Saturday, January 15, 2011

Not all cases with reciprocal ST depression are acute STEMI

This patient has concentric LVH and presented with chest pain.

There is sinus rhythm.  There is high voltage in aVL and typical "hockey stick" appearance of the ST-T complex (LVH with repolarization abnormalities. This also results in reciprocal ST elevation in inferior leads. 
Due to the ST elevation in leads aVF and III, with reciprocal ST depression in I and aVL, the cath lab was activated.  Coronaries were normal.

Later review of old records showed this to be her baseline ECG.

Without an old ECG to compare, one would be very suspicious of inferior STEMI. One should know that not all reciprocal ST depression is due to STEMI.   Inferior LV aneurysm, WPW, LVH, and LBBB may all have inferior ST elevation with reciprocal ST depression in aVL.
Here is an example of this in LV aneurysm:
http://hqmeded-ecg.blogspot.com/2010/10/tachycardia-must-make-you-doubt-acs-or.html


Had the treating physicians known this, they might have looked for the previous ECG and realized that the patient was not having a STEMI.

Conversely, absence of any reciprocal ST depression of any amount almost completely rules out inferior STEMI. We presented this research in Boston June 2011 SAEM.  Here is the abstract:

In acute inferior STEMI, Reciprocal ST depression in aVL and T-wave inversion in aVL are both more sensitive than ST elevation criteria and appear earlier in the course of STEMI
Christine Worrall
Emily Vogel
Stephen W. Smith

Background:  A previous study found that reciprocal ST depression (rSTD) is present in only 82% of inferior ST elevation (STE) acute myocardial infarction (MI).  However, we believe that changes in lead aVL are far more sensitive.  Objectives: To find the incidence of any rSTD or T-wave inversion (TWI) in angiographically proven inferior STEMI.  Methods: We searched the catheterization laboratory database for all cases coded as acute Inferior STEMI from January 2002 through March 2008.  All cases were reviewed and the presenting ECG, as well as the first ECG that was used for diagnosis of acute STEMI, were analyzed.  “True STEMI” was defined as 100% occlusion or as a culprit lesion with maximum troponin I (trop) > 10 ng/ml.  STE was measured in leads II, III, aVF; aVL was scrutinized for any rSTD or TWI.  TWI was defined as a T-wave mostly down, or a biphasic T-wave that is first down, then up (not up then down, which is associated with lateral AMI).  Reperfusion criteria were defined as STE of at least 1 mm in 2 of 3 of inferior leads II, III, aVF.   Results: There were 160 unique cases.  107 had 100% occlusion, and 35 had < 100% occlusion, but had a maximum trop > 10 ng/ml, for 142 true STEMI; 18 (11%) had < 100% occlusion and a max trop < 10 ng/ml.  85% of the diagnostic ECGs of true STEMI, and 84% of all cases, met STE criteria.  No true STEMI had absence of reciprocal depression in lead aVL. Of the 107 with 100% occlusion, 100 (93%) had at least 0.5 mm of rSTD; the remainder had rSTD of < 0.5 mm.  Even among those without true STEMI, 94% had some rSTD in aVL.  Additionally, in 44 cases (28%), there was no STE whatsoever on the presenting (first) ECG; all of them had either rSTD or TWI.  See Table.  Conclusion: STE criteria for inferior STEMI are insensitive, especially on the presenting ECG.  Changes in aVL, both some amount of rSTD and also TWI, are more sensitive than STE criteria in the diagnosis of inferior STEMI and are nearly universally present in inferior STEMI.  These changes also appear earlier than STE.

5 comments:

  1. Hearing these things sort of rocks the world of the initial prehospital provider education :) However, without access to prior ECG's I would likely call a STEMI, although I don't quite have 1mm in 2 leads.

    ReplyDelete
  2. This question might be a little off topic but since measuring STE or STD is important in almost every ECG I will still post it here:

    Every Book or paper on ECG gives me a different "rule" of how and where to measure th ST Segment alterations. The problem is, if doctors can't even agree on where to measure STE, how can such clear guidelines like "STE >2mm" be used consistently in practice?

    Here are some examples I found:
    - STE at the J-point, use end of PR as baseline
    - STE at the J-point, use TP as baseline
    - STE at 60ms after J-point, use TP, others say use PR
    - STE at 80ms after J-point.... etc. etc.

    I am VERY confused! Since there doesnt seem to be a consensus on the method, I will strive to copy the method you use Dr. Smith, being a true expert in theory AND in practice.

    Could you comment on the "best" method to stick to? Thank you very much!

    ReplyDelete
  3. This is so true.

    In fact, studies show that a subjective interpretation of ST elevation diangoses MI (by biomarkers) better than any ST elevation critierion.

    I just completed a study, submitted as abstract and as part of my paper comparing 171 early repol to 143 proven subtle anterior STEMI, that compared the diagnostic characteristics of 12 different STE criteria. The best criterion was the one below, as measured at the J-point relative to the PR interval. Sens, Spec, and Accuracy were: 67%, 54%, 60%. In other words, the best criterion performed miserably. My corresponding logistic regression equation numbers were 86%, 91%, and 89%. This takes into account the R-wave amplitude in V4 and the QTc, as well as ST elevation at 60ms after the J-point in lead V3.

    Rule that performed the best (Sens, Spec, and Accuracy were: 67%, 54%, 60%):

    ≥ 1mm in V1, V4-V6;
    ≥ 2 mm V2-V3 (men);
    ≥ 2.5mm in V2-V3 (men < 40 years old);
    ≥ 1.5mm in V2-V3 (women)

    ReplyDelete
  4. As a pre-hospital provider with this I would Think cath lab activation would be something to consider. Also i have to call the hospital in my town to go to the cath lab that is 25 minutes away. I would probably call and ask to go to cath hospital with this patient due to this ecg. So I am asking is it wrong to think this is a STEMI and go to a cath hospital.

    ReplyDelete
  5. If you are uncertain, and depending on how many false positive activations your cath lab resources will allow, it is not wrong to activate. But the better you get at reading the ECG, the less likely you'll have false positive activations which may deplete limited resources (especially fatigue in on-call personnel).

    ReplyDelete