Sunday, September 8, 2013

Male in his 50's with chest discomfort

A male in his 50's with a history of type I DM was riding his bike to work when he developed squeezing chest pressure and a sensation that "something wasn't right."   He rode his bike directly to the ED.  Here was his initial ECG:
There is very subtle, nondiagnostic (but suspicious) ST elevation in II, III, and aVF.  aVL is particularly worrisome as it has a biphasic T-wave (down-up) which is almost always ischemia. Down-up is usually reciprocal to reperfusing inferior MI, though there is no evidence of reperfusion in inferior leads.  V2 has a suspiciously flat/downsloping ST segment as well.

He was given one sublingual NTG and became pain free.  

There was, at this moment, no absolute indication for immediate angiography, as the patient was pain free and the ECG was not diagnostic of STEMI.  However, it is nearly diagnostic of ischemia, there is minimal ST elevation, and we know that a high percentage of NonSTEMI, when they do get their angiograms at 24 hours, have an occluded infarct-related artery even though the patient has remained asymptomatic.  These patients have larger infarct size, higher incidence of heart failure, lower EF, and higher mortality. 

Also, it was daytime, and the cath lab was free, so why not go immediately to the cath lab?

He went for immediate cath and had a 95% thrombotically occluded mid-RCA that was opened and stented, with thrombectomy.

Here is the post-cath ECG:
The inferior ST elevation is entirely resolved.  The T-wave in III is fully inverted (reperfusion), now with a fully upright T-wave in aVL (reciprocal to inferior reperfusion).  The T-wave in V2 is now larger and more upright (reperfusion).
The last troponin I measured was 1.0 ng/mL.  The echo showed a possible mid to basal inferior wall motion abnormality.  (Remember, wall motion abnormalities frequently disappear if ischemia is mild or brief)

The physician made a great call on this ECG; I like to think that, having seen so many similar cases here (as he had), made a difference.

See the very important question below in the comments section, and my answer.


  1. Is this a case of 'mission creep'? This is not a STEMI. Large trials (albeit a few years old now) only demonstrate benefit of Primary PCI for STEMI. I'm concerned if the recommendation is to expand the role of PPCI to include "very suggestive of ischemia" ECGs. You may be right that PPCI made a difference for this guy, but shouldn't we wait for the trial evidence to suggest we do more good than harm for a population before we recommend sending these type of patients for emergent cath? Very interesting case. Thanks for posting.

    1. That's a great question. The analysis of aVL is that it is "almost always" ischemia. So I don't think the diagnosis was in doubt in a previously healthy person with typical chest discomfort he had never had before. I did not say that emergent angiography is necessarily indicated, but it is clear that the patient will need it within 24 hours. It is daytime and the cath lab is free, so I asked, "why not take him now?". Is there a good reason not to take him now? There are good reasons to take him now, though no randomized studies to prove benefit of now over 24 hours from now. No randomized trial has ever looked at patients who have evidence of occlusion on the ECG but without meeting the diagnostic "criteria" for STEMI, but as I mentioned, those who have NonSTEMI have a high incidence of occlusion and worse outcomes than the NonSTEMI without occlusion.

  2. great case, what i noticed is a suspecious T waves in V3 V4 so my question how were the other arteries specially LAD ?

    thank you a lot

    Dr bensekrane Lotfi Djilali

    1. Sorry I don't have access to the report on the other arteries. But to my eye, T-waves in V3 and V4 look normal.
      Steve Smith


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