Thursday, April 25, 2019

Can you see through this paced rhythm?

Written by Pendell Meyers

An elderly female with known CAD and multiple stents, pacemaker, stroke, and COPD presented with 2 hours of midsternal, nonradiating chest pain at rest. Apparently on arrival to the ED the patient described her pain more as "crampy" abdominal pain, but also chest discomfort.

Here is her initial ECG during active symptoms:

What do you think?

There is dual chamber paced rhythm (atrial and ventricular pacer spikes) with resulting LBBB-like morphology. There is massive excessively discordant STE in II, III, aVF, as well as V4-V6. There is reciprocal excessively discordant STD in I and aVL. Additionally, if you use your eyes to correct for the upsloping baseline in V2, there is clearly concordant STD. Thus, this is an obvious OMI of the inferior, posterior, and lateral walls until proven otherwise.

The ratios are:

II: 5.5 / 7 = 0.79
III: 8.5 / 11 = 0.77
aVF: 5 / 9.5 = 0.53

V4: 3.5 / 9 = 0.39
V5: 3.5 / 6 = 0.58
V6: 3.5 / 3 = 1.17

Of course, the modified Sgarbossa criteria only require 1 lead with at least 25% (0.25).

Looking back at prior records, there were both paced and non-paced prior ECGs to compare with:

The EM and cardiology teams recognized this as a paced rhythm, and commented that there was "no clear STEMI in the setting of paced rhythm," which is true and appropriate in the setting of the current STEMI vs. NSTEMI paradigm.

They started medical management and consulted cardiology.

Approximately 45 minutes later, there was a spontaneous change in the rhythm on the monitor. The patient was still having symptoms at this time, and this repeat ECG was obtained:

Although there are still ventricular pacer spikes, the QRS is now narrow, meaning the ventricular pacer spikes are not responsible for the QRS complex, but rather near-simultaneous with anterograde ventricular activation from the intrinsic conduction system (most likely initiated from the atrial pacer spike). Obvious STEMI of the inferior, posterior, and lateral walls.

Now that it became obvious, the cath lab was activated.

At the time of cath they found a 95% thrombotic lesion of the ostial RCA. There was a large thrombus that required aspiration, resulting in a good angiographic outcome.

Post-cath ECGs showed the expected reperfusion pattern:

Peak troponin T was just over 10.0 ng/mL (very high).

The patient survived for 1 month but ultimately succumbed of cardiogenic shock and multiple complications thereof.

Learning Points:

In the current guideline recommended STEMI vs. NSTEMI paradigm, there is no such thing as a STEMI in paced rhythm. Our current paradigm has no comment on these patients, no recommendation for how we are supposed to decide which patients need emergent catheterization. 

This a powerful example of how the STEMI vs. NSTEMI paradigm distracts us from remembering that ACS is in fact an arterial occlusion syndrome. 

Because there is no such thing as STEMI in paced rhythm, many practitioners are blinded from the fact that their coronary arteries occlude just like any other patient without a pacemaker. For any other possible arterial occlusion, practitioners would have no confusion about what to do if a suspected arterial occlusion were in the differential but not easily accessible: they would emergently and definitively confirm or exclude the occlusion, rather than act like there was no occlusion.

Look out for our upcoming multicenter PERFECT study on the accuracy of the modified Sgarbossa criteria in the setting of paced rhythm. Hint: just like LBBB, it's the best we have.

Smith comment: this really illustrates the absurdity of the idea that one cannot diagnose MI in the presence of a ventricular paced rhythm.  One must take that idea to an extreme to not see the obvious STEMI here.

In this online quiz, 49% of respondants chose the answer: "One cannot diagnose an infarction from ventricularly paced complexes."

