A woman in her 30s with several days of chest pain and an episode of altered mental status.

Written by Pendell Meyers, reviewed by Smith, Grauer, McLaren

A woman in her early 30s with history of diabetes had 2-3 days of gradual onset nonradiating chest pain with associated nausea, malaise, and shortness of breath. Then she had an "abrupt change in her mental status and became more somnolent and less responsive" at home in front of her family. Her family called EMS, who found the patient awake and alert complaining of worsening chest pain compared to the prior few days.

En route to the ED, they recorded this ECG and transmitted it, asking whether the cath lab should be activated:

What do you think?

There is sinus rhythm at just under 100 bpm. The QRS has high leftward voltage consistent with LVH more than simple healthy young voltage. There is large STE in V1-V3, as well as aVL. There is STD in V5-6, II, III, and aVF. The T waves are questionably hyperacute in V1-V4, but the QRS is also very tall and dramatic. We have very few cases of LVH with large voltage present simultaneously with anterior hyperacute T waves, but the concern is that this could be one of them. A baseline ECG would help greatly (available below).

The subtle LAD OMI vs. normal variant STE formula is not applicable due to the presence of inferior reciprocal STD and lateral STD, and because it was not trained on LVH patients. 

If you had erroneously applied the formula, it would be falsely reassuring due to the large QRS voltage present in this case:

A prior baseline was available (though I doubt it was at hand when EMS asked for a prehospital decision on the ECG above):

Baseline (assuming baseline, no clinical info available) from last year.

With the baseline (just LVH with some normal variant STE), it is obviously easy to see that the initial ECG above is LAD OMI.

Here is her ECG immediately on arrival to the ED:

Obvious STEMI(+) OMI.

An ED echo reportedly showed an anterior wall motion abnormality and grossly depressed EF.

"Given patient's change in mental status, CTA of the chest was ordered to rule out dissection." 

Meyers note: I think CT angio for dissection is unnecessary in this case, as it is in almost all OMI cases. As Jesse McLaren pointed out to me, STEMI or OMI secondary to dissection is very rare (https://pubmed.ncbi.nlm.nih.gov/28511806/), so looking for it in the absence of compelling reasons (eg focal neuro or pulse deficit) will just delay reperfusion (https://pubmed.ncbi.nlm.nih.gov/22534052/).

"While at CT scanner, the patient lost pulses and appeared to have polymorphic VT cardiac arrest, then she achieved immediate ROSC with one defibrillation."

The initial high sensitivity troponin I returned at 34 ng/L.

The CT showed no dissection.

She proceeded to cath where they found total thrombotic proximal LAD occlusion (see images below).

ECG hours after PCI:

Next day ECG:

Troponin peaked at 23,591 ng/L.

Cardiac MRI done 5 days later:

EF 35%. Severe hypokinesis of the entire septum, anterior wall, and distal/apical segments. No LV thrombus. 

Learning Points:

LVH can make OMI interpretation more difficult. It is rare to see high LVH voltage in the same leads as OMI. But this one is an excellent example.

The first troponin is minimal when the benefit of reperfusion is maximal.

Comparison to baseline, and serial ECGs, can make a difficult interpretation easy. 

Sudden syncope or "seizure" in sick patients should be assumed to be cardiac arrest until proven otherwise.

Young people and women have OMI, and like other populations they may have delayed recognition.

OMI always evolves on ECG, if you have the ECGs to see it.

Young Women do suffer from thrombotic coronary occlusion!!

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MY Comment by KEN GRAUER, MD (8/15/2022):

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I saw the initial tracing in today’s case ( = ECG #1) — knowing only that the patient was a woman in her 30s on her way to the ED. I presumed she must have been having chest pain — but didn’t know how worrisome the history was (or was not) for a new cardiac event. I focus my comment on this initial tracing — which for clarity I’ve reproduced below in Figure-1. My thoughts on this initial ECG were the following:

• The rhythm is sinus at ~90-95/minute. Intervals (QR, QRS, QTc) and the frontal plane axis are normal (about +20 degrees).
• QRS amplitudes are greatly increased — especially in the chest leads, where there is significant "lead overlap" of complexes.

Regarding Q-R-S-T Changes:

• There are small and narrow Q waves in lateral leads (I,aVL,V5,V6) — which are almost certain to be normal septal q waves.
• R wave progression is normal (with transition appropriately occurring between leads V2-to-V3).

The KEY Question is whether ST-T wave appearance in ECG #1 is (or is not) suggestive of an acute cardiac event.

Figure-1: The initial ECG in today’s case.

Should the Cath Lab Be Activated?

As emphasized by Dr. Meyers — assessment of the initial ECG in today’s case was complicated by the presence of LVH. It is simply not common to see the picture of markedly increased QRS amplitude, in association with hyperacute T waves in the anterior leads.

• Dr. Meyers also emphasized that on occasion — finding a baseline tracing on the patient for comparison can be diagnostic. This was the case with today’s patient — as a quick comparison with the previous ECG left NO doubt that the chest lead ST-T wave peaking in ECG #1 was a new (and therefore acute) finding. Unfortunately, baseline ECGs are not always available at the time they are needed for initial triage decision-making of whether or not to activate the cath lab. So HOW to proceed?

