Is this ST elevation normal or abnormal?

Written by Pendell Meyers

A male in his 50s with history of HTN, DM, HLD presented with chest pain of less than one hour duration.

Here is his triage ECG:

What do you think?

Here is the computer interpretation at the top of the page:

Algorithm: Marquette/GE 12SL

There is sinus rhythm. There is fairly high QRS voltage, however the morphology of the QRS is otherwise normal, i.e. there is no LVH morphology (although voltage is high) or other QRS abnormalities that would adjust your expectations for the repolarization findings. There is a small amount of STE in V2 and V3, with a very small amount of STD in V4-V6. The T-waves are not definitively hyperacute. There was no prior for comparison. The lateral and inferior leads neither help to confirm or deny the suspicion of LAD occlusion. The subtle LAD occlusion vs. early repol formula is contraindicated because of the very slight ST depression.

This ECG was texted to Dr. Smith with no clinical context. He responded: "Very interesting! V4 and V5 ST depression make this very unlikely to be a normal variant." He is implying that LAD occlusion is suspected based on the STE in V2-3 with STD in V5-6.

The ECG was interpreted as non-ischemic. The patient was closely monitored.

Here is a repeat ECG 45 minutes later with persistent chest pain:

Obviously progressing into a clear STEMI. Meets formal STEMI criteria in V2-V3. Also notice clearly hyperacute T waves in V2-V4, as well as worsening STD in V5-6 and II, III, aVF. 

Several more repeats were obtained while waiting for the cath lab to be ready:

At cath they found an acute, thrombotic lesion in the proximal LAD with 95% stenosis and TIMI 2 flow, with an associated full thrombotic occlusion at the ostium of the 1st diagonal (TIMI 0 flow). Here are the images before and after intervention:

Here are the ECGs collected after intervention, showing the expected findings of reperfusion:

Trop T peaked at only 0.91 ng/mL. This is likely due to rapid presentation by the patient and appropriate rapid repeat ECGs with quick intervention. Most sustained LAD occlusions without rapid intervention will generate a troponin higher than this.

The patient did well.

Learning Points:

In our experience (no literature for or against as far as we know) the combination of abnormal STE in the right precordial/anterior leads with STD in lateral leads seems to be indicative of very early or impending LAD occlusion. You will see many patients with chest pain and ST elevation in the anterior leads, however you cannot assume it is normal variant ST elevation when there is STD in the lateral leads, which is essentially never normal in the setting of a normal QRS.

Repeat ECGs make difficult decisions easier.

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Comment by KEN GRAUER, MD (12/29/2018):

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Superb case by Dr. Pendell Meyers, which highlights recognition of subtle acute findings. Although I arrived at the same conclusion as Drs. Smith and Meyers in this case — my path for getting there differed slightly … I illustrate the rationale for my approach in Figure-1.

Figure-1: The initial ECG in this case. R wave amplitudes in several leads are noted in RED (See text). 

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The “magic” of electrocardiography (and its fascination) — lies with the different perspectives experienced interpreters sometimes provide when assessing the same tracing. The rhythm in Figure-1 is sinus. Intervals are normal (PR, QRS, QT). The frontal plane axis is normal, albeit relatively vertical at ~ +80 degrees. My thoughts on the rest of this ECG were as follows:

• The KEY finding on this tracing lies with the ST-T wave in lead V3. As per Dr. Meyers — there is slight ST elevation in this lead. I thought the T wave in lead V3 was disproportionately tall with respect to the R wave in this lead, and the base of this T wave was wider-than-it-should-be. This T wave just looked “out of place” to me, given ST-T wave findings on the rest of the tracing. Therefore — the ST-T wave in lead V3 could represent an early finding of acute LAD occlusion ... 
• I was not impressed by the ST-T wave in lead V2. I thought the amount and shape of the ST-T wave in lead V2 was comparable to what may be seen in a normal tracing.
• There is definite voltage for LVH. A R wave ≥20 mm in any inferior lead (II, III, or aVF) satisfies voltage criteria. In association with overall generous voltage, with definite voltage criteria for LVH satisfied in 2 of the inferior leads — I interpreted the ST segment flattening with slight ST depression in lead V6 + the slight J-point ST depression in lead V5 as a “strain” equivalent. In view of the clinical setting (a 50yo man with diabetes and hypertension) — I thought these findings more than enough to qualify for an ECG determination of LVH.

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My Initial Impression of ECG #1: I was not at all certain from this initial tracing if the findings in ECG #1 represented an acute event. Without availability of a prior tracing for comparison — I felt there was no way to distinguish the subtle lateral chest lead findings from being a longstanding marker of LVH (as a “strain” equivalent) — vs potential new ischemia. This left me with lead V3 as the single lead of definite concern — and, a single lead is not enough to make a definite diagnosis … BOTTOM LINE: This patient’s age and clinical history (diabetes; new-onset chest pain presenting to an ED) — automatically place him in a high prevalence group for an acute event. Clearly, more information is needed before a definite decision can be reached — but the “onus of proof” is on the clinician to rule out acute LAD occlusion.

• The 2nd ECG done 45 minutes later removed all doubt!

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Comment Regarding ECG Diagnosis of LVH:

As I discussed in detail in Dr. Smith’s blog post from December 27, 2018 — more than 50 criteria have been proposed in the literature for the ECG diagnosis of LVH. Whenever there are so many potential answers to any clinical question — it means that none of “the answers” are nearly as good as we would like.

• Even in the best of hands — sensitivity of the ECG for assessing LVH is no more than 60%. The “good news” is that despite this poor sensitivity — when certain criteria are satisfied, specificity for LVH may be excellent (ie, >90-95%).
• Specificity of the ECG for LVH is greatly enhanced if, in addition to fulfilling one or more voltage criteria: i) the patient is of a certain age (ie, patients under ~35 often manifest larger QRS amplitudes not indicative of true chamber enlargement); ii) the patient has a condition(s) that predisposes to LVH (such as hypertension, as in this case); and, iii) ST-T wave changes consistent with LV “strain” are present in one or more of the lateral leads. NOTE: Even if the classic, slowly downsloping (sagging) ST-T wave depression of LV “strain” is not present — a more subtle picture of lateral lead ST-T wave abnormality (ie, ST flattening and/or slight depression as seen in this case) qualifies as a “strain equivalent”, and serves to enhance specificity for LVH when voltage criteria are met in association with a predisposing condition.
• The presence of LVH on ECG often makes it much more difficult to assess for acute coronary disease. That said, given the history of new-onset chest pain and the abnormal appearance of the ST-T wave in lead V3 in the initial ECG — one has to be concerned about possible acute LAD occlusion until you prove otherwise.
• CLICK HERE — for more on My Approach to ECG Assessment of LVH (including the voltage criteria I favor).