A man in his 40's presented with severe back pain radiating to the chest. Here was his ECG, with pain:
This is diagnostic of hyperacute T-waves and LAD occlusion or subtotal occlusion. There are subtle de Winter's T-waves in V4-V6, in which the large T-wave is preceded by ST depression.
Apparently, it was not recognized (which is not unusual, this is subtle and difficult). Aortic dissection was on the differential diagnosis, and a CT of the chest ruled this out. Troponins were negative, the pain was resolved, and the patient was discharged.
He returned the next day with 9/10 back pain. Here was his ECG:
The fact that the T-waves are so different from the previous day's confirms the ischemia of the previous day. There is ST segment elevation in precordial leads. Is it normal variant ST elevation ("early repolarization")?
Even without a previous ECG for comparison, this is unlikely to be normal STE because of the poor R-wave progression. In our study of early repol vs. subtle anterior STEMI, only 5% of early repol had an average R-wave amplitude from V2-V4 of less than 5 mm. Here it is 1 + 2 + 9 = 12 divided by 3 = 4mm average. If you use the formula (see sidebar) which incorporates the ST elevation at 60 ms after the J-point in lead V3, and the QTc (393ms), then the result is 23.8, which is greater than 23.4 which indicates anterior STEMI.
His pain resolved spontaneously, and he had the following ECG:
The troponin returned positive this time and the patient went for cath and had subtotal stenosis of the LAD just distal to the first diagonal. It was stented.
I don't know the peak troponin, or echo results, or how much myocardium was lost. But here again is a "NonSTEMI" that really should be treated like a STEMI. The ECG 1 week later is consistent with significant myocardial loss:
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| What is your diagnosis? |
This is diagnostic of hyperacute T-waves and LAD occlusion or subtotal occlusion. There are subtle de Winter's T-waves in V4-V6, in which the large T-wave is preceded by ST depression.
Apparently, it was not recognized (which is not unusual, this is subtle and difficult). Aortic dissection was on the differential diagnosis, and a CT of the chest ruled this out. Troponins were negative, the pain was resolved, and the patient was discharged.
He returned the next day with 9/10 back pain. Here was his ECG:
 |
| What do you think? |
The fact that the T-waves are so different from the previous day's confirms the ischemia of the previous day. There is ST segment elevation in precordial leads. Is it normal variant ST elevation ("early repolarization")?
Even without a previous ECG for comparison, this is unlikely to be normal STE because of the poor R-wave progression. In our study of early repol vs. subtle anterior STEMI, only 5% of early repol had an average R-wave amplitude from V2-V4 of less than 5 mm. Here it is 1 + 2 + 9 = 12 divided by 3 = 4mm average. If you use the formula (see sidebar) which incorporates the ST elevation at 60 ms after the J-point in lead V3, and the QTc (393ms), then the result is 23.8, which is greater than 23.4 which indicates anterior STEMI.
His pain resolved spontaneously, and he had the following ECG:
 |
| This is now obviously diagnostic of MI, and with T-wave inversion and absence of pain, the artery is likely to be open. The Q-waves indicate that the MI has probably been going on for quite some time. |
The troponin returned positive this time and the patient went for cath and had subtotal stenosis of the LAD just distal to the first diagonal. It was stented.
I don't know the peak troponin, or echo results, or how much myocardium was lost. But here again is a "NonSTEMI" that really should be treated like a STEMI. The ECG 1 week later is consistent with significant myocardial loss:
 |
| Near total loss of R-waves from V2-V4 |
What I noticed in the first two ECGs, in addition to apparent hyperacute T waves in the precordial leads through V4, was ST segment elevation in aVR and V1. This coupled with a symptomatic patient is suggestive of a proximal LCA occlusion isn't it?
ReplyDeleteThere is no ST elevation in aVR (compare it to the PR interval). There is some STE in V1 in the second ECG, and that is consistent with the LAD occlusion.
DeleteWhen you say "LCA occlusion", do you mean circumflex? If so, neither of the findings you suggest would be typical of circumflex occlusion.
