This post was written by one of our fantastic Hennepin County Medical Center Emergency Medicine interns
who is an ECG whiz, Daniel Lee.
A man is his late 50’s presents to the ED with 1 hour of post exertional chest pressure associated with diaphoresis and nausea. He has a history of known CAD, diabetes, and dyslipidemia.
By pure clinical appearance, he looked like the textbook patient with acute MI.
This is his first ECG in the department, which I saw as it was being printed:
What do you think?
Here is a previous baseline ECG from 3 years prior to compare:
This was my interpretation of the first ECG:
|Sinus bradycardia with less than 1mm ST elevation in V4-V6, elevated compared to the previous ECG, suggestive of lateral MI. Looking to the high lateral leads, instead of ST elevation that one might see in a lateral MI there is subtle ST depression in aVL less than 1mm along with new T-wave inversion.
Leads II, III, aVF show about 0.5 mm ST elevation that is new compared to the previous ECG. Furthermore there is a new positive T wave in lead III.
Subtle changes, but with the history is very nearly diagnostic of acute inferior MI.
Let’s look at the 2 ED ECGs side by side:
Now you can see the differences more clearly
|Acute ECG on the left, with slight STE in left precordial leads,
compared to the previous ECG on the Right.
This patient had had two prehospital ECGs recorded, and these were viewed:
30 minutes after reported onset of pain:
|Sinus rhythm with only a small amount of elevation in V5 and V6. No ST elevation in the inferior leads, no T wave in III, no ST depression in the lateral leads.
T-waves are small in inferior leads.
This is a negative ECG.
10 minutes after first prehospital ECG, with continued pain:
|Smith comment: This shows ST depression in multiple leads, most pronounced in V2-V4. This is very suggestive of posterior MI.
There is also some subtle ST depression in II, III, and aVF, and it is followed by T-waves of increased size over the previous.
Notice how useful serial ECGs are!
More Smith comment: it is true that ST depression (STD) due to subendocardial ischemia does not localize [it is usually diffuse ST depression, in multiple leads and not reciprocal to ST elevation in an opposite territory], this ST depression is different! The STD in V2-V4 is almost certainly reciprocal STD, reciprocal to STEMI in the posterior wall; this is evident because it is maximal in V2-V4, not in V4-V6.
So what is the STD in II, III, and aVF? While de Winter’s T-waves have only been described in the LAD territory, there is no reason that they might not also exist in other territories. Since this is upsloping ST depression followed by an enlarged T-wave, I believe these are Inferior de Winter’s T-waves.
There is evidence that de Winter’s T-waves really represent a tiny trickle of blood through the thrombotic stenosis. There is enough limitation of flow to cause subendocardial ischemia with ST depression, and even enough limitation of flow to have hyperacute T-waves, but too little flow to have ST elevation! I believe this based on much experience of seeing dynamic changes from STE to deWinter’s and back again and correlating this with angiograms.
So this is an infero-posterior MI, with affected leads inferior (de Winter’s and later STE), posterior (STD V2-V4), and lateral (STE V4-V6).
The interesting thing is that they manifest ischemia at different times:
–When there is clear ST depression of posterior MI in V2-V4, and inferior de Winter’s T-waves, there is no ST elevation in V5 and V6.
–When there is STE in V4-V6, and in inferior leads, there is no ST depression in V2-V4.
The ED ECG in the context of the prehospital ECGs was indeed diagnostic of acute coronary occlusion.
The cath lab was activated and co-culprit lesions were found: 99% circumflex and 95% right coronary artery (RCA). Both were stented.
Peak troponin was (0.446 ng/mL) — very low due to rapid reperfusion.
Subsequent echo showed no wall motion abnormality.
Lead aVL is incredibly useful. New ST-depression (without LBBB or LVH) in aVL that cannot be blamed on an abnormal QRS is worrisome, and in the context of a patient with acute chest pain is almost certainly due to ischemia. In patients with suspicion of acute MI who have any ST elevation, aVL is also a very useful lead to differentiate between pericarditis and MI.
This paper by Bischof and Smith compared inferior MI to pericarditis and found that of 154 patients with inferior STEMI, 17% of whom had less than 1 mm of STE in any inferior lead, all 154 had at least 0.25 mm ST depression in aVL. Among 49 patients with pericarditis who had inferior ST elevation, zero of 49 had ST depression in aVL (though there are always rare exceptions such as this case). Interestingly this study also looked at 54 “subtle” inferior MI’s, and of these 49 had some ST depression in aVL. Thus it is not surprising that the current case of subtle inferior MI had ST depression in aVL. Moreover, T-wave inversion in aVL was also found to be 100% sensitive and 86% specific for inferior STEMI.
Here is a magnified in view of aVL side-by-side with the baseline ECG.
|Presenting with STD and TWI
|Old with no STD
In additions, this paper also found that all 33 patients with inferolateral MI, as manifested by STE in V5 and V6, still had ST depression in aVL. V5 and V6 are caudal to aVL and so an inferior ST vector towards lead aVF is also slightly towards V5 and V6 but away from aVL!! So V5 and V6 will have some ST elevation while aVL has ST depression. Thus, even inferolateral MI has reciprocal ST depression in aVL.
This patient functionally had an inferolateral MI given his two culprit lesions and in retrospect the elevation in leads V4-V6 were indicative that there was lateral wall involvement as well. The lateral involvement may also explain the very subtle nature of the acute ECG findings given that much of the voltage in inferior and lateral occlusions are directly opposed to each other.
This is the post cath ECG:
|Resolution of ST depression and T wave inversion in aVL, as well as the new T wave that had been present in III. There is some residual ST elevation in the inferolateral leads.
|Summary of Learning Points:
1. New ST depression and T wave inversion in lead aVL is highly suggestive of inferior MI.
2. Even very subtle inferior MI will likely have ST-depression in aVL. These ECGs must be scrutinized very closely!
3. Inferolateral MI will have ST depression
in aVL in addition to ST elevation
in V5 and V6.
4. de Winter’s T-waves may occur in any coronary distribution.