Saturday, April 2, 2016

A Patient with Ischemic symptoms and a Biventricular Pacemaker

This case was sent by Gary Giorgio from Summa Health Emergency Medicine Residency in Akron, Ohio.  He frequently sends very interesting cases.


There are many who say that STEMI cannot be diagnosed in the setting of a ventricular paced rhythm.  In a recent survey, as part of a case posted on Medscape by my mentor, K. Wang, 48% of respondants answered that "One cannot diagnose an infarction from ventricularly paced complexes."


An elderly woman presented with 6 hours of arm, back, jaw pain, diaphoresis, and dyspnea (no chest pain!).  There was an unclear history of CAD as previous care was at another hospital.

Here was her initial ED ECG:
There is clearly a ventricular paced rhythm (VPR).  What else (ok, it's obvious)?

In right ventricular pacing, which was formerly by far the most common, the pacing lead was usually in the apex of the RV and, therefore, the depolarization vector was usually away from the apex, resulting in a negative QRS in all of V1-V6
Here, the QRS is positive in V1, which suggests left to right ventricular activation, at least of the septum.

Biventricular pacing 
(especially "cardiac resynchronization therapy") is common now because it has been shown to improve cardiac function in patients with heart failure who also have a QRS duration greater than 130 ms.   A biventricular pacer has a lead in the RV and a lead that goes through the coronary sinus (the large vein that drains myocardial blood supply into the right atrium) and then into a branch vein on the epicardium of the LV.  Its location can be somewhat variable.  Thus, the QRS morphology is variable.  

Nonetheless, the principle of appropriate discordance which we use in left bundle branch block, applies in paced rhythm.  Furthermore, it is my belief, based on many many cases, that the Smith-modified Sgarbossa criteria (both derived and validated) apply not only to LBBB, but also to VPR.   Thus, we expect the ST segment to be in the opposite direction from the majority of the QRS and to be proportional (ST elevation less than 0.20-0.25 of the preceding S-wave).

Here is one case that Brooks Walsh and I reported.
Here is another that I reported with Jeffrey Tabas and Sarah Schaaf (full text).
Both are in in JAMA Internal Medicine.

In this ECG, there is both:
1) Concordant ST elevation (same direction as QRS) in leads V2 and aVL
2) Proportionally excessively discordant STE in:
a) V3 (3.5/2 = 1.75)  
b) V4 (3.5/5.5 = 0.63)
c) V5 (2.5/7.0 = 0.36)

In this case, there was an old ECG for comparison:
VPR and QRS are the same.
All ST segments are appropriately discordant and NOT out of proportion.
This proves without doubt that the presenting ECG represents STEMI

The cath lab was activated and a 100% LAD occlusion was opened and stented.

The interventionalist noticed something very interesting on the monitor prior to opening the artery:
What do you see?

Here I have it annotated with arrows:
The red arrows indicate beats that are initiated by the pacer
The black arrows show pacer spikes that occur AFTER the beat has been initiated, creating a fusion beat

Notice that the fusion beats do NOT show the STEMI, but the Paced beats DO shows the STEMI.

This is counter to conventional wisdom (which is often not so wise) that states that no further interpretation is possible in VPR.

In this case, the VPR beats show the STEMI.  The Non-VPR beats do NOT show it.

Furthermore, the VPR showed reperfusion changes after PCI:
There is electrical alternans of unknown etiology.
There is resolution of most ST elevation (indicating reperfusion) and T-wave inversion ("Wellens' waves, reperfusion T-waves) in V2 and V3, and also in half of the V5 and V6 waves, depending on the QRS.
Thus, even T-wave inversion may manifest in reperfusion of VPR cases. 

Here is the next day ECG:
Deeper T-wave inversion, evolving just like in Wellens' syndrome (which is a condition of reperfusion of the LAD after brief occlusion).

Learning Point:

STEMI may be diagnosed in VPR!!

