Written by Jesse McLaren (@ECGCases), with comments by Smith and Grauer
A 50 year old presented with chest pain radiating to the
shoulder. They had a history of an LAD stent 10 years ago and alcohol use
disorder, with repeated visits for chest pain and two code STEMIs two years ago
that found no occlusive disease.
What do you think?
There’s normal sinus rhythm, normal intervals, normal axis,
and normal R wave progression. There’s LVH with repolarization abnormalities,
including discordant ST depression and T wave inversion inferolaterally and
discordant ST elevation and tall T wave in V2.
Are there any primary ischemic changes? How can we identify
OMI in the presence of LVH?
1. prior ECGs
Below are the
first and last ECGs from that the visit resulting in a code STEMI, which found
a patent LAD stent but no occlusive disease (as per the discharge summary, further angiogram details not available):
This shows the benefits and limitations of prior ECG. On the
one hand, we can see prior secondary repolarization abnormalities. But we can
also see that they fluctuate over time, and can vary with differences in lead
placement.
2. proportionality
The secondary ST/T changes from LVH can make it difficult to
assess primary ischemic abnormalities, and the STEMI paradigm doesn’t even
try—defining STEMI as ST elevation in the absence of LVH. But the OMI paradigm
can draw from the principle of proportionality. As Drs. Aslanger, Meyers and
Smith explain in Recognizing
electrocardiographically subtle occlusion myocardial infarction and
differentiating it from mimics: ten steps to or away from the cath lab: “If there is high voltage indicating
left ventricular hypertrophy (LVH), some STE may be seen in leads with deep S
waves (usually V1-V3) and may mimic STEMI. If the amplitude of STE is more than
one-sixth of the amplitude of S-wave in one of these leads, it is highly
suspicious for OMI.”
This patient has a baseline ST/T ratio in V2 of >15% but
it is greater on the new ECG. Both the second ECG from the last visit and new
ECG have 3mm of ST elevation in V3, but the S wave has diminished from 14mm to
11mm, raising the ST/T ratio from 21% to 27%.
Very important post for understanding anterior ST Elevation in the presence of LVH:
3. patient
With the patient's repeated visits with chest pain, prior stable angiograms and repolarization changes on ECG, it would have been easy to dismiss. But the cardiologist was concerned about the patient’s
description of the pain, which was worse than prior episodes and in a patient with prior coronary artery disease, so they activated the cath lab. The LAD stent was patent
but there was a 90% ulcerated plaque in the right posterolateral branch, which
was stented. There was also 30% proximal RCA and 50% proximal circumflex lesions.
Because of a cath lab activation and culprit lesion
requiring a stent, the patient was diagnosed as “STEMI”. But they never had a
rise in troponin, and the initial and post-cath trop were the same: 14ng/L
prior (normal <26 in males and <16 in females) and 13 after. So was this unstable angina?
Smith: I don't think you can even make this conclusion. It might or might not be unstable angina, probably not, and with fluctuating ECG.
Here is the post-cath ECG:
There’s the same ST elevation in V2 and similar S wave, but
now the T wave seems even larger. Is this a posterior reperfusion T wave, given
the location of the culprit? But there should be at least a tiny increase in
troponin with reperfusion injury.
A few days later the patient presented again with chest
pain, and EMS brought in again as code STEMI based on anterior ST elevation and inferior ST depression. This time the patient declined cath and serial trops remained at 13. Echo findings: "a normal size of the LV with concentric remodeling and overall normal left systolic ejection fraction. Mild anterior septum segment, mid septum segment, and mid inferior segment wall motion abnormalities were noted. RV was normal in size and function, and there was no relevant valve pathology." The patient was diagnosed with non-cardiac
chest pain. Below are the initial and discharge ECGs:
Again we see some of the variations in repolarization
abnormalities, exaggerated by lead placement (R/S ratio is different V2-4 and the V1-2 are
placed too high on the second—with fully negative P in V1 and biphasic P in V2).
Take home
1.
Problem: LVH produces secondary repolarization
abnormalities which can make it difficult to identify primary ischemic changes,
and STEMI criteria don’t help
2.
Prior ECGs can show baseline repolarization changes, but these
can fluctuate over time and with variations in lead placement and patient position
3.
Proportionality: disproportionate ST elevation
can help identify OMI—with ST/S>15% concerning—but there can still be false
positives
4.
Patient: patients with high-pretest probability and
ischemic symptoms deserve investigation even if prior angiograms have been
unremarkable or ECGs are nonspecific
5.
Paradigm: code STEMIs leading to stents does not
mean the patient had a “STEMI”. ACS should not be classified by whether the
presenting ECG has ST elevation, but by whether the patient had Occlusion MI
(OMI) or non-Occlusive MI (NOMI)-- or unstable angina.
Smith: How would we conclude in retrospect that this was, or was not, OMI?
1. Any ECG which manifests ischemia should have evolution. This fluctuating LVH probably would not fulfill that criterion.
