Monday, February 8, 2016

Subacute STEMI. Should the patient go for emergent PCI, or can he wait until the next day?

This was sent by a very good medical student, who had a very good question.  He wishes to remain anonymous.

A 56 y/o male presented with Chest Pain radiating to the left jaw, starting at 8pm the previous night (15 hours prior), which was 10/10 at that time.  He decided to wait it out at home, then presented at around 11 AM, pain now reported at 2/10.

Here is the initial ECG (see the patient's previous ECG below for comparison):
There is sinus rhythm and new inferior QS-waves with less than 1 mm of inferior ST elevation, and reciprocal ST depression in aVL, and T-wave inversion.  
Such T-wave inversion is common not only in reperfusion, but in persistent and prolonged occlusion after formation of Q-waves, especially QS-waves.

Here is the patient's previous ECG:
This old ECG confirms that the first ECG shows a new MI

So this patient has a subacute STEMI.   

The initial troponin T returned at 0.47 ng/mL (quite high for Troponin T) and rose from there to 0.81, then 1.96 (typical of a large STEMI).  Whether the troponin continues to rise or not says nothing about ongoing ischemia: it takes time for complete troponin rise and fall even after infarction is completed.  Only the ECG and pain can tell you prospectively whether ischemia is ongoing.

The patient was admitted with "NonSTEMI" and did not undergo emergent angiogram and PCI.  He went the next day.

This is a nearly completed STEMI (a very advanced subacute STEMI). To call it a NonSTEMI is misleading.

Is it too late for emergency cath lab activation?  Should he go now, or with less urgency (tomorrow)?

My answer is this: 

If there is:
1) persistent ST elevation (as there is here) or 
2) persistent pain (as there is here)

Then the patient should go emergently.

But I know of no data to support this.

There are 2 excellent articles addressing whether a patient with completed MI should undergo PCI at all (vs. medical therapy alone), but none addressing this situation.

Schomig et al. published this in JAMA in 2005:  
Data presented shows benefit of PCI (vs. medical therapy alone) for patients who present between 12-48 hours after STEMI if there was persistent STE, or simply new Q-waveseven in the absence of pain.  But they did not assess the urgency of PCI.

Hochman et al. published the Occluded Arteries Trial (in the New England Journal).  
In this article, they assessed arteries occluded for 3 days or more, and found that PCI resulted in worse outcomes than medical therapy.

The question this student posed was slightly different: beyond 12 hours, is emergent PCI better than delayed PCI (both groups getting PCI).

ACC/AHA 2013 STEMI guidelines say this:

Primary PCI is reasonable in patients with STEMI if there is clinical and/or ECG evidence of ongoing ischemia between 12 and 24 hours after symptom onset (94,95). (Level of Evidence: B).  This means if there is chest pain, persistent ST elevation, or especially upright T-waves.

But the ACC/AHA guidelines do NOT address the timing (emergent vs. urgent) and they reference two studies, one of which is the Schomig article above, and the other of which also does not address emergent vs. urgent PCI.  

94. Schömig A, Mehilli J, Antoniucci D, et al. Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom onset: a randomized controlled trial. JAMA. 2005;293: 2865–72.

95. Gierlotka M, Gasior M, Wilczek K, et al. Reperfusion by primarypercutaneous coronary intervention in patients with ST-segment elevationmyocardial infarction within 12 to 24 hours of the onset ofsymptoms (from a prospective national observational study [PL-ACS]). Am J Cardiol. 2011;107:501–8.

Learning Points
1. I think if there is ongoing pain or ST Elevation, it is wise to go emergently to the cath lab to save any remaining viable myocardium.  Randomized data on this is lacking.  Probably, most researchers would be reluctant to test such management.  Similarly, no one has ever conducted a randomized trial of emergent vs. delayed PCI for NonSTEMI with refractory (continued) symptoms.
2. PCI at some point within the first 12-48 hours of STEMI is definitely indicated.

