This is another one from Amandeep ("Deep") Singh, with many comments by Smith.
Dept Emergency Medicine, Highland Hospital, Oakland.
Case
67yo male with h/o schizophrenia and who has become increasingly distrustful of Western medicine presents with chest pain radiating to the right shoulder associated with shortness of breath for 24 hours duration. He states that he was unable to sleep secondary to the pain. The patient seems very worried about his right shoulder and is requesting a x-ray. An x-ray was obtained, as well as an ECG and a troponin.
Prior to the troponin result, the RN notes that the patient was "pacing at the doorway, stating he wants to leave and be called with lab values. Pt. does not want to wait any longer. MD aware."
Here is the initial ECG.
Would you allow this patient to leave the ED?
I sent this ECG without any clinical information to Steve Smith, and he responded:
"Ischemic ST depression in V4 and V5. So if this is someone with symptoms compatible with ACS, this ECG is diagnostic of ACS."
Analysis of 2 issues: STD V4-5, and Delayed Activation Wave
Despite baseline wander, the initial ECG shows subtle
ischemic ST depression in V4-V5.
1. ST Depression in V4, V5 (by Smith):
Meyers and Smith recently wrote this article: Ischemic ST depression maximal in V1-V4 (vs. V5-V6) of any amplitude, is specific for Occlusion Myocardial Infarction (vs. non-occlusive ischemia)
In this analysis, if the ST depression was maximal in V1-V4, that was 96% sensitive for OMI requiring PCI.
In 196 cases, the STD was maximal in V5-6; 97 of these (51%) were ischemic (other STD max in V5-6 was due to LVH and other causes).
48/97 (25% of 196, 50% of ischemic ST Depression), were due to OMI, and 22 of the 48 had STEMI as seen in other leads.
Thus, of those ischemic STD in V5-6 not due to an obvious STEMI, 26 of 75, or about 1/3, were due to subtle OMI. The remainder of the ischemic STD was due to subendocardial ischemia.
In other words, if the ischemic ST depression was maximal in V5, V6, without STEMI elsewhere, then such subtle OMI was only present in about 1/3 of cases; 2/3 were subendocardial ischemia.
However, we can get even more granular:
There were 7 borderline cases: Suspected Ischemic STD Borderline/
Equal Between V4 and V5:
Quote from the article: "Although the determination of STDmaxV1–4 versus
STDmaxV5–6 was dichotomized for all other analyses
presented, there were 7 patients with STD for which
the interpreter noted that STD was basically equal in
leads V4 and V5, making this distinction especially difficult in this small subset. All 7 underwent angiography,
5 had culprit lesions (all LCX), 4 had OMI, and 3 received PCI.
2. Delayed Activation, or "N" terminal wave (by Deep).
In addition, there are "N" terminal or
delayed activation waves in leads II, III, and aVF.
The "N" wave is
defined as a notch or deflection in the terminal QRS complex and is
typically seen in leads II, III, aVF or I, aVL in association
with occlusion of the left circumflex artery. In the original
description, four criteria were required to define an "N" terminal wave:
1) a notch (or deflection) in the terminal QRS complex
2) the height
of the notch > 2mm (compared to PR segment)
3) disappearance
of the notch within 24 hours, and
4) slight QRS prolongation in leads
with the notched wave
--Niu et al. (see references below)
A recent study
comparing outcomes between patients with left circumflex occlusion
showed equivalent clinical outcomes between STEMI patients and NSTEMI
patients with an "N" terminal wave. The
"N" terminal wave in our case may have been possibly resolving,
explaining why it doesn't meet the 2mm criteria mentioned above.
The "N" terminal wave differs from the J wave.
Case continued
The patient eloped prior to any discussion about leaving against medical advice.
About
1 hour later, his first (4th generation, not high sensitivity) troponin I returned at 11.3 ng/mL (this is a level consistent with OMI, including STEMI). He was
contacted by phone and agreed to return to the emergency department for
evaluation.
A repeat ECG was obtained at 1am when the patient returned
to the hospital.
In this ECG, there has been loss of QRS voltage and resolution of
the ST segment depression in leads V4-V5. The "N" terminal wave is no
longer present in the inferior leads. Lead III appears to have more QRS
fragmentation compared to the presenting ECG.
Cardiology was consulted and recommended medical management
overnight with a plan for coronary angiography in the morning. A repeat
troponin returned at 14.9 ng/mL, which prompted cath lab activation at
4am (about 3 hours after he re-presented to the emergency department).
Cardiac cath showed a 100% proximal left circumflex occlusion.
