Saturday, June 18, 2011

Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 ng/ml)

This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. 

3 hours prior to calling 911 he developed typical chest pain. 

The medics recorded this prehospital ECG at 1535:
There is ST elevation and tall T-waves in precordial leads, with reasonably good R-wave progression.  He is a 45 year old male, so this could be male pattern benign early repolarization (BER, or ER).  But it could be anterior STEMI.  40% of anterior STEMI has upward concavity in all of leads V2-V6.

How can one decide whether this is ER or MI?  First, if an old ECG is available, then compare.  Only rarely does early repolarization change from date to date, though it is possible. 

Second, I have developed a score that helps to differentiate the two.  His BER score, based on ST elevation at 60 ms after the J-point in lead V3, QTc (400), and R-wave amplitude in V4 is 23.9 (> 23.4 is likely anterior STEMI).

(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc) - (0.326 x RA in V4 in mm)

Third, one can do an immediate cardiac ultrasound.

Medics gave him nitroglycerine sublingual and his pain resolved.  He arrived in the ED and had this ECG recorded at 1544
It is essentially the same as the previous, and the score is again about 24 (MI more likely than early repol).  Also, compare with the patient's previous ECG below; concentrate on reciprocal leads III and aVL.  The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology).  The new ECG has relative reciprocal ST depression in lead III, with ST elevation in aVL.  This rules out pericarditis, which essentially never has reciprocal ST depression.


Here is a blow-up of V1-V3:

A previous ECG was found:
This has no ST elevation, and T-waves are not tall.  Notice the ST elevation in lead III that follows a deep Q-wave. This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology".  LV aneurysm is very different for inferior vs. anterior MI.
Here is V1-V3 of the old ECG:

The patient remained pain free, and this ECG was recorded at 1606:

Here is V1-V3:

He remained pain free.  A bedside ultrasound was done by an emergency physician and simultaneously read by a cardiologist.  They could see no anterior wall motion abnormality.  Diagnosis of ACS was in doubt. 

His old angiogram was reviewed and it was known that his disease was not amenable to PCI.  He needed CABG.  He was therefore treated with eptifibatide, heparin, and aspirin, and referred for CABG, but not immediately.

The next AM, this ECG was recorded:
There is some residual ST segment elevation.  The T-waves are far less tall. 
Here is V1-V3:

8 days later.  All ST elevation resolved.

Here are V1-V3 8 days later:
There is finally no ST elevaton whatsoever
It is often difficult to see changes unless they are directly side-by-side.  Here are V1-V3 from start to finish.  I did not include the prehospital because it is identical to the first ED ECG:
Self explanatory, no?

All troponins were undetectable (< 0.04 ng/ml). 

The patient had a critical LAD stenosis.  Flow had spontaneously been restored, perhaps aided by nitroglycerin.  He underwent CABG.  

Conclusions:
1.  Anterior STEMI can look very much like early repolarization.  There are means to distinguish the two.
2. Transient ST elevation is very hazardous.  Even when the serial troponins are negative, the ECG is critical to the diagnosis of ACS. 
3. When flow is restored, wall motion may completely recover so that echocardiogram does not detect the previous ischemia.
4. This is not pericarditis because:
            a. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG)
            b. There is relative reciprocal ST depression in lead III.
                      Pericarditis does not have reciprocal depression.
            c. ST elevation of pericarditis  is maximal in leads II and V5, V6. 
                      Here the ST elevation is maximal in V2-V4.
            d. Pericarditis does not have hyperacute T-waves.
            e. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL.

6 comments:

  1. Hello everyone.

    In the first EKG we notice widespread ST elevation without mirror and PR depression, in aVr there's ST depression with PR elevation : why don't we consider the diagnosis of pericarditis ?

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  2. 1. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG)
    2. Pericarditis ST elevation is maximal in leads II and V5, V6. Here the ST elevation is maximal in V2-V4.
    3. Pericarditis does not have hyperactue T-waves.
    4. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL.

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  3. This is one of the lowest QTc by far I've seen with ACS. Thanks. BTW, our interventionist won't even look or consider QTc as a possible help for those unclearcut ECGs.

    On another issue, Dr Smith would you comment on the supersensitive TnT that is out in some hospitals. Ours have it at pg/mL. I don't know if I would just have to multiply the ng/mL by a factor of 100 to get the equivalent in pg/mL

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  4. Remember, this is only to be applied when the question is: is this ER or anterior STEMI? Then the QTc by itself, unless very high (> 430 = 90% specific, > 440 = 95% specific) or low (< 384 ms = 95% sensitive) is not great, but combined with STE and R-wave in the equation, it works well.

    As for troponin, you'd have to tell me exactly which assay you're referring to. The product, whether troponin I or T. The critical information is its 99% reference value, its limit of detection (LoD), and its 10% coefficient of variation (CV).

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  5. I know this is a shot in the dark but do you have sensitivity, specificity of QTc for ER too?

    The 99% percentile is at 14 pg/mL of Troponin T, there was also a lab qualifying statement of WHO criteria:
    30-60 pg/mL - equivocal for MI
    >60 probable

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  6. It all depends on the cutoff. And you have to remember this is in my study of patients whom cardiologists call "ER" and who have at least 1 mm STE in one lead. Versus patients with LAD occlusion that is not obvious. For this group, 384ms was 95% sensitive for MI, but only 44% specific. >438 was 95% specific for MI, but only 29% sensitive. The AUC of the ROC curve for QTc was 0.82. Pretty good, but not great. The AUC for R-wave amplitude was 0.87.

    As for troponin, the 99% is the cutoff for MI or not, with appropriate rise and fall. So the 99% reference range cannot be 14pg/ml but 30-60 be "equivocal" and > 60 probable.

    It unfortunate, but interpretation of troponin levels is incredibly complex and impossible to cover in a blog posting.

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