Dr. Goldsmith of our Cardiology Department added his opinion in an email:

This is a gray zone. Apropos of your general thinking that we should act to make a clinical difference and not just on the basis of guidelines (!) the issue of timing here relates to how much salvage is likely. Points in favor of going now: the relatively low trop on presentation (suggests possible opening/closing of an artery) with pain. If the trop had been 20 I probably would not have gone.....pain and ST elev are problematic guides because both can persist for many hours after there is no chance of successful reperfusion (MI pain in the old days required morphine for 24 hours, usually, as I remember from my residency!). So these are tough, and as you say there is no firm guidance. The low trop with a rise suggest a new event or recurrent event to me, rather than a done deal, so I probably would have argued for earlier study knowing it might or might not help but would not likely hurt. Perfect Pathway B case, by the way!


  1. GREAT case sent in by this astute anonymous medical student! Your review of the literature is appreciated! I’ll add a few comments to your excellent discussion.

    These 2 ECGs provide fertile ground for making a series of important points. The baseline (B&W) tracing showed sinus rhythm with LAHB and IRBBB (incomplete RBBB — as QRS duration is < 0.10 second with an rsR’ in V1 and narrow terminal s waves in I,V6). There is some nonspecific ST-T wave flattening, but nothing acute. In addition to the limb lead ST-T wave changes described by Dr. Smith — the T waves in V1,V2 are clearly more prominent in the new (RED) tracing compared to the baseline ECG (possibly with hint of ST depression). This is consistent with reperfusion following acute posterior infarction (so this was a recent acute infero-postero STEMI).

    It is interesting how while r waves were tiny in each inferior lead in the prior ECG — they nevertheless WERE present. These r r waves have now been replaced by the Q waves from the new inferior infarction. Note the notching in leads II and aVF at different points in the downslope of the S wave in the new tracing. There is often question as to whether a patient with a small r wave but predominantly negative inferior QRS complexes (as in the prior tracing) has had inferior infarction, LAHB or both. The presence of notching in the downslope of the S wave (as seen in the new tracing) — especially the kind that is seen in lead II of the new tracing where we have an initial negative deflection — then small positive — and finally deep negative deflection — is virtually diagnostic of inferior infarction. And, in the new tracing — I interpret QRS morphology as consistent with both LAHB + inferior infarction.

    As per Dr. Smith’s review of the literature — there are unanswered questions in the literature regarding when to take this patient to cath. I think it might be different if this patient presented at midnight and had no more than minimal chest pain — in which case the relatively limited potential for benefit from emergent cath in the middle of the night (as opposed to first thing the next morning) might easily be outweighed by potential detriment by having to mobilize all staff for a procedure that is most optimally performed during regular hours. But this patient presented at 11:00 am — so I completely agree with Dr. Smith that catheterization during this current working day would be what I would want if it were me or my loved one presenting to the hospital.

    THANKS again for presenting this excellent case!

  2. Dr. Smith,
    I wonder why that patient's ECG shows a R wave in avR? I have learnt that such phenomenon occurs when there is TCA toxicity, wrong lead placement or dextrocardia, but all the three seem not to be reason for this case, as both ECG show the same phenomenon and other leads do not suggest the latter two.
    Thank you!

    1. Good question. See Ken's note above. This is due to an incomplete RBBB.

  3. In red background there's no T wave inversion in lead avl & v2
    At the sametime in lead avl 1st two beat show less than 1mm depression & 3rd beat almost normal
    Dr Ken said about reciprocal changes pz elaborate

    1. Ilyas,
      With inferior T-wave inversion, you expect T-wave to be upright in aVL. III and aVL are nearly opposite. aVL has a reciprocally upright T-wave.
      As for reciprocal changes: I don't understand the question. There is clearly inferior ST elevation and reciprocal ST depression in aVL, though neither is 1 mm. We know that ANY such WPW, that it is almost always due to MI, whether new or old (LV aneurysm).
      Steve Smith


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