistent with acute coronary occlusion, so to does the Echocardiogram!

    Sam

    ReplyDelete
    Replies
    1. If the EKG is suspicious for an LAD lesion i would strongly recommend obtaining apical views, especially 2 chamber. The A2C is often the toughest TTE view to acquire (lots of lung artifact at the anterior wall), but there is a lot of bang for your buck as you can see 4 of the LV segments perfused by the LAD (basal, mid and apical anterior and apical inferior).

      Resting WMA's are horribly insensitive for the diagnosis of ACS, although Sam makes a good point that with an acute occlusion and ongoing ischemia, serial echo exams are more likely to reveal an abnormality. I am not going to debate whether or not an anterior WMA was actually present on the presented PSAX images (lack of thickening with appropriate inward excursion is my interpretation), it is simply a misapplication of a bedside diagnostic test by the physicians, although i'd contend that using it did not delay the patients care.

      As for speckle tracking strain, it is highly likely that longitudinal strain would have been substantially impaired in the anterior wall in this patient. Determining this would of course require apical views (4 chamber, 2 chamber and long axis). See the attached paper for the best study to date on using longitudinal strain to evaluate for ACS.

      mark

      https://www.dropbox.com/s/xsbv5ydc4t4bbks/Dahslett%20T%20et%20al.%20Early%20Assessment%20of%20Strain%20Echocardiography%20Can%20Accurately%20Exclude%20Significant%20Coronary%20Artery%20Stenosis%20in%20Suspected%20NSTEMI%20ACS.%20JASE%202014.pdf?dl=0

      Delete
  5. The anterior septum is not thickening as much as the other segments, maybe not so clear on the first clip, but on the other two.

    ReplyDelete
    Replies
    1. Ana,
      You have a good eye.
      Thanks for the comment!
      Steve

      Delete
  6. Appreciate your ECG blogs very much Steve,

    The parasternal short axis (PSSA) views ideally should cut through the papillary muscles to get a good view of the mid-LAD wall. Other than the end of the loop of the first video, the transverse cut is through much of the mitral valve thus demonstrating more of the base (top) of the LV. From the PSSA view at the papillary muscle level, one can also scan down toward the apex to pick up a focal apical wall motion abnormality--also well seen in a four chamber view. Good job by the ED team as usual. Ron Johannsen

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  7. Dear Steve,

    There's an obvious lack of R wave uprise in V2 and V3 lead, and a convex ST elevation in V1 in the 1st recorded EKG compare to the previous EKG recorded weeks or months before. In this case, the comparison (rarely available in my hospital) gives the Dx.

    ReplyDelete
    Replies
    1. Nicolas,
      We looked at V1 in our series of early repol, and it looked like this or worse in 14%. It was not a useful marker. Inferior ST depression certainly was. As you say, the comparison makes the diagnosis.
      Steve

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  8. GREAT case with lots of nice learning points. Agree there is subtle abnormality on the Echo — but for me, it is lead V3 in the 1st ECG that most heightened my concern. The T wave in V3 is just disproportionately tall with respect to the R wave and QRS in this lead. Given that — are the series of subtle-but-real findings in a bunch of other leads that should make one highly suspicious of an acute event just from this 1st ECG. Just to list them once more, these other findings are: i) ST segment flattening in aVF + slight ST-T dep in III (which in that context, makes the ST segment in lead II suspicious also because it is flatter-than-it-should-be); ii) slight-but-real ST elevation in both leads I and aVL; iii) relatively small r waves in V1 and V2 (not abnormal by itself — but consistent with early ant. stemi given the ST-T wave in V3; iv) ST coving and elevation in V1 (which by itself isn’t necessarily abnormal — but which is not normal given other findings seen on this tracing); and v) an ST-T wave in lead II that by itself wouldn’t be abnormal — but which is in my opinion suspicious given what we see in neighboring leads V1 and V3.

    And then when we find the prior tracing — the above findings become diagnostic because in addition to the change in ST-T waves — note how much larger anterior R waves were in the prior tracing …

    My point in mentioning this large list of admittedly VERY subtle findings is to highlight that it is the COMBINATION of findings (rather than any single finding by itself) that should lead one to be very suspicious in a patient with new chest pain of an acute event from ECG #1 — and to be able to confirm this once the prior tracing is found — regardless of what tropoinins might show. And it is in THAT context — that the subtle-but-real Echo abnormality can more readily be detected.

    THANKS for presenting this great case Steve!

    ReplyDelete
    Replies
    1. Oops — I meant to say in v) above an ST-T wave in lead V2 (not II) that by itself wouldn't be abnormal ...

      Delete
  9. Dr. Smith,

    thank you so much for your reply.
    Back to the Early Repol - LAD occl formula:
    why is it sometimes falsely positive in case of ST depression? It should not affect (at least from the mathematically point of view) the calculations on precordial parameters (ST60, QTc, R4 voltage).What’s your explanation.
    Many thanks again.
    Mario Parrinello

    ReplyDelete
    Replies
    1. Mario,
      It may be falsely NEGATIVE. I can't say the reason. But this is the fact: we excluded patients with inferior ST depression, and other exclusions which I consider to be "obvious LAD occlusion." My goal was to come up with a rule for the subtle cases only. I do not consider it subtle if there is inferior ST depression, so we did not either derive or validate the rule on cases like this. We just assumed they were positive.
      Steve Smith

      Delete
  10. I mean falsely negative, sorry.
    Mario

    ReplyDelete
  11. Great case there. Suprised they didnt see motion abn on ant wall. But also high suspicion made a good result for patient. Well done for whole team! Thx.

    ReplyDelete

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