2. There should be at least some troponin rise and/or fall, even if they do not reach the 99th percentile. Furthermore, it would be very rare for this to be OMI without at least one troponin going over the 99th percentile. Our research definition of OMI requires either a) diminished flow in the artery (TIMI 0-2) or b) culprit plus a very high troponin. There can be OMI that does not meet these criteria (but that does manifest on the ECG and has evolution) due to a) occlusion that is too brief, or b) inability to identify a culprit, but there must be SOME troponin rise and/or fall, even if it is unstable angina with all of them below the 99th percentile. The definition of acute MI includes a rise and/or fall of troponin with at least one value over the 99th percentile for that assay.
Therefore, this patient had Non-ischemic ST Elevation and a chronic, stable stenosis that was intervened upon. There was some non-ischemic fluctuation in the ECG.
This patient should carry around a copy of their ECG!
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Comment by KEN GRAUER, MD (6/20/2022):
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Superb discussion by Dr. McLaren about the difficult topic of how to assess and manage the patient who has a history of coronary disease — but who also has a history of repeated ED visits for chest pain, which have led to cardiac catheterization that previously failed to show occlusive coronary disease. Additional features of today's case that complicate assessment include:
- The history of "alcohol use disorder". While this most definitely does not rule out the possibility of new acute cardiac disease — in my experience, it always made it more difficult for me to assess such patients.
- A series of prior ECGs on the patient that showed fluctuation of ST-T wave abnormalities. That said — differences in lead placement made assessment of these fluctuations more difficult.
- Some unusual findings on the initial ECG (including LVH) — that left me uncertain about how to proceed.
I thought the initial ECG in today's case was worthy of further comment. For clarity — I have reproduced this initial tracing in Figure-1.
- ECG #1 shows a normal sinus rhythm at a rate just over 60/minute. The PR interval is normal, and the QRS is narrow — but the QTc is prolonged (I estimate ~480 msec.). The frontal plane axis is normal at +20 degrees.
As noted above by Dr. McLaren — there is LVH on this initial ECG. That said — there are some atypical features about this ECG diagnosis:
- I have previously reviewed "My Take" on a user-friendly approach to the ECG diagnosis of LVH (See My Comments in the June 20, 2020 and April 27, 2019 posts in Dr. Smith's ECG Blog). Voltage criteria are not quite met in the chest leads in Figure-1. There are met in lead aVL (R ≥12 mm in aVL) — and the very tall R wave in lead I is probably also qualifying.
- As I've emphasized in previous posts — the fact that more there are more than 50 criteria in the literature for the ECG diagnosis of LVH means that none of these criteria are optimal. It also means that the ECG is far from a perfect assessment tool for LVH. For practical purposes — when QRS amplitude appears increased and ST-T wave changes consistent with LV "strain" are present — the probability is high that "true" LVH is present if the patient is an adult of a certain age who has a history of heart disease. I therefore thought the diagnosis of LVH to be secure.
I found the most striking ECG finding in
Figure-1 — to be the 2+ mm of J-point ST elevation in
lead V2, that occurs in association with a disproportionately tall T wave with wide base. That said — I was
not convinced that the upward concavity (
"smiley"-configuration) ST segment with angled J-point in
ECG #1 was acute. While the overall shape of this ST-T wave in lead V2 looked most consistent with the type of ST elevation seen in anterior leads with LVH (
June 20, 2020) — the S wave in lead V2 was
not nearly as deep as I would expect if the ST-T wave in lead V2 was simply the result of LVH.
- There was subtle ST elevation in the high-lateral leads I and aVL of ECG #1 — with what appeared to be some mirror-image opposite ST depression in the inferior leads. Could this be acute? (especially since the ST-T wave depression of LV "strain" was nowhere to be seen in these high-lateral leads?).
- There was moderately deep and symmetric T wave inversion in lateral chest leads V5,V6 (with terminal negativity of the T wave in lead V4). Was this consistent with ischemia? with LV "strain"? — or — with a combination of the two?
- My Impression of ECG #1: I was not at all certain from assessment of this initial ECG as to how I would answer Dr. McLaren question about whether to activate the cath lab. My "hunch" — was that acute OMI was less likely — but I felt I'd need more information (ie, the degree of concern from the patient's history and symptoms, comparison with other tracings, troponins, etc.) to make my decision.
- Review of the 2 prior tracings from the patient's last code STEMI visit did not resolve my uncertainty. While ST-T wave changes seemed a bit more marked on ECG #1 than on the prior tracings — I did not think they provided a definitive answer.
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| Figure-1: The initial ECG in today's case. |
Bottom LINE in Today's Case:
As emphasized by Dr. McLaren — Patients with high pre-test probability and ischemic symptoms sometimes deserve investigation, even if prior caths have been unremarkable and/or ECGs are nonspecific. This was the case for today's patient.
- Unfortunately — assessment of this patient in the future may remain problematic if he again returns for chest pain, but without definitive ECG changes or troponin elevation.
- P.S.: Very important point highlighted by Dr. Smith's last comment = Just because there is a high-grade stenosis (ie, a 90% narrowing in today's case) — does not necessarily mean that this is a "culprit" lesion responsible for symptoms.
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