Case sent in by Alex Bracey, written by Pendell Meyers, edited by Smith:
A male in his 60s woke up from sleep with chest pain radiating to the back with nausea. There was no vomiting, diaphoresis, palpitations, or other associated symptoms. Vitals were within normal limits, and the exam was unremarkable, the patient appeared well.
He arrived in the ED approximately 1 hour after onset of pain. Here is the initial ECG, as well as the prior ECG on file from several months ago which was immediately available:
Presentation ECG interpreted alone:
Sinus rhythm at approximately 60bpm, with normal QRS complex. No pathologic Q-waves. Without the prior ECG for comaparison, the T-waves are not clearly hyperacute. There is slight STE in V3-V5. There is 1-2mm STE in II, III, and aVF with slight J-point depression in aVL and marked, large T-wave inversion in aVL.
If you consider only the ST elevation in the inferior leads out of context, this amount and morphology would not be incompatible with a baseline ECG of a young man with high voltage and diffuse baseline ST elevation.
The ST depression and T-wave inversion in aVL, however, is NOT compatible with a baseline abnormality, and makes the ECG diagnostic of acute coronary occlusion. As has been shown through many prior cases and publications by Dr. Smith, lead aVL holds the key to understanding inferior ST elevation. ST depression in aVL should always be assumed to be due to inferior MI, unless there is: limb lead LVH, WPW, LBBB, paced rhythm, etc. If there are well-formed Q-waves, it could be due to inferior LV aneurysm as well.
For review, see Dr. Smith's study comparing the findings of lead aVL in inferior ACO versus pericarditis, showing almost perfect reliability of aVL in this scenario:
http://www.sciencedirect.com/science/article/pii/S0735675715008189
Although the study did not incorporate a cohort with normal variant inferior ST elevation, it is extremely unusual to have reciprocal ST depression in aVL in this setting.
Comparison with baseline ECG:
The STE in the inferior leads is larger than baseline, but only by a small amount. The inferior T-waves are hyperacute in comparison to the baseline. Although there was a very small negative T-wave at baseline, the STD and large bulky negative T-waves seen on the presentation ECG are clearly new changes and must be taken to be reciprocal evidence of inferior ACO. The precordial leads are basically at baseline, and specifically there is no obvious evidence of posterior or lateral ACO accompanying the inferior ACO.
Case Continued:
The ED physicians were immediately suspicious of inferior STE and reciprocal STD and inverted T wave in aVL. They called the interventional cardiologist and began recording serial ECGs.
Bedside echo was limited but showed no effusion, no obvious wall motion abnormality.
The initial troponin was undetectable (as you would expect for an acute coronary occlusion of less than 2 hours duration).
The patient was taken for emergent cardiac cath and found to have 100% in-stent restenosis of his prior RCA stent (this history was withheld above for educational purposes).
Here are the cath images:
Here are the post-cath ECGs:
Troponin T was first positive approximately four hours after onset of symptoms, and peaked at 2.09 ng/dL approximately 10 hours after onset.
Echo later that day showed EF 59%, with severe hyperkinesis of the basal inferior wall and inferior septum.
A male in his 60s woke up from sleep with chest pain radiating to the back with nausea. There was no vomiting, diaphoresis, palpitations, or other associated symptoms. Vitals were within normal limits, and the exam was unremarkable, the patient appeared well.
He arrived in the ED approximately 1 hour after onset of pain. Here is the initial ECG, as well as the prior ECG on file from several months ago which was immediately available:
 |
 |
| What is your interpretation? |
Presentation ECG interpreted alone:
Sinus rhythm at approximately 60bpm, with normal QRS complex. No pathologic Q-waves. Without the prior ECG for comaparison, the T-waves are not clearly hyperacute. There is slight STE in V3-V5. There is 1-2mm STE in II, III, and aVF with slight J-point depression in aVL and marked, large T-wave inversion in aVL.
If you consider only the ST elevation in the inferior leads out of context, this amount and morphology would not be incompatible with a baseline ECG of a young man with high voltage and diffuse baseline ST elevation.
