Guidelines would (erroneously) say that this patient who was defibrillated and resuscitated does not need emergent angiography

A patient had a cardiac arrest with ventricular fibrillation and was successfully defibrillated.

Here was his initial ED ECG:

Formal interpretation by interventional cardiologist:

There is "Non-diagnostic" ST Elevation in V2-V4 and aVL.  

Therefore, according to ACC/AHA guidelines based on the COACT and TOMAHAWK trials, this patient should not go emergently to angiography.

But there are hyperacute T-waves and this is obviously diagnostic of a proximal LAD occlusion.  It can't be anything else.

Would you enroll this patient in a study that randomizes patients with VF arrest to immediate vs. delayed angiography?

Of course you wouldn't!!  Because the diagnosis is obvious.

The PMCardio Queen of Hearts AI bot knows it is OMI with high confidence:

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The cath lab was activated in spite of the guidelines.

https://www.ahajournals.org/doi/10.1161/CIR.0000000000001194

The COACT trial was fatally flawed (see below).  They did not keep a register of patients who were not enrolled. A patient like this one would not be enrolled because no clinician (ER doc or cardiologist) would enroll such a patient.

A reliable study would keep track of all patients with shockable arrest and analyze the ones who were not enrolled to see their outcomes.  This study failed to do so.  The proof of this is that only 5% of patients enrolled had acute coronary occlusion.  This is FAR LESS than all other studies of shockable arrest.  

First high sensitivity troponin I = 4 ng/L (nearly below the limit of detection)

Angiogram:

--Culprit is 99 % stenosis in the proximal ostial LAD

--LCX is a large OM with a large lateral segment, the lateral segement has a diffuse 90% disease in the ostial proximal segment of it. It will be staged later on this admission.

Echo:

Decreased LV systolic performance with estimated ejection fraction of 35 - 40 %.

Regional wall motion abnormality- mid to distal septum, anterior, anterolateral and apex.

Troponin profile (peaks at 33,672 -- a large MI):

Post PCI ECG:

2 days later:

Summary of the COACT and TOMAHAWK

According to these 2 randomized trials (TOMAHAWK and COACT, references at bottom), there is no utility of emergent angiography for cardiac arrest "without ST Segment elevation."

These studies did not address OMI ECG findings!!!

--There were many problems with the COACT trial.  See my discussion at the bottom.

--And in the more recent TOMAHAWK, most patients were comatose and died of cerebral anoxia.  So if the patient is awake and has ECG OMI findings, there is no reason to believe that angiography should be withheld.

COACT:

The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab.

Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. N Engl J Med [Internet] 2019;Available from: http://dx.doi.org/10.1056/NEJMoa1816897

Should all patients with shockable arrest be taken to angiography regardless of STEMI or No STEMI?

There has long been controversy about whether to take patients with a shockable rhythm without ST Elevation to the cath lab, and a recent randomized trial showed no benefit: Coronary Angiography after Cardiac Arrest without ST-Segment Elevation (COACT).  This study had a fatal flaw: they did not keep track of all the "Non-STEMI patients" who were NOT enrolled, but instead were sent for immediate angiogram.  It was done in Europe, where the guidelines suggest taking all shockable arrests emergently to the cath lab.  So it is highly likely that physicians were very reluctant to enroll patients whom they suspected had Occlusion MI (OMI), even if they did not have STEMI. These physicians did not want a patient with an OMI that was not a STEMI to be randomized to no angiogram.  This strong suspicion is supported by their data: only 22 of 437 (5.0%) patients in this study had OMI.

What percent of shockable arrests without STE have an OMI?  

This large registry in Circulation 2010 reported that at least 1 significant coronary artery lesion was found in 128 (96%) of 134 patients with ST-segment elevation on the ECG performed after the return of spontaneous circulation, and in 176 (58%) of 301 patients without ST-segment elevation. 

5% vs. 58%!!  It is clear that there was signficant enrollment bias in COACT.

