This comes from a paramedic in Hungary named Farkas László:
This patient had chest pain that then resolved:
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| There is diffuse ST depression, with ST Elevation in aVR and a hyperacute T-wave in lead V3 V3 is likely a de Winter's T-wave (ST depression with large upright T-wave) |
Since this T-wave is not obviously massive, one might think this is a posterior MI (right precordial ST depression) or simply diffuse subendocardial ischemia (diffuse ST depression with STE in aVR).
11 minutes later, the chest pain was gone, suggesting spontaneous reperfusion (autolysis of thrombus).
This ECG was recorded:
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| All ST depression in V3 is gone Only residual ST depression remains The T-waves in V2 and V3 are smaller This rules out posterior MI: as an artery reperfuses in posterior MI, the T-wave gets larger! (Posterior reperfusion T-waves) |
See posterior reperfusion T-waves:
2 Examples of Posterior Reperfusion T-waves
Here is our research on this topic: http://emj.bmj.com/content/34/2/119
8 minutes later:
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| All precordial T-waves are smaller still |
7 minutes later:
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| There is less ST depression |
Another 16 minutes later:
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| There is new ST elevation, but, in addition, Wellens' waves are emerging (Wellens' pattern A, terminal T-wave inversion in V2-V4, and a little in V5) |
Another 7 minutes later
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| ST Elevation is resolving, terminal T-wave inversion remains |
Here is a .gif of lead V4 from T = 0-11-19-26-42-49 minutes:
The cath lab was activated and a 90% thrombotic subtotal occlusion with flow was found.
I think that de Winter's T-waves really represent very tight subtotal occlusion of the LAD. Complete occlusion results in ST Elevation. Very tight stenosis results in subendocardial ischemia with diffuse ST depression and STE in aVR. de Winter's is a point halfway between these two: a hybrid of STEMI and diffuse ST depression with STE in aVR.
Here is another example of this:
Is the LAD really completely occluded when there are de Winter's waves?
Of course, when the LAD reperfuses, we usually get Wellens' waves (reperfusion T-waves). So even though the ECG never manifested outright STEMI, the small amount of infarct that resulted from this subtotal occlusion resulted in the same T-wave evolution that we would have seen with outright STEMI.
Silly question - is there not initially ST elevation in V1 in the first ECG? If so how do you interpret that in this context?
ReplyDeleteCheers,
Ben
PGY1
Good observation. Yes, and it could be analogous to septal STEMI, but it is also just as likely reciprocal to ST depression as due to subepicardial ischemia. V1 and aVR are similarly opposite to V5 and II.
Deleteinteresing topic
ReplyDeleteDr. Smith, looking at the two examples of hyperacute T-waves in your book on pg. 76 and 77 and de Winter's paper from 2008 show the T-wave to be of much greater amplitude than the R-waves. I've been looking at ECG 1 and your interpretation and I'm curious how the T-wave in V3 meets large/hyperacute criteria. In absolute terms I count 6 mm of T-wave amplitude from the depressed J-point. The V3 QRS voltage appears normal to me, and the T-wave amplitude ratio to the 7 mm R-wave, while close in amplitude, is less than one. They also don't seem very wide and their concave morphology looks normal.
ReplyDeleteThanks
Tom,
DeleteThere are no criteria for hyperacute T-waves. Maybe some day someone will figure it out. Right now, it is a subjective recognition, with confirmation by follow up ECGs. In this case, you can tell by follow up ECGs that, indeed, the first T-wave was much larger than it is at baseline. When I look at the T-wave in V3 in the context of the ST depression, I suspect that it is a hyperacute T-wave for this patient, but I don't know for certain. Only after the ischemia changes, and the T-wave becomes smaller, is my suspicion confirmed.
Steve Smith
Ok, I understand now. I see that it will take me some time/many ECGs to develop the subjective recognition ability.
ReplyDeleteThanks for your your reply.