Hyperacute T-waves, missed by computer, short DBT, but large myocardial infarction

This 57 yo male with no past medical history had sudden onset of chest pain while sleeping.  He called 911 at midnight and his prehospital ECG (unavailable) showed acute MI and the cath lab was activated 20 minutes prior to arrival, giving cath lab personnel time to drive into the hospital as the patient was being transported.

Computerized QTc was 410 ms.  First ED ECG, only 1 mm ST Elevation in V2, V3, and aVL, but marked ST depression in inferior leads and V5, V6.  Notice the T-wave towers over the R-wave in V2 and V3, and there is an upright T-wave in V1.  In early repolarization, there are well developed R-waves in V2-V4, so this ECG cannot be early repolarization.  Even without the changes in inferior and lateral leads, the hyperacute T-waves in V2 and V3 are diagnostic of STEMI.  The computer missed this.  

If you used the formula, you would only come up with 22.9, which is less than 23.4 (86% sensitive at this cutoff, and 90% specific), but greater than 22.0 (96% sensitive and 81% specific)

The Door to Balloon time was 34 minutes, time from symptom onset to opening of a 100% occluded wraparound (type III) LAD was about 80 minutes (very short).  Nevertheless, the patient suffered a large myocardial infarction, with a peak troponin I of 290 ng/ml.  There was a large anterolateral, anteroseptal, anteroapical, and distal inferior wall motion abnormality, with EF of 30-35%.  The convalescent echo several weeks later will tell us how much of this is due to (irreversible) infarction vs. temporary "stunning".   His follow-up ECG the next day is shown below. 

There are "reperfusion" T-waves in V1-V6 and I, aVL.  There is a QS-wave in V2, and QR-wave in aVL, and poor R-wave progression in V3 and V4, all diagnostic of anterolateral MI, subacute.

This demonstrates:

1) hyperacute T-waves, with loss of R-wave amplitude such that the T-wave towers over the R-wave
2) that the computer again misses a clearly diagnostic STEMI
3) that a large STEMI may not meet any millimeter criteria for STEMI (there are several published criteria, and the only one met here is 1 mm in two consecutive leads, an extremely non-specific criterion.  In fact, no STE millimeter criterion has adequate accuracy)
4) that even with rapid reperfusion, much myocardium may be lost.

Not all cases with reciprocal ST depression are acute STEMI

This patient has concentric LVH and presented with chest pain.

There is sinus rhythm.  There is high voltage in aVL and typical "hockey stick" appearance of the ST-T complex (LVH with repolarization abnormalities. This also results in reciprocal ST elevation in inferior leads. 

Due to the ST elevation in leads aVF and III, with reciprocal ST depression in I and aVL, the cath lab was activated.  Coronaries were normal.

Later review of old records showed this to be her baseline ECG.

Without an old ECG to compare, one would be very suspicious of inferior STEMI. One should know that not all reciprocal ST depression is due to STEMI.   Inferior LV aneurysm, WPW, LVH, and LBBB may all have inferior ST elevation with reciprocal ST depression in aVL.
Here is an example of this in LV aneurysm:
http://hqmeded-ecg.blogspot.com/2010/10/tachycardia-must-make-you-doubt-acs-or.html


Had the treating physicians known this, they might have looked for the previous ECG and realized that the patient was not having a STEMI.

Conversely, absence of any reciprocal ST depression of any amount almost completely rules out inferior STEMI. We presented this research in Boston June 2011 SAEM.  Here is the abstract:

In acute inferior STEMI, Reciprocal ST depression in aVL and T-wave inversion in aVL are both more sensitive than ST elevation criteria and appear earlier in the course of STEMI

