A male in his 60's had a history of previously stented infero-posterior-lateral STEMI due to an occluded dominant circumflex, which had been opened and stented.
He called 911 for acute chest pain.
Here is the first prehospital ECG at time zero. The computer read "Nonspecific ST-T abnormalities."
Time zero:
There is minimal ST elevation in V2 and V3.
T-waves are large in V2 and V3.
There are minimal down-up T-waves in III and aVF.
This is LAD occlusion until proven otherwise. One must explain the minimal ST elevation in V2 and V3. It is not due to LVH, LV aneurysm, or pericarditis.
Thus, it must be either normal variant ST elevation (loosely called "early repolarization") or acute LAD occlusion. To me it is clearly LAD occlusion.
One can use the LAD occlusion/early repol formula to differentiate. There is an iPhone app for it which really helps to be certain you are applying the formula correctly.
It is critical to use this formula only when the differential is subtle LAD occlusion vs. early repol (normal variant ST elevation). There must be ST Elevation of at least 1 mm. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI.
If you use these values:
Computerized QTc = 431 ms
ST elevation at 60 ms after the J-point in lead V3 (STE60V3) = 1.5 mm
R-wave amplitude in V4 (RAV4) = 6.5 mm
The resulting value = 25.1. Any value greater than 23.4 is very likely to be LAD occlusion.
Case continued
This was recorded 22 minutes later: Again, nonspecific ST-T abnormalities
Now there is straightening of the ST segment in V2. A straight ST segment is very rare in normal variant ST elevation, and the change makes it diagnostic of LAD occlusion. Inferior ST segments have also evolved. aVL has suspicious coving; it is probably a proximal LAD occlusion.
The ST elevation "criteria" are incorrect.
The patient arrived in the ED and had this ECG recorded at 25 minutes after the 2nd ECG (t = 47 minutes)
So this is the first ED ECG:
The cath lab was activated.
This ECG was recorded 26 minutes later, just before the patient was transported to the cath lab:
My interpretation when I saw this was that the LAD thrombosis was at the ostium of the first diagonal (D1) and that it had partly reperfused, leaving D1 open and the LAD still occluded.
A 100% proximal LAD occlusion was found, with left-to-left collaterals (from the circumflex) perfusing the 1st diagonal. This explains the reperfusion of the high lateral wall.
Here is the next day ECG:
Peak Troponin I: 99 ng/mL (very high)
Echo:
He called 911 for acute chest pain.
Here is the first prehospital ECG at time zero. The computer read "Nonspecific ST-T abnormalities."
Time zero:
 |
| The computerized QTc was 431 ms. The computer read "nonspecific ST-T abnormalities" What do you think? |
There is minimal ST elevation in V2 and V3.
T-waves are large in V2 and V3.
There are minimal down-up T-waves in III and aVF.
This is LAD occlusion until proven otherwise. One must explain the minimal ST elevation in V2 and V3. It is not due to LVH, LV aneurysm, or pericarditis.
Thus, it must be either normal variant ST elevation (loosely called "early repolarization") or acute LAD occlusion. To me it is clearly LAD occlusion.
One can use the LAD occlusion/early repol formula to differentiate. There is an iPhone app for it which really helps to be certain you are applying the formula correctly.
It is critical to use this formula only when the differential is subtle LAD occlusion vs. early repol (normal variant ST elevation). There must be ST Elevation of at least 1 mm. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI.
If you use these values:
Computerized QTc = 431 ms
ST elevation at 60 ms after the J-point in lead V3 (STE60V3) = 1.5 mm
R-wave amplitude in V4 (RAV4) = 6.5 mm
The resulting value = 25.1. Any value greater than 23.4 is very likely to be LAD occlusion.
Case continued
This was recorded 22 minutes later: Again, nonspecific ST-T abnormalities
 |
| What do you see here? The computer still reads "nonspecific ST-T abnormalities" Note the computer reads the ST segment: For V2, it is 1.03 mm For V3, it is 1.58 mm "Normal" for a male over age 40 is up to 2.0 mm in V2 and V3. |
Now there is straightening of the ST segment in V2. A straight ST segment is very rare in normal variant ST elevation, and the change makes it diagnostic of LAD occlusion. Inferior ST segments have also evolved. aVL has suspicious coving; it is probably a proximal LAD occlusion.
The ST elevation "criteria" are incorrect.
The patient arrived in the ED and had this ECG recorded at 25 minutes after the 2nd ECG (t = 47 minutes)
So this is the first ED ECG:
 |
| The computer interpretation: "Possible old inferior myocardial infarction." Very similar, but now with more ST depression in inferior leads and subtle ST elevation in aVL. Again, diagnostic of LAD occlusion, with evolution of findings. |
The cath lab was activated.
This ECG was recorded 26 minutes later, just before the patient was transported to the cath lab:
 |
| Very interesting: 1. The ST depression in the inferior leads is gone, as is the STE in aVL, suggestive of reperfusion of the high lateral wall. 2. There is T-wave inversion in aVL, also suggestive of reperfusion. 3. V3 has developed terminal QRS distortion (loss of S-wave), suggestive of evolution of injury to the anterior wall. 4. There are the beginnings of Q-waves in V2-V4 Thus, it appears as if there has been worsening of the anterior wall and reperfusion of the high lateral wall. |
My interpretation when I saw this was that the LAD thrombosis was at the ostium of the first diagonal (D1) and that it had partly reperfused, leaving D1 open and the LAD still occluded.
