Monday, March 1, 2021

Chest pain with ventricular paced rhythm - will you be able to rise above the STEMI paradigm and figure out what to do?

 Submitted by Marie Wofford MD and Mark Kastner MD, edits by Smith and Meyers


An 86 year old with prior history of CAD and PCI, aortic stenosis, pacemaker, atrial fibrillation on warfarin, hypertension, etc., presents with sudden onset mid back pain radiating to the left shoulder and chest. His vital signs were within normal limits with the exception of tachypnea at 22/min. The EMS ECG is shown below:

What do you think?



The ECG shows ventricular paced rhythm (the pacer spikes are barely visible to me in lead V2), resulting in almost LBBB morphology (LBBB morphology would require upright usually monophasic R waves in I and aVL, which is not present in this ventricular paced rhythm). 

There is STE in V1 through V5, and in leads II, III, and aVF. The inferior leads all show concordant STE, most less than 1.0 mm. In the precordial leads, the STE is excessively discordant (greater than 25% of the preceding S wave) in many leads in a row (see exact numbers below). 

Lead V5 is the transition lead, and it is difficult to say whether the positive or negative component is greater. 

When the QRS is nearly equally positive and negative, the ST segment should be isoelectric (no STE or STD).  Any STE in this situation is indicative of OMI.  

But this is an issue only for that one lead.  Several leads meet the Smith Modified Sgarbossa Criteria, and only one is necessary to make the diagnosis of OMI.

V1: 1.0 / 6.0 = 17%

V2: 3.0 / 17.0 = 18%

V3: 5.0 / 17.5 = 29%

V4: 3.5 / 12.5 = 28%

V5: 1.0 / 2.0 = 50%


This ECG is diagnostic of transmural ischemia involving the inferior and anterior / anterolateral walls, with the most common etiology being, of course, OMI. This combination of anterior and inferior makes a large LAD the most likely culprit (or at least whatever artery is acting like the LAD usually acts, supplying both of these territories).


Initial troponin I was 25 ng/L  (URL 20 ng/L for men, 12 ng/L for women).


He was taken for cath within an hour of arrival. 

RCA: ostial lesion, 99% stenosis, prior prior prox RCA stent which was patent

LAD: mid-LAD lesion 99% at site of prior stent, with "limited" collateral flow from first RV marginal to distal LAD

LCX: minor luminal irregularities

RPDA: 100% stenosis (unclear whether this was chronic)


The RCA lesion was deemed the culprit lesion and stented. There is no comment on the acuity of the mid-LAD lesion, but judging by the fact that they did not intervene on it and did not describe any reasons why they were unable to intervene on it, it seems to me that they thought this was not an acute lesion.

In retrospect, it does make sense to me in this coronary context that the RCA lesion alone could explain the ECG findings. At baseline, his RCA supplies both the inferior and anterior walls, because there is a severely limiting stenosis in the LAD with collaterals from the RCA. When such an RCA suffers acute OMI, both the inferior and anterior walls have acutely lost blood supply, causing a pattern that is much more commonly seen in large LAD occlusion.


Here is his ECG the next day:

Resolution of prior findings, and reperfusion T wave inversion in the inferior leads, as well as likely posterior reperfusion T waves.


Troponin I levels:

1900: 8,019 ng/L

2200: 10,207 ng/L

No further troponins measured.


Formal (noncontrast) echocardiogram on day 2 showed LVEF 55%, distal inferior hypokinesis, RV systolic function mildly reduced.


He was discharged 2 days later without further complications.


Learning Points:

Use the modified Sgarbossa criteria to evaluate for OMI in LBBB and ventricular paced rhythm (stay tuned for big publication on paced rhythm coming out soon!!!) The ACC/AHA guidelines give us no advice on how to diagnose OMI in paced rhythm. 

There is huge variability in coronary anatomy, but the ECG findings don't lie about which walls are infarcting.

Troponins are least when the benefit of reperfusion is maximal! This patient's initial troponin was barely over the URL for this assay.


6 comments:

  1. Is the results from PERFECT study finally about to be published? :) //Peter Hammarlund

    ReplyDelete
    Replies
    1. Peter, good to hear from you! Yes, it is In Press at the Annals of EM.

      Delete
  2. 『When the QRS is nearly equally positive and negative, the ST segment should be isoelectric (no STE or STD). Any STE in this situation is indicative of OMI.』->Why? Just for LBBB/paced rhythm or any rhythm? How to explain?

    ReplyDelete
    Replies
    1. Because it cannot be discordant or concordant if the QRS has equal positivity and negativity.

      Delete
  3. great review on modified Sgarbossa criteria once again
    I have been told that you can't identify culprit on ECG by using Sgarbossa criteria
    The following were copied from amal mattu's teaching point
    ""infarct localization or identification of the culprit coronary artery using the ECG in patients with a LBBB is inaccurate""
    Want to know your thought
    Great article once again

    ReplyDelete
    Replies
    1. I strongly disagree with that. We have a paper in Press at Annals of EM on the OMI in paced rhythm. Should be out soon.

      Delete

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