References
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MY Comment by KEN GRAUER, MD (3/26/2022):
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Insightful recognition of some extremely subtle but important findings by Drs. Singh and Smith! For clarity — I’ve put the 2 ECGs in this case together in Figure-1 — to which I’ll add the following comments:
-USE.png) |
| Figure-1: The 2 ECGs in today’s case (See text). |
MY Thoughts on the Initial ECG:
This is a challenging ECG to interpret because: i) The ischemic findings highlighted above by Dr. Smith are subtle!; ii) There is baseline artifact that makes it difficult to know which of the 2 or 3 complexes in each simultaneously-recorded lead set are “real”; and, iii) Entities other than ischemia may produce similar findings:
- In the limb leads — baseline artifact is most marked in leads II, III and aVF — and absent in lead I — therefore most likely caused by “something” going on in the Left Leg (CLICK HERE — for Review on HOW to identify the “culprit” lead producing baseline artifact). Rapid identification of the “culprit” lead producing the artifact is relevant in today’s case — since I would have really liked to see a better quality tracing given subtlety of the abnormal findings — and a quick look at this paient’s left leg might have solved this problem.
- In addition to the inferior lead N waves and localized ST depression identified by Drs. Singh and Smith — there is an overall picture of nonspecific ST-T wave flattening on this tracing and fairly prominent U waves are seen in the mid-precordial leads (BLUE arrows in ECG #1). Knowing serum K+ and Mg++ levels is therefore highly relevant to optimal interpretation in this case — since low levels of these electrolytes might produce similar ECG findings (See My Comment at the bottom of the page in the March 18, 2022 post for more on ECG findings with low K+/Mg++).
- In my opinion — the History is the most important piece of information in today’s case. This patient is clearly “old enough” (67 years old) to have coronary disease — and the reason this man who is “distrustful of Western medicine” nevertheless presented to the ED — is new chest pain that was severe enough to prevent him from sleeping. The fact that his symptoms had been ongoing for 24 hours is relevant — because this may indeed account for why findings in ECG #1 are so subtle (ie, this tracing might reflect “pseudonormalization” following resolution of OMI-related ST elevation that was in-process of evolving to reperfusion T wave inversion).
- Awareness of this history is why despite an ECG picture suggestive of low K+/Mg++ in ECG #1 — our attention needs to be focused on considering acute coronary disease until proven otherwise.
It is because the History in today’s case has us focused on thinking, “this patient has had a coronary event a day ago until we prove otherwise” — that my “eye” focused on several additional subtle findings suggestive of postero-lateral localization from a LCx (Left CircumfleX) “culprit” artery:
- There is early transition in ECG #1 — as the initial R wave in the small-amplitude QRS complex in lead V1 is relatively tall (considering small size of the S wave in this lead) — and the R wave becomes predominant already by lead V2. Among the causes of early transition are posterior MI (CLICK HERE — for Review of the Causes of a Tall R Wave in lead V1).
- Although ST-T wave morphology varies in each of the 3 simultaneously-recorded complexes in leads V1,V2,V3 of ECG #1 — the “theme” that I see is that of uncharacteristic ST segment straightening and flattening — which in association with early transition (taller-than-expected R waves in V1,V2,V3) — is a "picture" that to me suggests posterior MI of uncertain age in a patient with symptoms (NOTE: I've commented on this "picture" of a positive "Mirror Test" multiple times in Dr. Smith's ECG Blog — See My Comment in the January 3, 2022 post — the September 28, 2020 post — and the October 11, 2020 post — to name just a few).
- There is an “imbalance of precordial T waves” — in that T waves in lateral chest leads (ie, in V5,V6) are of very low amplitude or flat — and, the T wave in lead V1 is actually taller than the T wave in lead V6. This finding is not seen very often — and in the “right” clinical setting, has been associated with recent OMI from a LCx culprit artery (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM).
MY Thoughts after seeing ECG #2:
The etiology of today’s patient’s symptoms of course became clear when he returned to the hospital at 1 am with worsening symptoms — and — with return of positive troponin values. But from an ECG perspective — a number of confirmatory findings stand out when one carefully compares ECG #2 with ECG #1 (See Figure-1):
- As noted by Drs. Singh and Smith above — there has been loss of QRS voltage, as well as resolution of the localized ST depression that was initially seen in leads V4-5. As I’ve emphasized in previous posts — among the entities to consider for acute loss of QRS amplitude is myocardial “stunning” from a large infarction (See My Comment in the August 28, 2020 post in Dr. Smith’s ECG Blog). Loss of the localized ischemic ST depression in V4,V5 suggests there have been “dynamic" ST-T wave changes.
- Despite overall loss of QRS amplitude in ECG #2 compared to ECG #1 — there has been an increase in R wave size in lead V1, such that the R in V1 is now predominant. In addition — T wave amplitude in leads V1,V2 has clearly increased — whereas the T wave in lead V6 has remained flat. These findings confirm ongoing “precordial T wave imbalance” — and are highly correlated with a LCx “culprit”. As noted by Drs. Singh and Smith — cardiac cath confirmed 100% proximal LCx occlusion.
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“Take-Home” PEARL: When T waves in each of the chest leads are upright (or at least not inverted) — the T wave in lead V1 is usually not taller than the T wave in lead V6.
- NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “strain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found that recognition of a tall, upright T wave in lead V1 that is clearly much taller than the T wave in lead V6 is a CLUE to an acute coronary syndrome that I might not otherwise have recognized.
- The “culprit” artery in such cases is likely to be the LCx (Here is another case = ECG Blog #182).
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