A 100% proximal LAD occlusion was found, with left-to-left collaterals (from the circumflex) perfusing the 1st diagonal. This explains the reperfusion of the high lateral wall.
Here is the next day ECG:
 |
| Reperfusion T-waves in I and aVL, and V2. Some persistent, minimal, ST elevation. |
Peak Troponin I: 99 ng/mL (very high)
Echo:
The estimated left ventricular ejection fraction is 50%
The estimated pulmonary artery systolic pressure is 39 mmHg + RA pressure.
Regional wall motion abnormality-distal septum anterior and apex akinetic
.
Regional wall motion abnormality-inferolateral (from previous STEMI).
Normal estimated left ventricular ejection fraction lower limits of normal.
Note there is no lateral wall motion abnormality because of the reperfusion, through collaterals, of that wall
Unless one is a true expert interpreter (ie, this means you’ve interpreted at least several hundred thousand tracings over MANY years, and require no more than 3-5 seconds to recognize 90-95% of the abnormalities on most tracings) — you should NOT look at the computerized report until AFTER you have made you own INDEPENDENT interpretation of an ECG. The reason is simple — you might see “nonspecific ST-T abnormalities” for a tracing like this, and thus be dissuaded into thinking there is a possibility of something non-acute. There should be NO DOUBT in the context of a 60yo man with new-onset severe chest pain that this 1st ECG represents acute LAD occlusion until proven otherwise. Significant findings (as per Dr. Smith) include: i) ST elevation in the chest leads beginning in lead V2 through to V5; ii) most definitely more peaked-than-they-should-be T waves especially in V3,V4 (but also in V2,V5); iii) subtle-but-real ST elevation with slight T inversion in aVL; and iv) subtle-but-real reciprocal changes in the inferior leads (with biphasic T in lead III). The inferior Q waves may or may not be related to the acute event … but we KNOW that “the action” is in anterior chest leads.
ReplyDeleteOverall, I like computerized ECG interpretations. They literally tripled my speed for interpretation back in the days when I was reading large piles of tracings for all of our providers. But that’s because I know exactly what the computer can and cannot do. For anyone who is not a true expert (definition above in my 1st sentence) — you should use the computer as a “check” to ONLY be looked at AFTER you have already made your own independent interpretation of the ECG. The computerized report might then suggest something you didn’t see. But if the computerized report says, “non-specific changes” for a tracing like this — Do NOT believe it, because the computer is wrong … THANKS to Dr. Smith for this highly illustrative post!
This was a very concerning story and ECG series from the start. What is most interesting / worrying for me is that my hospital is 2,000km from a cath lab and he did not meet our thrombolysable criteria. Who reading this would have thrombolysed him at this stage? Clearly, he would have almost certainly gone on to widespread ST elevation, which would have been 'thrombolysable', but more damage would have been done by then.
ReplyDeleteDavid, criteria are meant to ensure high specificity for interpreters who are uncertain. A full 25% of acute 100% coronary occlusions do not meet STEMI criteria. Thrombolysis is indicated here.
DeleteSteve Smith
Steve...
ReplyDeleteThe first ECG is is the kind of ECG that I remember most when giving expert testimony. As Dr. Grauer stated, this is not all that subtle to someone who is an expert based on years of interpreting thousands of ECGs, but it is dangerously subtle to a much less experienced emergency or critical care physician who is probably overworked and sleep-deprived at 4 am.
Three things in the first ECG grabbed my attention immediately and instantaneously: the wide T waves in the precordial leads, the straightening of the ST segment into the T wave in aVL (most evident in the second complex in that lead) and the subtle planar ST depression in II and aVF with distinct ST-T junctions.
I teach advanced electrocardiography and I find so many physicians who only recognize hyperacute T waves when they are very tall and peaked (i.e., when they look most like hyperkalemic T's). WIDE hyperacute T waves are more frequent and (I feel) more typical (though some are tall and peaked).
Also, a straight, upward sloping ST segment that continues to the apex of the T wave - especially in the setting of a patient with credible ACS symptoms - should always, ALWAYS be a red flag! That is an ST segment that is transitioning from upward concavity to upward convexity. I also find that many of my students tend to overlook Lead aVL, especially because the QRS is often very small, being perpendicular to Lead II and the majority of mean QRS axes in the frontal plane. Sometimes you just have to use a magnifying lens to see that the ST segment begins with a J point elevation that is at times =/> 50% the height of the R wave. During my residency I trained under a number of cardiologists, all of whom impressed on me that Lead aVL alone was probably the source of more malpractice litigation than one could imagine.
The planar ST depression in Leads II and aVF with the distinct ST-T junction also caught my eye immediately. The ST depression is very, very subtle but I wouldn't need it to strongly suspect a reciprocal change. A flat ST segment and the distinctive take-off of the T wave would have been enough.
This is an excellent teaching case!
Thanks.
Exactly right on all counts, Jerry. Thanks!
DeleteSteve