A man in his 50s with a history of hypertension, dyslipidemia, type 2 diabetes mellitus, and prior inferior OMI status post DES to his proximal RCA 3 years prior presented to the emergency department at around 3 AM complaining of chest pain onset around 9 PM the evening prior. He described it as severe, sharp, and substernal with associated nausea, vomiting, chills, and diaphoresis. The following ECG was obtained. Note that the machine read is "normal sinus rhythm, normal ECG." Cardiology over read the tracing and signed the interpretation without modification.
ECG 1
The Queen of Hearts sees no OMI but only with low confidence. She seems concerned about a few leads.
I sent this ECG to Dr. Smith and Dr. Meyers with no clinical context.
Dr. Smith said "That is a tough one. I would say OMI low confidence."
Dr. Meyers noted the presence of South African Flag sign, indicative of high lateral OMI.
Smith comment: in clinical context, (middle aged with acute chest pain), the ECG is diagnostic and the cath lab should be activated.
The patient was given aspirin 324 mg PO, nitroglycerin 0.4 mg SL, and morphine 2 mg IV all simultaneously. Twenty minutes later, his pain was unchanged and he was given an additional dose of morphine 2 mg IV. Thirty minutes later he reported significant improvement in his chest pain. Cardiac troponin I drawn around that time resulted at 0.323 ng/mL (ref. <0.049 ng/mL).
Smith comment: this troponin alone should be enough data to activate the cath lab, regardless of the ECG.
Also: As we always say, do not give morphine until you are committed to the cath lab. The pain will resolve and you will think the ischemia is gone when it is only hidden!
Case continued: The hospitalist admission H&P an hour later describes 6/10 chest pressure, but also notes that he "has chest tenderness and upon palpation it reproduces his chest pain." This is classically taught as a strong argument for musculoskeletal etiology of pain. Note that as many as 7% of patients with acute coronary syndrome have chest pain reproducible on palpation [Lee, Solomon]. This equates to a negative likelihood ratio of 0.3, which reduces the pre-test probability of acute coronary syndrome by less than 30% [McGee].
Smith comment: But the tests (ECG and troponin) are extremely specific and so the post test probability is nearly 100%.
Repeat cTnI drawn at around 8 AM was 3.910 ng/mL. Cardiology consult note written around that time documents that "Pain improved with NTG, morphine in ED but still present." (This patient was not one of the lucky 6.4% of patients taken for immediate heart catheterization due to uncontrolled chest pain [Lupu].) The note also says "slight lateral ST elevations noted, likely early repolarization since unchanged compared to 2014."
Brief aside: "Early repolarization" is a frequently proclaimed and poorly understood electrocardiographic phenomenon which mostly serves to reassure clinicians that not all ST elevations are ischemic (something readers of this blog know well). The original term "benign early repolarization" has fallen out of favor since the seminal paper by Haïssaguerre et al. linking the finding with long term risk of idiopathic ventricular fibrillation. The link is quite modest, increasing the chance of VF from 3.4 per 100,000 to 11 per 100,000 [Rosso].
In an attempt to clarify language, a consensus definition was developed. The definition requires the following three components:
- An end QRS notch (sometimes called a J wave) or slur, in the case of a slur it must lie entirely above the isoelectric baseline
- The peak amplitude of the notch or slur should be ≥ 0.1 mV in 2 or more contiguous leads (excluding V1-V3)
- The QRS duration should be < 120 ms
ECG 2
Compared to the presenting ECG, the Queen of Hearts sees no OMI with high confidence.
Notice that the old ECG does meet the consensus definition for early repolarization, but the current ECG does not. This is shown in the enlarged picture below.
It is therefore inaccurate to say that the ECG shows "unchanged" early repolarization. Here are the South African Flag Sign leads shown side by side, the older tracing on the left, the current tracing on the right.
Older tracing Current tracing
In lead I we see the disappearance (or marked diminution) of a previously prominent end QRS notch. In leads aVL and III, we see a change in ST segment morphology from markedly concave to much more angular. V2 has some changes, but at least to me it is not as clear what to make of them.
Fortunately, the patient was taken for heart catheterization that morning.
The first view shown below is right anterior oblique caudal. This view is usually best for visualizing the left circumflex and its branch vessels (called obtuse marginals).
