A man in his 50s with acute chest pain and LVH

Sent by Drew Williams, written by Pendell Meyers

A man in his 50s with history of hypertension was standing at the bus stop when he developed sudden onset severe pressure-like chest pain radiating to his neck and right arm, associated with dyspnea, diaphoresis, and presyncope. EMS arrived and administered aspirin and nitroglycerin. He reported several weeks of intermittent chest pain similar to the active pain, worsening over the past 2-3 days, some of them as long as an hour, but all spontaneously resolved and were of less intensity than the current symptoms.

There are 2 very instructive posts which we link to at the bottom. Do not miss them!

Here are his three EMS ECGs:

EMS1 at 0735

This was sent to Dr. Smith with no other information.  What did he say?

Meyers sent this ECG to Smith without any other info and this was the response:

Smith interpretation: "A very rare anterior OMI w high S-wave voltage." 

Meyers: "I said I would have to say OMI until proven otherwise. But I was not certain. The inferior reciprocal part was the most helpful for me.  Steve, tell me more about how you know this one. The LVH makes it hard."

Smith: "I would not say I know it. But I highly suspect it due to the hyperacute T wave in V3, but especially, as you say, the inferior reciprocal ST depression, with ST elevation in aVL."

Another ECG was recorded: EMS2 at 0746

EMS3 at 0755

Baseline (4 months ago) (not available to EMS at that time)

The three EMS ECGs above show initially concerning findings for anterior and high lateral OMI in the setting of LVH, followed quickly by deflation and terminal T wave inversion, all together suggesting transient LAD OMI with reperfusion.

His symptoms were reportedly resolved upon arrival to the ED.

ED ECGs:

0814

0830

These show continued reperfusion with no evidence of reocclusion.

Initial high sensitivity troponin I returned at 103 ng/L (URL 20 ng/L, and the patient's prior troponin from 4 months ago was 14 ng/L).

Cath at approximately 0945:

"The LAD had a 90% proximal stenosis with TIMI 3 flow which corresponds to his ECG although LV function remains preserved. With nitroglycerin there is improvement in the 90% stenosis but still persistent stenosis consistent with the dynamic nature of his presentation. I am going to code this as an acute STEMI as he had transient ST elevation which started to evolve in the emergency department but I think this is most appropriately termed STEMI."

Pre-intervention:

Post-intervention: 

Post-cath ECG:

1030

Second high sensitivity troponin I returned at 594 ng/L, and no further were ordered.

No formal echo was done, and EF was normal on ventriculogram during cath, with no obvious wall motion abnormalities.

Next day ECG:

2 Very instructive posts on LVH and OMI and Pseudo-OMI

1. Is this Acute Ischemia? More on LVH.

2. LVH with anterior ST Elevation. When is it anterior STEMI?

Learning Points:

It is rare to see high voltage of LVH at the same time as OMI findings in the same leads as the high voltage. It is so rare, that Dr. Smith has been unable to study it due to difficulty finding such cases. We think that, in most cases, acute LAD OMI causes diminution of S-wave voltage in V1-V3 (we have proven that LAD OMIs have less QRS voltage than normal variant STE, for example), which results in being unable to find many cases of high voltage LVH with active OMI findings. This case's first EMS ECG shows a rare example of LVH with active anterior and high lateral OMI.

Comparison to prior ECG can be very helpful. 

Reperfusion of OMI indicates at least partial thrombolysis of occluding thrombus, but still unstable plaque rupture, which can reocclude at any moment. We believe the best care of such patients would be angiogram as soon as possible (while receiving maximal medical therapy of course), in order to secure this unstable lesion and prevent reocclusion.

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Comment by KEN GRAUER, MD (12/14/2022):

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We've reviewed many cases that illustrate the challenge posed by distinguishing between marked LVH — vs — LVH + superimposed acute OMI. Today's case presents another facet of this challenging differential diagnosis, namely recognition of a true acute OMI on top of longstanding LVH.

• As per Drs. Williams, Smith and Meyers — It is rare to see high voltage from LVH at the same time as we see ECG findings of acute OMI.

I focus My Comment today on a number of KEY aspects regarding the challenging differential diagnosis between LVH vs LVH + acute OMI. For clarity in Figure-1 — I've put together and labeled the initial 2 tracings recorded in today's case.

