This ECG is from an adult w/ h/o of HTN, dyslipidemia, s/p PM, smoker came in due to chest pain.
Figure 1 - ECG case
The strip shows pacing at 60 with AF as intrinsic rhythm + something else.
Do you see the difference when compared side-to-side?
Figure 2 - Side-by-side comparison of the ECG case (right side of the screen) vs. old ECG (left side of the screen)
Typically in paced rhythms the morphology is that of a left bundle branch block (LBBB) but as you can see here it is not the typical LBBB morphology that is seen in V1. This makes the usual Sgarbossa criteria for AMI in LBBB a challenge.
In the GUSTO-I trial by Sgarbossa EB, et al (17 pts with PM were analyzed -
(read this article and go back to the strip)
*They found that ST-segment elevation = 5 mm was most indicative of AMI in leads that had predominantly negative QRS complexes.
*Any degree of ST-segment elevation in a lead with a predominantly positive QRS complex was a highly specific sign of AMI. (***ST-segment elevation concordant with the QRS polarity is not expected in uncomplicated ventricular pacing)
*ST-segment depression in leads V1, V2, or V3, had a specificity of 82% for acute infarction (could represent either posterior “Q wave” infarctions or "ST depression (subendocardial)” infarcts.(***V1,V2 and V3 should not be present in these leads)
For the case, LHC revealed LAD lesion and intervention was done.
Other articles (free on the web):
Interesting post. First — I’m looking for the DATE that this post was made? (Did I miss it?). Second — I’m GLAD you told us that a pacemaker was present — because I otherwise just don’t see pacemaker spikes … (Did I miss those?).ReplyDelete
Third — It doesn’t say what Figure 2 is trying to show? Could you clarify what it is that you are showing on the left vs the right in that figure …
Fourth — I think the concept of recognizing likely acute STEMI in the setting of ventricular pacing can be far simpler than is put forth in Table 1 from that 1995 GUSTO-1 article by Sgarbossa et al that you reference. The one figure (from their too-small-to-develop-reliable-criteria retrospective series of 17 paced patients with acute MI) shows an obvious acute STEMI that NO specific “criteria” are needed to make the diagnosis.
So, to simplify — you are looking for “primary” ST-T wave changes beyond-that-expected for QRS morphology in the paced tracing. I submit that there really can be NO fully encompassing set of criteria that will cover all possibilities — because QRS morphology will just be different depending on specifics of the pacer and its location in the ventricles. What one looks for most is ST elevation in leads where it should NOT be present. In this example of this paced 12-lead (shown in your Figure 1) — there is subtle-but-real ST elevation in lead aVL that just shouldn’t be there. To me, the shape and amount of ST elevation in leads V2,V3 is clearly MORE than what I would expect for a simple paced rhythm. Therefore, in a patient presenting with new symptoms — these qualitative findings to me are clear suggestion that an acute STEMI may be evolving.
THANKS for considering the above comments.
Thank you sir for dropping some comments. This was posted 2.17.16. In this blog, I omitted the date of posting. The label in Figure 2 must have been deleted when I copied it from the original file. I will try to correct it. Figure 2 is the side-by-side comparison of the old ECG compared to the ECG case presented. I agree with your fourth comment. This post was intended to highlight STEMI can be diagnosed in paced rhythms. Again, thanks for the comments.ReplyDelete