Tuesday, February 15, 2011

Syncope, Chest pain: subtle, dynamic ST elevation and hyperacute Ts with preceding ST depression

This 63 yo male with no cardiac history had 30 seconds of syncope.  When he awoke, he complained of progressively worsening substernal chest pain associated with nausea and diaphoresis.  He had 2 prehospital ECGs and 4 hospital ECGs before he was taken to cath.  Here is the succession:

Prehospital ECG with ST elevation and tall T-waves that looks like early repolarization. The ST segment and T-wave in lead III should raise suspicions for LAD ischemia.

First ED ECG 0349.  There is an apparent junctional rhythm.  The ST elevation is gone.  The T-wave in lead V2 is no longer tall.  Lead III still looks suspicious.  LAD high grade ACS is certain with these changes.  This was not appreciated.  A Pulmonary embolism workup was done.

Second ED ECG 0432.  There is new ST depression in leads I, III, and V3-V6.  V3, with a large T-wave and ST depression, is "A New Sign of LAD occlusion" de Winter et al. N Engl J Med 2008;359(19):2071.  Still the cath lab was not activated.

See this post for more of these T-waves: http://hqmeded-ecg.blogspot.com/2009/02/hyperacute-t-waves.html


3rd ECG 0439.  Hyperacute Ts and ST depression mostly resolved.  The patient was admitted to cardiology.

4th ECG 0605.  Recurrence in V3 of hyperacute T with ST depression.
At this point, the patient was taken for cath. He was found to have 100% LAD occlusion just after the D1 takeoff, but also had a severe 90% RCA co-culprit ruptured plaque.The LAD was getting some flow through right to left collaterals, which explains the subtlety of the ECG.  Maximum troponin I was 36 ng/ml.

After cath and PCI.  The R-waves are gone.  There are only QS-waves in V2 and V3.  There is some persistent ST elevation.  There is T-wave inversion in aVL.
Next day ECG: T-waves are beginning to invert in V2 and V3

7 comments:

  1. God bless adherence to serial ECGs! I often encounter a single ECG similar to one of those above, and wonder where at in the evolution of ACS the patient is. It is lessons from cases like this that help bring me clarity in such situations.

    Thank you Steve!

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  2. is it just me or providers really love considering pulmonary embolism in a lot of cases, often at the expense of some other entity, as in this case?

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  3. Interesting observation. It does seem that physicians like to do workups for PE, when the diagnosis is much more likely to be ACS. Especially in this case in which there is syncope with bradycardia. If there had been syncope with tachycardia, PE would be high on the differential.

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  4. steve, in the first two ECGs you mean V3, not lead III, correct? I can't find much wrong with III - thanks!

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  5. No, I indeed meant lead III. It has a down-up biphasic T-wave which is highly suspicious as the reciprocal findings for ischemia in the area of aVL.

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  6. On the ECG recorded 4:39 there is a reduction in the R waves (compared to all the other ECGs) in V3-6 and also pathologic Q waves in these leads. The P waves are also smaller, so one would say in this case the V3-6 electrodes were placed too high. But the difference in the R waves are so big and the pathologic Q waves cannot be explained by lead misplacement.

    Maybe this was the result of ischaemia because of which some part of the anterior wall became electrically inert transiently.

    What do you think, Dr. Smith?

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    Replies
    1. I don't see the Q-waves, but I agree that there is diminution of R-waves. good observation.

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