Christine Worrall

Emily Vogel

Stephen W. Smith

Background:  A previous study found that reciprocal ST depression (rSTD) is present in only 82% of inferior ST elevation (STE) acute myocardial infarction (MI).  However, we believe that changes in lead aVL are far more sensitive.  Objectives: To find the incidence of any rSTD or T-wave inversion (TWI) in angiographically proven inferior STEMI.  Methods: We searched the catheterization laboratory database for all cases coded as acute Inferior STEMI from January 2002 through March 2008.  All cases were reviewed and the presenting ECG, as well as the first ECG that was used for diagnosis of acute STEMI, were analyzed.  “True STEMI” was defined as 100% occlusion or as a culprit lesion with maximum troponin I (trop) > 10 ng/ml.  STE was measured in leads II, III, aVF; aVL was scrutinized for any rSTD or TWI.  TWI was defined as a T-wave mostly down, or a biphasic T-wave that is first down, then up (not up then down, which is associated with lateral AMI).  Reperfusion criteria were defined as STE of at least 1 mm in 2 of 3 of inferior leads II, III, aVF.   Results: There were 160 unique cases.  107 had 100% occlusion, and 35 had < 100% occlusion, but had a maximum trop > 10 ng/ml, for 142 true STEMI; 18 (11%) had < 100% occlusion and a max trop < 10 ng/ml.  85% of the diagnostic ECGs of true STEMI, and 84% of all cases, met STE criteria.  No true STEMI had absence of reciprocal depression in lead aVL. Of the 107 with 100% occlusion, 100 (93%) had at least 0.5 mm of rSTD; the remainder had rSTD of < 0.5 mm.  Even among those without true STEMI, 94% had some rSTD in aVL.  Additionally, in 44 cases (28%), there was no STE whatsoever on the presenting (first) ECG; all of them had either rSTD or TWI.  See Table.  Conclusion: STE criteria for inferior STEMI are insensitive, especially on the presenting ECG.  Changes in aVL, both some amount of rSTD and also TWI, are more sensitive than STE criteria in the diagnosis of inferior STEMI and are nearly universally present in inferior STEMI.  These changes also appear earlier than STE.

Cardiac Arrest, Wide Complex, Is it STEMI?

For other cases of cardiac arrest, see these posts

Case
This 200 kg patient was watching TV when he had a witnessed v fib arrest, and had a prolonged resuscitation. In the ED, his pH was 7.20, K of 4.9, and this was his initial ECG:

One might be tempted to diagnose ventricular tachycardia. However, there are p-waves best seen in lead I, with a slightly long PR interval. There are also PVCs which are unlikely to occur during V tach.
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Once it is determined to be sinus tach (with aberrancy, in this case a slightly unusual LBBB), one must find the end of the QRS (J-point, the start of the ST segment) in order to find the ST segment and to evaluate for ST elevation or depression. In this case, the end of the QRS is easily found in lead V6. Then, draw a line through that J-point an extend it up and down. I have done this in detail in this previous case:
http://hqmeded-ecg.blogspot.com/2010/11/wide-complex-tachycardia-its-really.html

Here are the lines for this ECG:
Then you can find the end of the QRS in any lead. After doing so, you can see profound concordant ST depression in leads V2-V5, and Concordant ST elevation in I and aVL with reciprocal ST depression in II, III, aVF.

70 minutes after the first ECG, this ECG was recorded:

Now the QRS is narrower. The sinus rhythm is obvious. There is a R-wave in V6 typical of LBBB, but the ST segment is not discordant as it should be. Rather, it is concordant. V1-V3 have concordant ST depression.
The patient's initial troponin was negative. Because of other factors, he was not taken for PCI. Troponin 5.5 hours later was 308. ng/ml. Echo was technically difficult but showed LVH and probable lateral wall motion abnormality. This was presumably a large posterolateral STEMI with LBBB.

Left Ventricular Aneurysm or Anterior Acute STEMI?

I am simply going to post a link to a nice presentation of this at the ems12lead.com blog by Tom Bouthillet.

http://ems12lead.com/2011/01/12/left-ventricular-aneurysm-vs-acute-anterior-stemi/

RV MI diagnosed by ST elevation in V1

The Importance of Serial ECGs