Steve Smith
Dr. Smith,
ReplyDeleteRegarding ECG #1 vs ECG #2..
There seems to be sublte ST depression in I and aVL (with TWI), and very subtle ST elevation in III.
In addition the QTc is significantly longer than in ECG #2 (421 vs 393).
Could you comment please?
thanks,
Dave B
Yes, there is subtle ST depression in I and aVL. There is also a biphasic T-wave (down then up, not up then down). This all suggests some involvement of the inferior wall, perhaps from a wraparound type III LAD. I do not have any further cath results, however. Also, down up in lead aVL would be reciprocal to up-down in lead III (which you can't see), and would suggest some reperfusion of the inferior wall that is affected.
DeleteAs for QTc, I can speculate that it is longer in the one with the larger T-waves because there is more active ischemia at that moment in time.
DeleteHis first ECG also has clear ST-depression localized in leads I and aVL that must be explained as well.
ReplyDeleteSee answer to Dave B above!
DeleteInstead of the very subtle De Winter T ( which i couldnt appreciate), there are some STE in V2-V3 with very very hyperacute T waves and this coupled with relatively long QTc already is diagnostic of LAD occlusion.
ReplyDeleteAnother thing: Could those be called De Winter T? I looked up in google and De Winter T is defined as 1-3mm upsloping depression at J point towards a high T wave. In V4-V6 instead of upslopong rather the ST segment is downsloping. Am i right?
Yes, I meant that the de Winter's T-waves were in addition to the hyperacute T waves in V2 and V3. De Winter may not have described the ones that are downsloping, but he should have.
DeleteIn the next couple days I will post 2 EKGs with downsloping de Winter's T-waves.
Sorry, the LCA should have read LMCA (or more probably LAD as V1 elevation was greater). Apparently I misread the aVR as I thought I detected about a 1mm elevation of the ST segment above the T-P segment.
ReplyDeleteIt is a misunderstanding that STE in aVR correlates with LMCA occlusion. It correlates with LMCA obstruction. See my post on the 5 primary patterns of ischemic ST depression:
Deletehttp://hqmeded-ecg.blogspot.com/2012/02/five-primary-patterns-of-ischemic-st.html
Dr Smith,
DeleteRegarding the suspected STE in aVR. I've got mixed messages from different physicians on whether you should compare the ST-segment with the PR segment or the TP segment. Any comment?
This is complex. There are published standards that are all over the map. Thrombolytic trials did not specify how to measure. In Kosuge's articles (most recent is Am J Cardiol 107(4):495-500; Feb 15, 2011) on the significance of ST elevation in aVR in ACS, he measured ST elevation at 20 ms after the J-point, relative to the TP segment.
DeleteHi Dr Smith
DeleteBeing only early in my career, I have also had a lot of confusion about where to measure STE relative to, with different answers from differing senior doctors. I have just read your article about BER VS anterior STEMI, where you mention measuring relative to the PR interval. Above, you talk about measuring relative to the TP segment. Could you please clarify on the optimal comparator for STE? Does the above only relate to aVR and left main/three vessel disease?
Thanks in advance
There is no good answer to that very complex question. Look at the table in my paper to see how ppor ST elevation measurements work. No thrombolytic trial specified the method of measurement, There are many conflicting recommendations, none based on any angiographic or treatment outcomes. Morphology is most important, and the subjective interpretation is better than any measurement.
Deletewhere are the changes show the myocardial loos in the last ECG ? may i Know ? thanx anyway
ReplyDeleteV2-V4 have lost R-wave amplitude
DeleteDr. Smith, I tried to repeat your calculation of the numbers for the first ECG, but I got a completely different total. It may be because of my screen resolution but I want to be sure I am doing this right at work if I am going to use it. I used 2 mm ST elevation in V3 60 ms after J point, qtc of 421, and 21 for R wave amplitude in V4, and I got 20.385. How is my number so different?
ReplyDeleteMaybe this is an argument for calipers and real ECG paper ?
Erin,
Deleteyou cannot apply the equation to the first ECG becase there is ST segment depression. See the red warning above the equation.