Posterior Reperfusion T-waves have never been described in the literature, until now. Dr. Brian Driver and Dr. Gautam Shroff have joined me in formally studying this and we show that this is a real phenomenon.
Here is the article (full text):
Here I provide 2 examples. Here are many other examples.
Case 1
ECGs of a patient with proven reperfused isolated posterior MI during pain and then 120 minutes later, after resolution of pain.
Elderly male who is perfectly healthy complained of chest pain on and off for 2 days, then much more severe just prior to evaluation.
Figure 1:
Figure 1a: ED ECG during pain.
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| The ST segments in right precordial leads are isoelectric and there is no definite evidence of acute infarction. |
Figure 1b. 120 minutes later after pain resolution.
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| Relative to the presenting ECG, the ST segments are relatively slightly elevated and the T-wave has enlarged signficiantly. This was not recognized by the treating physicians. |
No one saw these ECG changes which signify that the first ECG was acute posterior MI and the second represents reperfusion of the infarct related vessel.
When I saw them in reviewing ECG, I immediately knew that he had a posterior MI.
[Posterior MI is now unfortunately called "lateral" because MRI shows such infarct to be more lateral than posterior. However, the affected wall still has no overlying leads on the 12-lead, so this new terminology is counterproductive for ECG analysis.]
Peak TnI 46
Nuclear scan: Severe intensity, large perfusion defect involving the
lateral wall consistent with myocardial infarction in that
distribution.
Echo: Regional wall motion abnormality-lateral
No angiogram due to clinical considerations.
Case 2
Figure 2a. A patient with stuttering chest pain presents pain free:
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| There is evidence of reperfused inferior and lateral MI, with T-wave inversion. There is minimal ST depression in V2 and V3 highly suspicious for posterior MI |
Figure 2b. Here is the previous ECG:
Figure 2c. The patient developed chest pressure again
Figure 2d. I activated the cath lab and an occluded RCA was opened. Here is the ECG several hours after reperfusion:
Comment
If recorded on the posterior wall, the T-waves would be inverted, just like a posterior Wellens' syndrome. However, they are recorded from anterior, and are added to the upright T-waves of the anterior wall, so they result in added voltage to the right precordial T-waves!
(+) T-wave in anterior wall.
Add the (-) the T-wave of the posterior wall. This T-wave is a negative of a negative, and therefore positive, so adds to the total voltage.
1st negative: recording the posterior wall from anterior
2nd negative: negative T-wave on the posterior wall.
Recording a negative of a negative gives a positive.
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| Previous ECG - Normal |
Figure 2c. The patient developed chest pressure again
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| There is pseudonormalization of inferior and lateral T-waves, with some new, minimal inferior ST elevation and reciprocal ST depression and T-wave inversion in aVL. This is diagnostic of coronary occlusion. |
Figure 2d. I activated the cath lab and an occluded RCA was opened. Here is the ECG several hours after reperfusion:
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| There are inferior and lateral reperfusion T-waves (inverted). There are large right precordial "posterior reperfusion T-waves" in lead V2 |
Comment
If recorded on the posterior wall, the T-waves would be inverted, just like a posterior Wellens' syndrome. However, they are recorded from anterior, and are added to the upright T-waves of the anterior wall, so they result in added voltage to the right precordial T-waves!
(+) T-wave in anterior wall.
Add the (-) the T-wave of the posterior wall. This T-wave is a negative of a negative, and therefore positive, so adds to the total voltage.
1st negative: recording the posterior wall from anterior
2nd negative: negative T-wave on the posterior wall.
Recording a negative of a negative gives a positive.
Why never V7-V9 to confirm/prove ?
ReplyDeletemerci
Al
For the first case, I wasn't there and no one even recognized that this might be a posterior MI until the imaging studies were done later.
DeleteFor the second one, I recognized subtle coronary occlusion with posterior MI immediately. No need for posterior leads. My opinion on that is that they cannot help when you already have diagnostic ST depression. They can be falsely negative and dissuade cath lab activation -- I have posted at least 2 such cases in the past. When are they useful: They might reveal a posterior MI in cases that have an otherwise normal ECG.
Dr. Smith,
ReplyDeleteAccording to case #2 I noted that there was a loss of precordial Balance of "T" waves suggesting Acute Ischemia. The "T" wave in V1 is larger than in V6 suggesting a type of hyperacute "T" wave. Thoughts? My other question is from Case #2 figure 2b. Was the normal EKG from that day or from a previous date or earlier in that visit? Since there were relatively fat and slightly larger "T" waves in V1 than in V6 that this could have been CAD if it was an older EKG or early Ischemia if it was from that day. Thoughts? Always love your cases!
Garrett,
DeleteFirst, T-wave in V1 greater than T-wave in V6 may possibly be useful in 1) RV MI and 2) anterior MI. I have shown that it adds nothing to the diagnosis of LAD occlusion beyond what my formula adds (in that study we found that 15% of early repol had this finding and 30% of LAD occlusion, and that it had no independent value. Second, if it were of value, it would only be of value in the symptomatic state. Here, the T-wave in V1 is large because the posterior wall is reperfused, not because of any active ischemia.
Finally, the old EKG is from months ago. Again, the comment about V1 and V6 T-waves applies. I think this is a nearly worthless rule. Its evidence base is incredibly weak and, for LAD occlusion, I showed it to be of little use.
Steve Smith
Steve,
DeleteThank very much for the detailed reply. Very helpful!