Saturday, December 4, 2021

Do these Serial Prehospital ECGs show OMI?

A 50-something male with a history of hypertension called 911 after sudden onset chest pain in the middle of his chest radiating up to his neck. He reports that earlier in the day he had some chest pain that came on while he was teaching that subsequently resolved with rest.  + Diaphoresis and SOB, no radiation to the shoulders. 

He had 3 prehospital ECGs recorded:

What do you think?

The 1st ECG is may appear normal, but is ischemic.  There is a very tiny amount of ST depression in V2, but there is definitely a bit of STD in V3 and V4.  

The 2nd ECG has clear STD in V2-V4 and slightly larger inferior T-waves.  

The 3rd has still larger T-waves in inferior leads.  There is now RBBB (but QRS is only 120 ms), with rSR in V1, but no R' beyond V1.  Without an R'-wave in V2, there is no reason to have ST depression other than posterior OMI (RBBB with rSR' usually is followed by some STD that is discordant to that preceding large R' wave).

So this is highly suspicious, if not diagnostic, of inferior-posterior OMI.

For reasons I can't explain to myself, I was skeptical when I saw these prehospital ECGs.  I should know without doubt that in the context of acute chest pain, ANY ST depression maximal in V1-V4 is highly specific for OMI.  After all, Pendell and I wrote the paper.  This shows that even I am biased by the STEMI paradigm.

He arrived at the ED and had normal VS and normal exam.

On arrival, he had an ED ECG recorded:

What do you think?

It is now clearly diagnostic of inferior-posterior OMI.  T-waves inferior are markedly different, there is new subtle inferior STE, there is reciprocal STD in aVL, and there is diagnostic ST depression in V2 and V3.

The cath lab was activated.  


After leaving for the cath lab, the first hs troponin I returned at 40 ng/L .  The URL for this assay is 34 ng/L for men, but a value with a high (70%) positive predictive value at Hennepin for type I MI (which includes BOTH OMI + NOMI) is 200 ng/L.  (We don't know which initial value, if any, has a high PPV for OMI).

Thus, an isolated initial value of 40 ng/L tells us little about the probability of OMI/NOMI.  In the context of acute chest pain, it makes a type I MI very likely.  Only the ECG can tell us if it is OMI or NOMI.

The peak Troponin I was 6534 ng/L.  This is quite high and is seen in some NOMI but more often in very rapidly treated OMI.

Angiographic findings:

1. Left dominant system (the circumflex supplies the inferior wall).

2. Left main: large, no significant stenosis.

3. LAD: luminal irregularities in the proximal to mid segment and focal 70% stenosis in the distal segment. Very small diagonals. The diagonal territory is supplied mainly by a Ramus intermedius with luminal irregularities.

3. LCX: dominant. Supplies an early OM, LPLA and LPDA. There is a severe 95% stenosis in the distal LCX in the AV groove distal to an LPLA and proximal to an LPDA (supplying the inferior and posterior walls).

TIMI flow is not mentioned.  A 95% lesion could have normal (TIMI-3) flow, or it could have lower than normal TIMI 1 or 2 flow.  However, the ECG tells us that flow was not normal at the time of the ECG.  It might have been normal at the time of the angiogram.

4. RCA: non-dominant, no relevant stenosis.

Formal Echo:

--Normal LV size, wall thickness, and systolic function with an estimated LVEF of 63%.

--Regional wall motion abnormality - hypokinesis of basal inferior and inferolateral segments.

So this is consistent with inferior-posterior injury, but (since EF was good) also with only a mild to moderate amount of injury.  This minimal injury is attributed to very fast treatment and the fact that the artery was open at the time of the angiogram.

In our studies, we defined Occlusion (OMI) retrospectively: if there was very low flow in the artery (TIMI 0/1) or there was a culprit PLUS a very high troponin, we assumed that the artery was occluded at the time of the ECG.  The definition of "very high troponin" varied (all used contemporary (not high sensitivity) troponins.  In the DIFOCCULT study, it was a troponin I of 5.0 ng/mL (approximately equal to 5000 ng/L for hs troponin).  In DOMI-ARAGATO 2 and in all studies of the Modified Sgarbossa Criteria, including PERFECT (paced rhythm), we used contemporary troponins Troponin I of at least 10 ng/mL (equivalent to 10,000 ng/L for high sensitivity) or troponin T of 1.0 ng/mL (equivalent to 1000 ng/L for hs-cTnT).  

Thus, it is unclear whether this patient would have qualified for our definition of OMI.  The artery was open, but we do not know the TIMI flow.  The troponin was above 5000 ng/L, but below 10,000 ng/L.

No comments:

Post a Comment

DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

Recommended Resources