ECG Challenge: Is This Acute MI?  (you need to log in to Medscape to see it)

Comment by KEN GRAUER, MD (4/25/2019):
TRUE — It is often more difficult to diagnose an acute OMI in the setting of cardiac pacing. And, sometimes — it is simply not possible to diagnose acute OMI by ECG when there is pacing. But “sometimes” is not “always” — and as per Drs. Meyers and Smith, quantitatively or qualitatively ( = anyway you look at this! ) — the initial ECG in this case (which I’ve reproduced in Figure-1) — is OBVIOUSLY diagnostic of an acute STEMI in this older patient with known severe coronary disease and new-onset severe chest pain.
Figure-1: The initial ECG in this case. RED arrows illustrate the amount of abnormal ST elevation (See text).
Because assessment for acute ST-T wave changes is often more difficult when there is cardiac pacing — I begin by looking for one or more leads that I KNOW is (are) abnormal. The more leads in a given lead area that I can identify as definitely abnormal in a paced tracing — the most solidified is my diagnosis of acute OMI.
  • There should be NO DOUBT that the inferior leads in Figure-1 are of themselves absolutely diagnostic of acute STEMI despite the presence of a pacemaker. RED arrows indicate where the slope of the ST segment in these leads changes — and this is the amount of true ST elevation. In addition — note how “fat” (wide) the ST-T wave is in each of these leads. This is not a “normal” ST segment in a paced tracing.
  • Similarly — there should be NO DOUBT that leads V4V5 and V6 are also diagnostic of acute STEMI despite the pacemaker (RED arrows again indicating the amount of frank ST elevation). The shape of these elevated ST segments clearly establishes that something other than just pacing is going on.
  • Once established that these 6 leads are clearly abnormal — it becomes easier to recognize less striking changes in other leads that of themselves might not have been as readily recognizable. For example, in the context of abnormal inferior lead ST elevation — BLUE arrows in leads I and aVL indicate J-point ST depression consistent with acute reciprocal change. I would not have been as confident that this ST depression in leads I and aVL was abnormal without the obviously abnormal ST elevation in II, III and aVF.
  • Leads aVR and V1 are not helpful in diagnosis in Figure-1.
  • Whereas distortion/baseline wander of the complexes in lead V2 makes assessment more difficult — given obvious evidence of acute infero-lateral STEMI — the shelf-like shape with some ST depression, plus a much more pointed T wave than is usually seen in a paced tracing suggest from lead V2 that acute posterior MI is likely.
  • Lead V3 by itself would be difficult to assess in this paced tracing. By itself — I would not be certain that the relatively modest ST elevation with concave upslope to a fairly peaked T wave was abnormal. But in the context of the ST-T wave appearance in neighboring leads V2 and V4,5,6 — I think the ST-T wave in lead V3 is an extension of the clearly abnormal ST-T elevation seen in V4-thru-V6.
BOTTOM Line: The picture seen here of an acute STEMI despite cardiac pacing should be engraved in our memory. This picture should not be missedThere will be many paced tracings in which definitive findings of acute OMI are elusive. This is not one of them. On the contrary — Figure-1 is diagnostic of an extensive acute STEMI.


  1. Thank you for the nice case!
    Could you please explain why there is STE in V4-V6 if culprit is RCA?

    1. Occasionally the RCA is very large with large lateral and apical branches

  2. Even from QRSs originating from the ventricle (PVCs, QRSs during VT, accelerated idioventricular rhythm or ventricularly paced rhythm) STEMI can be diagnosed.
    K. Wang.

  3. If the only finding was a STE in avr, how would you localize the MI?

    1. Not sure why you're asking this here, but STE in aVR is always reciprocal to ST depression pointing toward the apex. The subendocardial ischemia represented by this ST depression does NOT localize the MI.

  4. Stephani HellwegeMay 6, 2019 at 2:36 PM

    Dear Dr. Smith and Dr. Mayers,
    this is a very high educational post. I may ask your permission to take this clinical case for educational purposes to show and discuss this topic with my colleges, cardiology residents and medical students as a presentation. Thank you very much.
    Many greetings from Germany.

    1. Stephani,
      Of course.
      Here are some other even better such cases:
      Steve Smith

  5. Thank you for this very interesting case. I will definitely be looking at your other posts.


    1. Andrew, it seems you've been looking through other posts for years!


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