Is this new LAD occlusion with ST Elevation superimposed on old QS-wave MI?

A middle-aged male with history of anterior STEMI complicated by prolonged cardiac arrest with near miraculous ROSC, who has an ICD, complained of 2 months of increasing dyspnea on exertion, without chest pain.  He works out, and his workouts had become severely limited.

He had a known EF of 35%.

On the morning of presentation to the ED, he complained of some choking feeling in his throat which was persistent upon arrival.  There was no SOB or chest pain at rest.

Vital signs were normal.  Exam was normal.  There was no throat pathology.

Here is his ED ECG:

This is pretty classic anterior LV aneurysm morphology:
QS-waves with some moderate ST elevation
However, the T-waves may be a bit large for typical LV aneurysm.
If any T/QRS ratio is greater than 0.36, then strongly consider that it is an acute MI, not just old.
In this case, here are the T/QRS ratios:V2 = 3.5/16 = 0.22
V3 = 2.5/6.5 = 0.38
V4 = 2.0/4.5 = 0.44
So 2 leads have a higher ratio than expected for LV aneurysm.

Of course, in this case we KNOW he has an old anterior MI.
And we have an old ECG to compare to:

This has zero ST elevation, and flat T-waves.
Thus, it would appear that there is new STE and enlarged T-waves superimposed on old LV aneurysm.
A faster heart rate will exaggerate ST elevation, but in this case the heart rate is slower.
We cannot blame the change on the heart rate.

Why, if there is a new LAD occlusion, would the findings be so subtle?

First, we have seen that LAD occlusion can be very subtle.
Second, when there is very little viable myocardium present, there will be less ST elevation and less T-wave enlargement.

I was very concerned about this choking feeling in his throat and the ECG.

I called cardiology, and the cardiologist on call knew this patient well and was also very concerned.

We activated the cath lab.

The coronaries were clean.


Later, his cardiologist remembered that he had increased the dose of beta blocker just before the new dyspnea on exertion began.  This appears to be a good explanation for the exercise limitation.

However, I don't know why his ECG shows these new, worrisome findings.

If I saw a similar case in the future, I would do the same thing.

No subsequent ECG was recorded to assess for change/evolution.


By the way, this was his ECG after being defibrillated 17 times several years ago:

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Comment by KEN GRAUER, MD (6/2/2019):

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A dictum that I was taught on my surgical rotation in medical school was, “If you are correct more than 80% of the time in diagnosing acute appendicitis — then you are not taking enough patients to surgery.” This dictum was of course developed before advanced diagnostic techniques were in practice (ie, ultrasound and MRI, which have greatly increased diagnostic accuracy) — but I believe the general principle remains valid today and applies to conditions in many medical specialties.

• As expert as one may become in clinical ECG interpretation — no one is able to predict with 100% accuracy which ECGs will indicate acute coronary occlusion at cardiac cath.
• Although experienced interpreters can get close to this ideal accuracy standard — no interpreter is perfect, and a single initial ECG is not infallible. As a result, despite clear suggestion on a tracing of acute ECG changes — prompt appropriate cardiac catheterization will sometimes reveal patent coronaries.

MORAL: This blog post illustrates one case in which acute cath lab activation was the correct course of action despite the fact that the cath turned out to be negative. 

• Were the same scenario to repeat itself — acute cath lab activation would again be the correct course of action, because this patient with a history of previous anterior STEMI and new symptoms — presented to the ED with new ECG changes that suggested acute ischemia.

Dr. Smith has detailed quantitative assessment of T wave/QRS amplitude ratios to demonstrate abnormal findings in the initial ECG. I focus my comments below on qualitative assessment of this initial ED tracing ( = ECG #1 in Figure-1) — and then hone in on the changes seen when comparing ECG #1 to a prior ECG on this patient ( = ECG #2).

Figure-1: The initial ECG in the ED — and comparison of this initial tracing with an old ECG on this patient (See text).

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My Thoughts on ECG #1:  First and foremost is the History! This patient with extensive prior anterior STEMI presented with a 2-month history of progressive dyspnea, with development of a “new choking sensation” on the day he presented, with persistence of symptoms at the time he arrived in the ED. Before looking at his initial ECG — we need to appreciate that this worrisome history describes a high-prevalence situation for acute ischemia.

• Descriptive Analysis of ECG #1: There is sinus bradycardia at ~55/minute. All intervals are normal. There is marked right axis deviation, with a predominantly negative qrS complex in lead I. There is no chamber enlargement.