We are starting a large study of this, at multiple sites.  We'll see how well the Modified Sgarbossa Criteria work for VPR.

Dr. Ken Grauer has some great comments on this post here:

Ken Grauer If EVER you wanted to learn more about how you may sometimes see definitive evidence of acute STEMI despite permanent pacing — then I suggest you check out Dr. Stephen Smith's newest blog post in its entirety (at the above link). I just submitted the following Comment at that link on this insightful case:
KEN GRAUER wrote the following — GREAT case for illustrating a series of important findings and observations during stemi evolution in a patient with a pacemaker. As per Dr. Stephen Smith — Acute STEMI can be diagnosed in some cases of paced rhythms. In addition to assessing for inappropriate discordance — the 1st ECG shown here clearly manifests primary ST segment elevation in many leads, any one of which in an older patient with new-onset worrisome chest pain should by itself be enough to strongly suggest acute evolving stemi. My “Go-To” lead is often lead aVL — which in this case shows subtle but clearly abnormal ST elevation (with beginning T wave inversion). Almost regardless of amount — this shape is highly suspicious. QRS amplitude of the paced complex in lead I is small — but the ST coving and elevation in that lead (which “neighbors” lead aVL) is clearly abnormal. ST segment assessment in the chest leads show typical ST segment shape and elevation characteristic of acute anterior STEMI, which begins in V1 and is maximal in V3,V4. The key point that I’d emphasize from this obvious acute stemi — is that ST segment appearance in any ONE of the above leads in an older adult with new-onset chest pain and a pacer should be enough to prime your suspicion of an acute evolving event.

That the above ST segment changes noted are clearly acute becomes even more obvious with revelation of the patients baseline pacer tracing (2nd 12-lead posted).

There follows with the 3rd and 4th ECGs posted a highly insightful example of how in some cases stemi evolution can clearly be seen on serial tracings. Electrical alternans, as seen on the 3rd 12-lead — may be seen in severe ischemia/LV dysfunction, both of which were doubtlessly present.

Finally — the fascinating rhythm strip highlights several findings. As emphasized by Dr. Smith’s BLACK arrows — the first 3 beats are fusion beats, as the pacer spike occurs after (not before) the QRS begins. I suspect that the fusion here may be between the paced impulse with an accelerated ventricular focus (ie, AIVR) — as AIVR is a common associated rhythm with evolving stemi. And it looks like the 2nd and 3rd (but not the 1st) fusion beats manifest retrograde atrial conduction. Measurement with calipers suggests slight increase in the RP’ interval for the 3rd fusion beat compared to the 2nd fusion beat — which probably reflects retrograde Wenckebach conduction. I suspect that it is this slightly later retrograde conduction for the 3rd fusion beat that allows the pacemaker to sense atrial activity and put out a completely paced complex (ie, the 4th beat). It may be that the reason ST elevation is minimal for these first 3 fused beats is reciprocal change from opposing electrical activity (depending on the site of the AIVR rhythm) that in part cancels out the primary ST elevation.

Of interest — a spontaneous P wave (that is upright) precedes the 5th beat. This 5th beat is also a fusion complex — but this time, the fusion is between partial conduction from this sinus P wave with the paced complex. Note there is more ST elevation for this 5th beat than there was for the first 3 fusion beats — which suggests to me that if we did see any non-paced spontaneously conducted P waves, that they might indeed show similar ST elevation as seen in the completely paced complexes on the 1st tracing.

Finally — AIVR-and-paced fusion resumes for the last 3 beats in the rhythm strip. Note similar amount of ST elevation and similar retrograde conduction for these last 3 AIVR-paced fusion beats as was seen for the first 3 AIVR-paced fusion beats. FASCINATING!

Thanks so much to Dr. Smith for posting this wonderful teaching tracing. Fortunately the patient’s acute evolving stemi was recognized despite permanent pacing, resulting in successful PCI.

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