I’d point out the following.

• There are many ECG criteria for the diagnosis of LVH. I list those that I favor in Figure-2 — and discuss in detail my approach to the ECG diagnosis of LVH at THIS LINK.
• Note addition of the patient’s age to the criteria I suggest in Figure-2. The reason for including age — is that younger adults often manifest increased QRS amplitudes on ECG without true chamber LVH. While there is no universally-agreed-upon discrete “maximal age dividing point” — I’ve found ~35 years of age to work well clinically in my experience over decades.
• 
  
• This number “35” facilitates recall — because, of the 50+ criteria for LVH in the literature — by far the most sensitive and specific criterion in my experience also involves the number “35” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 ≥35 mm satisfies voltage criteria for LVH in adults ≥35 years of age).
• 
  
• Assessment of LVH in the pediatric population is problematic — because of the difficulty determining reliable diagnostic voltage criteria for each age group (complicated further by technical issues of ensuring precise chest lead electrode placement in these smaller body frame patients). As a result — I routinely refer to tables for assessing maximal expected amplitudes for each specific age group.
• 
  
• To “simplify life” when assessing for LVH in younger adults (ie, patients in their late teens, 20s and early 30s) — I’ve found over the years that reversing the number “35” provides a quick “ballpark” assessment criterion as to whether there is sufficient voltage on the ECG of a younger adult (ie, who is under 35yo) to qualify for “LVH” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 ≥53 mm).

Figure-2: Criteria I favor for the ECG diagnosis of LVH. (NOTE: I’ve excerpted this Figure from My Comment at the bottom of the page in the June 20, 2020 post in Dr. Smith’s ECG Blog).

Is there Voltage for LVH in Figure-1?

The patient in today’s case was a woman in her 30s — therefore more likely to manifest increased QRS amplitude not necessarily the result of LVH. Given the challenge of confusing “amplitude overlap” in the chest leads of Figure-1 — I clarify the limits of QRS deflections by coloring the complexes in Figure-3.

• Note that even accounting for the fact that today’s patient is a younger adult — the 53 mm criterion threshold is attained, suggesting true voltage for LVH in this younger age group patient.
• 
  
• Remember: The ECG is an imperfect tool to assess LVH. If true chamber size is needed — then an Echo (which also provides information on cardiac function) is far superior to ECG for assessment of chamber enlargement. That said — “pre-ECG interpretation likelihood” for LVH is clearly increased in today’s patient because of longstanding diabetes.

Figure-3: I’ve colored the QRS complex in 5 of the chest leads — to illustrate the actual size of the QRS complex in each of these leads. The deepest S wave is in lead V2 ( = 27 mm, as shown in RED) + the tallest R wave in lead V5 ( = 27 mm, as shown in GREEN) exceeds 53 mm. Note that the S wave in lead V1 is also unusually deep ( = 26 mm) — and the R wave in lead V4 is of unknown amplitude, since it is cut off by the top of the ECG paper (See text).

A Final Look at the ECG in Figure-1:

I fully acknowledge that I was not at all certain from seeing the initial ECG in Figure-1 whether this patient was (or was not) having an acute event. Against an acute event was the following:

• The patient has LVH on ECG — and as we have mentioned, it is uncommon to see hyperacute anterior T waves in association with marked LVH. Among the types of benign repolarization variants is T wave peaking that is often surprisingly tall in anterior leads in which there are deep S waves.
• There is excellent R wave progression — with an extremely tall R wave in lead V3 (R wave amplitude is typically reduced when there is anterior OMI).
• The QTc is at most no more than minimally prolonged (whereas acute infarction often produces significant QTc prolongation).

On the other hand — In Favor of an acute event until proven otherwise are the following:

• Although the patient in today's case is a young adult — this woman in her 30s has diabetes mellitus (presumably for some period of time) — therefore she clearly is at greater risk of myocardial infarction at an earlier age.
• Even accounting for LVH — the T wave in anterior chest leads is taller than is usually expected. This is especially true in lead V3 — where the 15 mm tall T wave is nearly as tall as the R wave in this lead. The "shape" of LV "strain" when seen in anterior leads tends to be the mirror-image opposite of the slow downslope-faster upslope ST depression typically seen in leads V5,V6 with LVH. It would be unusual to see such a tall, pointed T wave with narrow base from LVH as we see in lead V3.
• Neighboring leads V2 and V4 also appear taller and pointier than is usually seen with either LVH or depolarization variants.
• Finally, while the ST-T wave may normally be negative in lead III when the QRS is predominantly negative — there usually is not the J-point depression seen in Figure-3 (RED arrow in lead III).

BOTTOM Line: This young woman in her 30s has diabetes mellitus — and presented with a history of "worsening chest pain". While I was uncertain from her initial ECG if an acute process was ongoing — the worrisome history and questionable ECG features described above combine to clearly merit diagnostic cath to clarify the anatomy.

• To Emphasize: Once the prior ECG became available for comparison — there no longer was any doubt that the ECG findings highlighted above were acute!