Q-R-S-T Changes:

• Q Waves — Numerous Q waves are seen on this tracing, consistent with the patient’s prior infarction. Small q waves are seen in leads I, II, III, aVF (albeit the inferior q waves are not-so-narrow); a large QS complex is seen in leads V1-thru-V3 (with fragmentation of the S wave downslope in V2 and V3 = [BLUE arrows]) — and then relatively large Q waves (especially given relative size of QRS amplitude in these leads) are seen in V4, V5 and V6.
• R Wave Progression — Transition is delayed until between lead V4-to-V5 or V6. The reason for this delayed transition is the large anterior QS complexes.
• ST-T Wave Changes — T waves are peaked in each of the inferior leads (as highlighted in lead II, within the BLUE oval) — with mirror-image but shallow T wave inversion in lead aVL. The ST segment takeoff looks straightened in leads V1-thru-V4 or V5 (parallel to the slanted BLUE lines), with slight ST elevation in these leads.

My Initial Impression of ECG #1: I was not at all certain about whether or not the above described changes in ECG #1 were acute. I was concerned by the history. I thought this might be an early acute OMI in process of evolving.

• This was one case in which I really wanted to see a prior ECG on this patient! That said, I made my initial impression before looking at ECG #2.
• There was obvious evidence of extensive prior infarction(s). At the least, there was prior antero-lateral MI — evidenced by deep QS complexes in anterior leads with fragmentation in V2, V3 (BLUE arrows) + persistent Q waves through to V6 with minimal r wave amplitude in high lateral leads I and aVL (and a small q in lead I ).
• I was uncertain IF the small-but-somewhat-widened inferior Q waves represented prior inferior infarction — or — if the more-peaked-than-expected T waves seen in each of the 3 inferior leads, in association with fairly shallow-but-mirror-image T wave inversion in lead aVL might reflect acute or recent injury.
• Given the clinical context (ie, worrisome new symptoms in this patient with known severe coronary disease) — I was concerned about the relative straightening of the ST segment takeoff in leads V1-thru V4 (possibly V5) + a T wave in leads V3 and V4 that looked like it might be hyperacute in view of the lack of R wave amplitude in these leads.
• Beyond-the-Core: I was not sure if the marked right axis with predominantly negative QRS in lead I + qR pattern in each of the inferior leads was indicative of: i) LPHB; ii) Prior infarction(s); or, iii) Both of these entities. Most of the time — LPHB does not manifest as an isolated conduction system defect, but instead is usually seen in association with RBBB. One also does not usually develop a small initial q wave in lead I with LPHB — though it certainly is possible given this patient’s prior history that limb lead QRS morphology is the result of prior infarction (with q waves and loss of high lateral lead R wave amplitude), with or without the conduction system defect of LPHB.
• Bottom Line: I was not at all certain about whether or not the above described changes in ECG #1 were acute. I felt we needed: i) More clinical information; ii) Access to one or more prior ECGs, so that we could determine which of the above findings might be acute; and, iii) To consider alerting the cardiologist on call that this patient was in the ED and might soon need cardiac cath.

My Impression After Seeing ECG #2: Lead-to-lead comparison of ECG #1 with a previous ECG on this patient suggests the following.

• That despite no appreciable change in frontal plane axis — the T wave peaking in each of the inferior leads of ECG #1 is a new finding (that was not present in ECG #2).
• Even accounting for slight change in R wave progression between the 2 tracings in Figure-1 (ie, there is no appreciable r wave until lead V6 in ECG #2) — the ST segment straightening that is seen in ECG #1 in 5 of the 6 chest leads (parallel to the slanted BLUE lines) — was present only in leads V2 and V3 on the previous tracing (ECG #2) — and none of the ST-T waves in ECG #2 looked hyperacute.
• Bottom Line: Given the clinical context of new worrisome symptoms — the new findings seen in ECG #1 compared to the previous ECG on this patient merit acute cath lab activation.
• Final Thought #1: Access to a prior tracing on this patient was invaluable in this case. That said, ideally we’d want to know when this prior tracing was obtained relative to the evolution of this patient’s previous extensive infarction and cardiac arrest — and, whether there was any evolution of ECG findings after hospital discharge.
• Final Thought #2: A superimposed new condition might not produce changes as dramatic as one might expect — IF the patient's baseline ECG showed baseline ST-T wave changes in the opposite direction ...

Our THANKS to Dr. Smith for presenting this highly insightful case!