This was a middle aged female with a h/o CAD who presented to the ED by EMS sudden onset of central chest pressure 45 min prior to ED arrival with associated diaphoresis and SOB.
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| There is LVH and there are ST-T abnormalities (large inferior T-waves and ST elevation, with reciprocal findings in aVL). There are also suspicious T-wave inversions in V2-V5; they look like Wellens' waves in V4 and V5. Though the ST Elevation does not meet STEMI criteria, it is an obvious OMI. |
In LVH, just like in BBB, the ST segment (and T-waves) are often discordant to the majority of the QRS (ST elevated if QRS negative, as in inferior leads, or depressed if QRS mostly positive, as in I and aVL). Here is a previous post that demonstrates this.
In this case, the inferior ST elevation appears to be too much to attribute it to LVH alone.
The cath lab was activated but the interventionalist cancelled the activation.
However, then a previous ECG was located:
This confirms that the inferior ST elevation is new and thus due to acute OMI.
However, then a previous ECG was located:
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| Previous ECG has LVH in aVL, but no "secondary" ST-T abnormalities. This demonstrates that the precordial T-wave inversion is new as well. |
This confirms that the inferior ST elevation is new and thus due to acute OMI.
This case was written in 2012, before we changed the paradigm to OMI/NOMI and years before the Queen of Hearts was in use.
Now, in 2023, I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:
Here is the ECG after PCI:
The culprit was 100 % thrombotic occlusion of the mid RCA. The Peak troponin I was 47 ng/ml (equivalent to 47,000 ng/L) -- a very large infarct. There was a regional wall motion abnormality in the inferior and posteriorior walls. The LAD was not involved.
This was called an NSTEMI by the cardiologists. Of what use is this nomenclature if a case such as this is called a NonSTEMI? There is occlusion of the infarct-related artery and ST elevation, but because it is not 1 mm at the J-point, it is arbitrarily called a NonSTEMI.
Had the patient not undergone immediate reperfusion therapy, much more myocardium would be lost.
That is why using any millimeter criteria for diagnosing STEMI is very insensitive (it is also nonspecific, as in LVH, BBB, early repol, etc.)
Great case Dr. Smith...
ReplyDeleteIt looks like RAE and concurrent LVH and RVH, with an RVH strain looking pattern in the first ECG that is not there in the older ones, if that is even correct.
How does concurrent LVH and RVH with strain pattern confound our ST segment analysis, if at all? Things become apparent with an old ECG that are not so apparent without it.
thanks,
David B
Dave, I don't see the RVH. There is RAE with the peaked tall P-wave in lead II, but the axis is normal, no S-wave in I, no tall R-wave in lead V1, so no RVH. Or am I missing something?
ReplyDeleteSteve
No, i am sure you are not missing anything.
ReplyDeleteWhat caught my eye was the RAE, the tallish R waves in V1-V4, and what looked like a RVH/strain in V1-V3, if the T wave inversions were not due to wellens. I have seen similar looking morphology attributed to RVH/Strain. Granted, they were only present on the first ECG.
Also, I did note the normal axis and lack of S waves, but I did not know if they were necessary for RVH to be present, and I did not know how concurrent LVH would change things.
Anyhow, if it's not there, it's not there! Thanks for your reply.
Thanks Dr Smith,
ReplyDeleteI was so busy looking at the biphasic anterior T waves it took a while before I looked at the inferior leads.
I think there is 1mm of elevation in lead III and aVF, I think that the j wave seen in lead II scews the J point in leads III and aVF. I think if you drew vertical lines the way you did in previous posts on BCT to find the J point as it appears in lead II that just on 1mm of STE in both III and aVF are met.
Regards
Matt
Steve,
ReplyDeleteGreat case- no one mentioned this, but this dead give away here are the absolutely classic Ischemic Hyperacute T Waves in the inferior leads!!
Sam
Absolutely!
DeleteAgree with Sam Ghali — what immediately caught my eye was also those very abnormal-looking much fatter-than-they-should-be T waves in each of the inferior leads. In a patient with chest pain, I’d call these hyperacute until proven otherwise (regardless of the ample QRS voltage that we see).
ReplyDeleteOtherwise — I disagree with Dave B, and would not call “RAE” on this 1st tracing. Although the P wave in lead II is peaked, it falls shy of the required 2.5 mm height for RAE, and the P wave axis is also NOT what one typically sees with RAE (in which there are tall, peaked P waves in each of the inferior leads). That said, it is well to keep in mind that both sensitivity and specificity of the ECG for atrial enlargement is poor. It is especially poor for LAE. It can be a bit better for RAE — but not when P wave axis is so “off” as it is here …
Otherwise — NICE case Steve!
Dr. Smith, in this case there are ST-T changes in precordial leads look like "Wellen waves" but the culprit is RCA, so I think these inverted T waves is the mirror-image of hyperacute T waves of posterior wall. What's your opinion?
ReplyDeleteI think that is true of V2 and V3, but this is an inferior, posterior, lateral MI. That the T-waves in V5 and V6 are inverted after PCI shows that this is reperfused lateral MI as well. Why are they already inverting PRIOR to PCI? Not sure, but there may have been some differential reperfusion due to collaterals, such that while there was still STEMI in inferior leads, there were reperfusion T-waves in lateral leads.
Delete