The ST depression and T-wave inversion in aVL, however, is NOT compatible with a baseline abnormality, and makes the ECG diagnostic of acute coronary occlusion. As has been shown through many prior cases and publications by Dr. Smith, lead aVL holds the key to understanding inferior ST elevation. ST depression in aVL should always be assumed to be due to inferior MI, unless there is: limb lead LVH, WPW, LBBB, paced rhythm, etc. If there are well-formed Q-waves, it could be due to inferior LV aneurysm as well.
For review, see Dr. Smith's study comparing the findings of lead aVL in inferior ACO versus pericarditis, showing almost perfect reliability of aVL in this scenario:
http://www.sciencedirect.com/science/article/pii/S0735675715008189
Although the study did not incorporate a cohort with normal variant inferior ST elevation, it is extremely unusual to have reciprocal ST depression in aVL in this setting.
Comparison with baseline ECG:
The STE in the inferior leads is larger than baseline, but only by a small amount. The inferior T-waves are hyperacute in comparison to the baseline. Although there was a very small negative T-wave at baseline, the STD and large bulky negative T-waves seen on the presentation ECG are clearly new changes and must be taken to be reciprocal evidence of inferior ACO. The precordial leads are basically at baseline, and specifically there is no obvious evidence of posterior or lateral ACO accompanying the inferior ACO.
Case Continued:
The ED physicians were immediately suspicious of inferior STE and reciprocal STD and inverted T wave in aVL. They called the interventional cardiologist and began recording serial ECGs.
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| T=20 mins from presentation: the ST segments in III and aVF show straightening, which further confirms inferior ACO. |
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| T=30 mins from presentation: STE in the inferior leads increasing. |
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| T=40 mins from presentation: STD in aVL increasing. Q-waves in III and aVF starting to increase in size and width. |
Bedside echo was limited but showed no effusion, no obvious wall motion abnormality.
The initial troponin was undetectable (as you would expect for an acute coronary occlusion of less than 2 hours duration).
The patient was taken for emergent cardiac cath and found to have 100% in-stent restenosis of his prior RCA stent (this history was withheld above for educational purposes).
Here are the cath images:
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| The LAD appears patent. What is missing in this picture? |
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| The right coronary artery shows occlusion of the mid-RCA stent. What is that other vessel right at the osmium? The patient has an anomalous circumflex artery which arises from the RCA rather than the left main. The |
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| The RCA is now patent after intervention. |
Here are the post-cath ECGs:
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| STE resolving, Q waves continuing to form. aVL normalizing. |
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| Continued normalization. No terminal T-wave inversions yet in the affected leads. |
Echo later that day showed EF 59%, with severe hyperkinesis of the basal inferior wall and inferior septum.
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| Leads II and III from all ECGs, side by side, showing the progression of changes from baseline to ACO to post-PCI. BL= baseline. Reperfusion was not available as no more ECGs were obtained. |
The progression above shows the morphology changes of ACO over time in this case. Visualize the STE, inflating T-waves, straightening of the ST-segments, all of which contribute to the overall increasing amount of area under the curve of the ST-T segment compared to the QRS complex, which then resolves after intervention.
Side note: We believe that the ratio of "area under the curve" from the J-point to the end of the T-wave (compared to the baseline) to the overall size and width of the QRS complex is a great way to visualize and monitor the ST-T segment changes of acute coronary occlusion. This concept incorporates the subtleties of hyperacute T-waves, proportionality, and is illustrated by almost all cases of ACO on this blog. If it could be quantified by a computer (rather than qualified by the eyes of an experienced electrocardiographer as it is now), I believe it would perform much better than the standard STEMI criteria that is currently recommended by guidelines.
Learning Points:
- Lead aVL almost always holds the key to evaluating subtle inferior STE
- Serial ECGs interpreted by those who know what to look for are invaluable
Nice case. Kind of on an unrelated note, don't you think V2 and V3 are reversed in all the EKGs done at presentation before cath lab? I'm assuming the leads weren't changed until the patient went to the cath lab because post cath lab EKGs look like normal V2/V3 leads.
