Just as hyperacute T-waves can be reciprocal to T-wave inversion (last case),.....
....T-wave inversion can be reciprocal to STEMI of opposite wall!
This case was sent by Arthur Lee.
Case:
A 50 yr old woman presented after a syncopal episode, with sweating and left arm numbness. There was no chest pain or SOB, at least none reported by Dr. Lee. Here is her presenting ECG:
Answer:
There is very abnormal T-wave inversion in aVL which is typical of subtle transmural/subepicardial (due to occlusion) ischemia to the inferior wall. This is reciprocal T-wave inversion. The high lateral wall is reciprocal to the inferior wall.
Similarly, the precordial T-wave inversions in V2-V4 are reciprocal to posterior wall transmural/subepicardial (due to occlusion) ischemia.
This ECG is typical of a very subtle and/or early inferoposterior MI. It is incorrect dogma that posterior MI has upright T-waves. That is wrong because the T-wave orientation depends on many factors, including the lead strength of the well perfused (normal) anterior wall (contributing an upright vector) and the state of the artery supplying the posterior wall. If open, it will contribute an upright vector -- (posterior reperfusion T-waves); if closed, it will contribute a negative, inverted vector because it is 180 degrees opposite to an upright (hyperacute) vector towards the posterior wall.
This negative vector can overpower the upright vector produced by the anterior wall and result in inverted T-waves.
Thus, this is a subtle inferoposterior MI, and the T-wave in III should then be scrutinized for any hyperacute features.
Indeed, when you look at the T-wave in lead III, it has just as much amplitude (voltage) as the QRS in lead III. This is not normal. This supports inferoposterior MI as the diagnosis.
Given that this patient has no chest pain, one must be skeptical of such a diagnosis. She does however have diaphoresis and arm numbness.
Fortunately, the symptoms resolved and the following ECG was recorded:
Outcome:
She ruled in for MI by troponins and went for angiogram. An 80% thrombotic RCA was stented.
....T-wave inversion can be reciprocal to STEMI of opposite wall!
This case was sent by Arthur Lee.
Case:
A 50 yr old woman presented after a syncopal episode, with sweating and left arm numbness. There was no chest pain or SOB, at least none reported by Dr. Lee. Here is her presenting ECG:
 |
Arthur asked: "How do we interpret the anterior T-wave inversion? Are they reperfusion T-waves of the anterior wall?"
What do you think?
|
Answer:
There is very abnormal T-wave inversion in aVL which is typical of subtle transmural/subepicardial (due to occlusion) ischemia to the inferior wall. This is reciprocal T-wave inversion. The high lateral wall is reciprocal to the inferior wall.
Similarly, the precordial T-wave inversions in V2-V4 are reciprocal to posterior wall transmural/subepicardial (due to occlusion) ischemia.
This ECG is typical of a very subtle and/or early inferoposterior MI. It is incorrect dogma that posterior MI has upright T-waves. That is wrong because the T-wave orientation depends on many factors, including the lead strength of the well perfused (normal) anterior wall (contributing an upright vector) and the state of the artery supplying the posterior wall. If open, it will contribute an upright vector -- (posterior reperfusion T-waves); if closed, it will contribute a negative, inverted vector because it is 180 degrees opposite to an upright (hyperacute) vector towards the posterior wall.
This negative vector can overpower the upright vector produced by the anterior wall and result in inverted T-waves.
Thus, this is a subtle inferoposterior MI, and the T-wave in III should then be scrutinized for any hyperacute features.
Indeed, when you look at the T-wave in lead III, it has just as much amplitude (voltage) as the QRS in lead III. This is not normal. This supports inferoposterior MI as the diagnosis.
Given that this patient has no chest pain, one must be skeptical of such a diagnosis. She does however have diaphoresis and arm numbness.
Fortunately, the symptoms resolved and the following ECG was recorded:
 |
| All inverted T-waves are now upright and the hyperacute T-wave in lead III has normalized. This confirms the previous interpretation and is diagnostic of reperfusion. |
Outcome:
She ruled in for MI by troponins and went for angiogram. An 80% thrombotic RCA was stented.
Medical student here, this might be a very silly question but how would you differentiate this from antero-lateral wall ischemia? I.e. how to differentiate ischemic T-wave inversion on lateral leads from reciprocal changes of infero-posterior MI?
ReplyDeleteFirst, it looks subtle different. Look up Wellens' cases on this blog. More to the point, however, T-wave inversion is either 1. reciprocal to active ischemia/occlusion (aVL in the setting of inferior MI, V2 in the setting of posterior MI (or posterolateral, inferoposterior), in which case the patient still has symptoms (e.g. chest pain) or 2. indicative of reperfusion of the myocardial wall beneath that lead (V2-V4 in anterior ischemia), in which case the pain is resolved (e.g., Wellens' syndrome); I call these "reperfusion T-waves".
DeleteCan you specify point one as how to distinguish between ischemic vs reciprocal TWI during ongoing symptoms?
DeleteIf the patient is now pain free, then the T-wave inversion is likely reperfusion of that wall. If the patient has active pain, the T-wave inversion is reciprocal to the hyperacute T-wave.
DeleteThanks!
ReplyDeleteThats really valuable stuff for a medical student. I have a doubt though. Why does unstable angina (subendocardial ischemia at rest) produce inverted T-waves?
ReplyDeleteAre you referring to the active ischemia state? Or the post reperfusion state? Are you referring to true unstable angina (with negative troponins). Too many variables here to answer the question.
Delete