• NOTE: By way of background — I'll add the following links to a sampling of 4 (from the many) cases on Dr. Smith's ECG Blog which address the question of acute changes in patients with obvious LVH. For discussion of these cases — Please see My Comment at the bottom of the page in the June 20, 2020 post — the July 29, 2022 post — the August 15, 2022 post — and the September 30, 2022 post.

Figure-1: I've labeled the initial 2 tracings recorded in today's case (See text).

MY Thoughts on the 2 Initial EMS ECGs:

The patient in today's case was a man in his 50s with a longstanding history of hypertension. Marked LVH is obvious from the initial EMS tracing:

• I've reviewed ECG criteria for LVH (including assessment for LV "strain") on many occasions (Please see My Comment in the June 20, 2020 post in Dr. Smith's ECG Blog). 
• 
  
• In EMS ECG #1 — Colored lines clarify R wave and S wave amplitudes that overlap in each of the 6 chest leads. These show very deep anterior S waves — and — very tall lateral chest lead R waves that easily exceed voltage criteria for LVH in multiple leads.
• 
  
• PEARL #1: Remember that QRS voltage is often "cut off" on pre-hospital tracings (ie, BLUE arrows showing S wave cutoff in lead V3 — and R wave cutoff in lead V4). In particular — We have NO idea as to how deep the S wave in lead V3 really is. While I agree that the amount of J-point ST elevation and the height of T wave peaking in lead V3 looks to be disproportionate — this assessment would clearly be far more difficult if it turned out that an additional 20 mm of S wave were cut off from the real size of the S wave in lead V3.
• 
  
• PEARL #2: Once again — Lead aVL comes through on today's tracing as the KEY lead for convincing me of the likelihood of acute OMI. Marked artifact throughout lead aVL in EMS ECG #1 complicates assessment for ST-T wave changes in this lead. That said — despite baseline wander and a different picture for each of the QRST complexes in this lead — each of the 3 complexes in lead aVL suggest that there is ST elevation! This should not occur in a patient with marked LVH, in whom lateral leads like aVL would be expected to show ST-T wave depression from LV "strain" (or at least not to show ST elevation!).
• 
  
• PEARL #3: A definitive answer is forthcoming in the repeat ECG done just 9 minutes later. The limb lead artifact that was so prominent in EMS ECG #1 — is no longer present in EMS ECG #2. We now clearly see an initial Q wave in lead aVL — with coved ST segments showing reduced ST elevation, but with new T wave inversion. Even accounting for slight change in the frontal plane axis between these initial 2 EMS tracings — the ST-T wave changes in lead aVL suggest dynamic change consistent with spontaneous reperfusion.
• ST-T wave changes of spontaneous reperfusion are even more evident in the precordial leads, which show typical evolution in the mid-chest leads of EMS ECG #2 — in that there is now reduced T wave amplitude with deepening T wave inversion. Serial ECGs (sometimes done as soon as minutes later) — will often be diagnostic in an acutely evolving process! (as is true in today's case from comparing EMS ECGs #1 and #2, done just 9 minutes apart!). 

PEARL #4: Once again — Careful review of the History proved to be the KEY to understanding serial ECG findings. The reason today's patient called EMS — was for persistence of his most severe chest pain episode. But the patient also reported a history of several weeks of progressively worsening chest pain, sometimes lasting as long as an hour — but always with spontaneous resolution of chest pain!

• This history of frequent chest pain episodes that always spontaneously resolve — is consistent with serial ECGs and the patient's history on the day that he called EMS. Because each of his prior episodes of chest pain spontaneously resolved — his initial ECG ( = EMS ECG #1) suggested abnormal ST elevation (at least in lead aVL, if not also in lead V3) — but no sign of completed infarction.
• Consistent with the history from prior episodes — the ST elevation seen in EMS ECG #1 resolved, and was replaced with the above described reperfusion T waves in EMS ECGs #2 and #3 — all of which occurred as the severe chest pain resolved! (ie, Severe chest pain was present with EMS ECG #1 — but had essentially resolved in association with development of reperfusion T waves by the time the patient arrived in the ED).

PEARL #5: As we have shown on many prior ECG Blog posts — correlation of the history in today's case together with serial ECGs — can effectively tell us IF the "culprit" artery is open or closed. The accuracy of this clinical correlation is especially remarkable in today's case given the background of such marked LVH!