ReplyDeleteDan
Dan,
Deleteyou are absolutely right!
Thanks,
Steve
ECG 1... the R wave progression and t waves look concerning in chest leads. Any comments on that? Can we use the subtle anterior STEMI formula here?
ReplyDeleteAlso, any reason for the TWI in aVL on baseline ecg?
Thank you doctor..
As Dan above noted, V2 and V3 are reversed.
DeleteAs for aVL, T-wave is often normally inverted
But the T wave in V4 is quite tall.. Can we use the formula?
DeleteIf you are worried that the small amount of ST elevation in V2-V4 is due to LAD occlusion, then you should use the formula. when I look at this ECG, I am worried about the inferior leads, so I then look at aVL and am very worried about inferior MI (RCA or circumflex occlusion). I am not worried about LAD occlusion with this ECG, so I don't use the formula. I don't have the computerized QTc so I can't use it here.
DeleteGreat case as usual...however, the R wave progression in V3 doesn’t make sense to me, as the R wave is present in V2 and V4, but virtually absent in V3. Additionally, in the post Cathy ECGs, the R wave progression is intact, with the morphologies of V2-V3 seemingly reversed from original ECGs. Is this due to initial lead misplacement, or is there another explanation?
ReplyDeleteThank you,
Dave B
Dave,
DeleteYou are correct, as Dan also above noticed.
Reversed leads
thanks!
Steve
Intern here. Marked large t wave inversions in aVL? The vector of the qrs is down and so are the T waves? What am I missing? I don't see t wave inversions.
ReplyDeleteIt's a great question. Let's assume for a second that we didn't have the baseline ECG, and we're looking only at the presentation ECG. The direction of the T wave, like you're saying, could be potentially be normal based on the QRS and normal QRST angle. But the area under the curve between the baseline and the ST-T segment is marked, wide, bulky compared to the size of the QRS, and constitutes definite downward movement of the J point, ST segment, and T wave compared to whatever is there before the inferior acute coronary occlusion took place. So "inversion" is probably the wrong word, you're right, but you should see this as suspected inferior deflection of the T wave.
DeleteAnd now when you look back to the baseline ECG: the T wave is already negative, still in agreement with the QRS and QRST angle. But you can see how the T wave is so much smaller and shallower in the baseline, confirming that there is in fact negative deflection of these components in the presentation ECG.
Also notice the T waves in the post-PCI ECGs: the T waves in aVL are positive! Is it due to reperfusion? But the inferior T waves are not inverted/negative, so how can you explain it as reperfusion? Maybe it's lead placement instead. I don't know. I don't personally put as much stock in TQRS angle, I find that more experience helps the eyes see when it is irrelevant.
So you're right it's not technically "inversion", but definitely markedly depressed. Is that helpful? Great comment
Dr.Smith
ReplyDeleteI have trouble seeing the 1-2 mm STE in the inferior leads if I use the TP- segment as the baseline. In your book The ECG in Acute MI you use the TP segment. Please explain this to me.
Ola
Norwegian IM resident
Ola,
DeleteIn the book I say to measure at the J-point relative to the PR segment (I should have said PQ junction). This is a complicated topic. Suffice to say that the only placebo controlled trials for intervention were the thrombolytic trials of the 1980s and they did not specify how to measure STE. The guidelines say to measure at the J point relative to PQ junction. Here they are both about the same! It really doensn't matter because ST elevation measurement just does not correlate all that well with presence or absence of acute occlusion.
Steve Smith
Thank you for your answer and I am sorry, I looked at the first chapter where the TP segment is used as baseline in the explenation of STE mechanism. With further reading I see you say use the PQ segment and J point for STE measurement. Other resources like Rosen’s recommend the TP segment. In my hospital in Norway there are discrepancies but most use TP segment. I understand it might not be that important when you are experienced at pattern recognition. In my hospital system the junior docs like me decide which patient should bypass our hospital and go to cath based on prehosp ecg. In this setting the millimeters becomes quite important since we are not yet experts in pattern recognition. For me this lack of standardization becomes frustrating, but thanks a lot for the answer.
DeleteOla