Pseudonormalization of T waves, Coronary occlusion without 1 mm ST elevation

See 6 even better cases of T-wave pseudonormalization here.

Here is another case.  Do not miss this one:

A Middle-Age Male with Chest Pain that Recurs in the ED

This 64 year old woman presented intoxicated with nausea and vomiting and epigastric pain, with no chest pain. She has a history of a stent, but unknown in which artery. She stopped taking clopidogrel 2 weeks ago because she ran out. Here is the initial ECG; there was no previous ECG for comparison.

Notice there is deep symmetric T inversions in inferior leads, and a large upright T wave in aVL. There is also some T inversion laterally. This is all suggestive of inferior (and lateral?) Non-STEMI, due to reperfused RCA or circ. Inverted T waves are also known as "reperfusion" T-waves. If they are in the anterior leads, they are often referred to as "Wellens' T-waves."

A troponin returned elevated, and a repeat ECG was recorded:

Now the inferior T-waves have become mostly upright, in this case biphasic. There is some ST elevation, but it is not quite 1 mm in two consecutive leads. There is new ST elevation in lead V1, which in this context is diagnostic of right ventricular STEMI.

This phenomenon is called "pseudonormalization of T-waves" because normal T-waves are upright (same axis as QRS), but become inverted in non-STEMI that is reperfused. They become deceptively upright (not normal, but "pseudo" normal) when the artery re-occludes. Thus, where reperfusion of the infarct-related artery (IRA) leads to T-wave inversion, if inverted leads become suddenly upright, this is diagnostic of re-occlusion of the IRA.

There is nothing magical about 1 mm of ST elevation. ST elevation is used as a very imperfect surrogate for coronary occlusion. Coronary occlusion that does not spontaneously reperfuse or is not compensated for by collateral circulation will quickly lead to irreversible myocardial loss. Reperfusion therapy is indicated for occlusion, even when there is not 1 mm of STE in 2 consecutive leads. However, the specificity of the ECG for occlusion becomes less as the STE is less. So expertise in interpreting the ECG is particularly important for these cases.

In this case, it was clear that there was a very unstable thrombus in the RCA or circ, and that if it was not 100% occlusive, it was very nearly so.

The cath lab was activated, a 100% proximal RCA stent thrombosis was seen and the artery was opened.

This also illustrates how chest pain or even discomfort may be completely absent in STEMI. Below is the post-cath ECG, showing T-waves are now inverted again (indicating reperfusion).

Posterior ST Elevation MI in the Setting of Right Bundle Branch Block, with Posterior Leads V7-V9

This is a 68 year old man who had a resuscitated cardiac arrest. His prehospital ECG looks identical to this one which was recorded upon arrival to the ED:

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There is sinus rhythm with a wide QRS, with rSR' in V1 and a wide S-wave in lateral leads, consistent with right bundle branch block (RBBB). ST elevation or depression in RBBB is not difficult to find if you identify the end of the QRS. In this case, the QRS duration is about 135 ms, and in V2 and V3 there are 2 small S-waves; only after these S-waves does the ST segment begin. There is also almost 4 mm of ST depression in right precordial lead V3. Some ST depression (up to 1 mm) in the opposite direction (discordant) to the positive QRS is normal in RBBB, as in V1 here. This much ST depression (V2 and V3) is always abnormal (ischemia).

Most posterior STEMI is in conjunction with either inferior STEMI, lateral STEMI, or both. Only 3-11% of all MI are isolated posterior. In this case, there is no ST elevation elsewhere on the ECG. Marked isolated ST depression in the right precordial leads in a clinical scenario consistent with STEMI is usually posterior STEMI. Such ST depression can also (much less likely) be due to subendocardial ischemia. Two modalities that can help are: 1) recording posterior leads V7-V9 and 2) echocardiography with a posterior wall motion abnormality. In this case, both were done. The posterior ECG is shown here and was done 31 minutes later. Leads labelled V4-V6 were actually recorded on the back as leads V7-V9 (V7 at posterior axillary line, even with tip of scapula; V9 paraspinal at same level; V8 between them).

There appears to be lead reversal of limb leads.  Notice opposite axis of I and aVL from first ECG.
The remainder is explained below.

There is only one lead with ST elevation, lead V9 (labelled V6). There is approx 0.75 mm of ST elevation. Up to 0.5 mm is within normal limits, but any amount in even one lead >/= 0.5 is abnormal and very sensitive and specific for posterior STEMI (Matetzky S. et al. JACC 1998;31:506-511. Matetzky S et al. JACC 1999;34:748-753. Taha B et al. J Electrocardiol 1998;31(Suppl):178-9. Wung SF et al. Am J Cardiol 2001;87:970-974;A4.) Moreover, the QRS amplitude in V9 is tiny, and the ST elevation is very high in proportion. Similarly, there is also now a small amount of ST Elevation (< 1 mm in context of very small QRS) in aVL, suggestive of lateral STEMI.

Emergency physician performed bedside echocardiogram showed evidence of posterior wall motion abnormality and no anterior WMA. Immediate angiography showed a thrombotic occlusion of the mid circumflex, as well as disease in the RCA and LAD. Formal Echo the next day confirmed posteriorlateral WMA. Max troponin I was 12 ng/ml.

Approximately 75% of posterior STEMI will manifest at least 1 mm of anterior ST depression. (Matetzky S et al. JACC 1999;34:748-753. Wung SF et al. Am J Cardiol 2001;87:970-974;A4.)