We at Hennepin recently published this study

Sharma et al. (with Smith and others) found that among patients with shockable cardiac arrest who had OMI, the initial and subsequent pre-angiogram ECG were only 75% sensitive for OMI, with similar specificity.

Sharma A, Miranda DF, Rodin H, Bart BA, Smith SW, Shroff GR. Do not disregard the initial 12 lead ECG after out-of-hospital cardiac arrest: It predicts angiographic culprit despite metabolic abnormalities. Resuscitation Plus [Internet] 2020;4:100032. Available from: http://www.sciencedirect.com/science/article/pii/S2666520420300321

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MY Comment, by KEN GRAUER, MD (6/29/2024):

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The question of which patients who are successfully resuscitated following cardiac arrest should undergo prompt cath remains under discussion.

• As per Dr. Smith — the intuitive answer should be obvious. IF the initial ECG following successful defibrillation shows evidence of acute OMI — such patients have much to gain from immediate cath with PCI.

For clarity in Figure-1 — I've reproduced the initial ECG in today's case. As per Dr. Smith — the KEY resides with accurate assessment of this tracing.

• The rhythm is ventricular trigeminy (ie, every 3rd beat is a PVC).
• Sinus P waves are clearly seen in lead II. The QRS complex is wide — with QRS morphology most closely related to LBBB (Left Bundle Branch Block) — as determined by the predominantly upright QRS complexes in left-sided leads I and aVL. (Many LBBBs do not develop all positive R waves until more lateral leads than V6 — so the RS configuration in lead V6 here does not rule out LBBB).
• Regardless of whether you classified this conduction defect as "LBBB" vs IVCD (IntraVentricular Conduction Defect) — QRS morphology should be assessed as for LBBB.
• With LBBB — Q waves are not normally seen in leads I and aVL (as the normal left-to-right direction of septal depolarization is reversed as a result of the damaged left bundle branch — which leads to a right-to-left direction for septal depolarization that essentially eliminates "normal" septal q waves). Thus, the Q waves that we see in leads I and aVL of Figure-1 (especially the wide Q in lead aVL) — is indication that septal infarction has occurred at some point in time. As per the bullets below — that "point" in time is most likely the cause of this patient's cardiac arrest.
• 
  
• As per Dr. Smith — the most remarkable ST-T wave findings in ECG #1 — is the ST segment straightening and markedly disproportionate increase in size of the ST-T wave in lead V2 (within the RED rectangle). Despite the conduction defect — there is no way this ST-T wave in lead V2 could possibly be normal. Instead, this obviously hyperacute T wave in lead V2 suggests LAD OMI until proven otherwise.
• 
  
• The next most remarkable ST-T wave findings are seen within the BLUE rectangles (ie, within Leads I and aVL). Normally — the ST-T waves with simple RBBB or LBBB are oppositely directed to the last deflection of the QRS in these left-sided leads (For more on these findings with LBBB — Please check out My Comment in the September 17, 2020 post in Dr. Smith's ECG Blog).
• Instead, in lead I — the ST segment is not in the least depressed, and the T wave is upright in this lead (whereas in lead I with LBBB — there should normally be ST-T wave depression). This is a primary ST-T wave change, that in a patient with chest pain (or cardiac arrest) — indicates an ongoing acute event until proven otherwise.
• Even more remarkable — is the ST segment coving with hint of ST elevation and T wave inversion in lead aVL. This shape of ST-T wave in lead aVL is the opposite of the ST-T wave depression expected in lead aVL when there is LBBB. Simply stated — the shape of the ST-T wave in lead aVL looks like an evolving acute MI (and further supports indication of acute LAD occlusion).
• 
  
• In SUMMARY: In a patient who has just been defibrillated following cardiac arrest — it is hard to imagine how ECG #1 could be interpreted in any way other than representing acute LAD OMI in need of prompt cath with PCI. 

Figure-1: I've labeled the initial ECG in today's case (recorded after successful defibrillation).