Just before 10 AM, the patient received a stent to the culprit OM. Peak troponin was 12 ng/mL. Before and after angiography is shown below. They are very slightly different angiographic views, the image on the left is right anterior oblique caudal, and the image on the right is more of an anteroposterior caudal (meaning no lateral angulation of the imaging).
You might be asking yourself: How does this qualifiy as OMI given that the culprit artery has TIMI 3 (meaning angiographically unimpaired) flow. Recall that approximately 20% of OMIs have TIMI 3 flow at angiography [Cox, Stone]. In this patient's case, there was also an ECG obtained the following morning, shown below.
Notice that there are now reperfusion T waves in I and aVL, confirming the diagnosis of OMI.
You might also be asking yourself why the ECG showed South African Flag sign given that the artery is more posterior than high lateral. The answer is probably that the proximal part of the artery is close to the high lateral position, and the distal part of the artery manifested extremely subtle posterior changes. Usually, posterior OMI manifests as anterior ST depression. The presenting ECG in this case did not show overt ST depression, but comparing to the old ECG, there is relative anterior ST depression. This is shown below side by side, old ECG on the left, new ECG on the right.
Old ECG New ECG with acute chest pain
Learning points:
- Patients with early repolarization pattern are still at risk for OMI, and the underlying early repolarization pattern may obscure the presence of OMI.
- Chest pain reproducible on palpation does not rule out acute coronary syndrome. It reduces pre-test probability by less than 30%.
- "Normal" machine read does not rule out OMI.
- Posterior OMI may manifest as relative anterior ST depression without overt ST depression below the isoelectric baseline.
MY Comment, by KEN GRAUER, MD (12/27/2023):
- For clarity in Figure-1 — I've put these first 2 tracings together to facilitate comparison.
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| Figure-1: Comparison between the first 2 ECGs in today's case. |
- This patient is a 50s man with known coronary disease (s/p stenting of a previous inferior OMI) — who presented to the ED for severe CP (Chest Pain) of at least several hours duration, that was still ongoing at the time ECG #1 was obtained. As a result, even before looking at this patient's initial ECG — he falls into a high-prevalence likelihood group for ACS (for an Acute Coronary Syndrome). We therefore need to assume and rule "out" ACS — more than having to rule it "in". I did not see anything in ECG #1 that helped me to "rule out" OMI (= my opinion).
- We have discussed repolarization variants on multiple occasions in Dr. Smith's ECG Blog — with detailed description of this entity in the May 23, 2022 post by Dr. McLaren (Please check out My Comment and illustrative Figure at the bottom of the page of this post). For practical purposes — I favor the term, repolarization variant when doubt exists as to whether or not strict criteria for the newer definition of ER (Early Repolarization) are satisfied.
- Given the history in today's case — I was not in the least contemplating whether there was (or was not) some type of repolarization variant after seeing ECG #1. There clearly is slight-but-real ST elevation in leads I and aVL of this initial tracing — which places the "onus of proof" on us as medical providers to rule out ACS.
- Finally (as per Dr. Frick) — mention is made of the hospitalist's notation of being swayed by the presence of chest tenderness "reproduced by palpation". While this physical exam finding may slightly increase likelihood of a musculoskeletal disorder — this is clearly a subjective finding associated with far-too-great of a false positivity rate to allow use in any meaningful way as a factor to rule out OMI. The "onus of proof" remains on us as medical providers to objectively rule out ACS.
- Especially given the context of a patient with new CP — ST-T waves are not "normal" in any of the inferior leads. Instead — the ST segment is straighter-than-normal in both lead II and lead aVF (RED lines that I've drawn in these leads in Figure-1). It is easier to appreciate this subtle change in lead aVF than in lead II — but although loss of the gradual smooth upsloping of the ST segment in both of these leads (leading to a more abrupt junction between the end of the ST segment and the beginning of the T wave) is not diagnostic — it is also not "normal".
- Lead III is of more concern — as it shows the magical mirror-image opposite ST-T wave relationship with lead aVL that so often indicates acute inferior or high-lateral OMI (See My Comments regarding this "magical" mirror-image opposite relationship at the bottom of the page in the March 27, 2023 — the November 21, 2020 — the October 6, 2018 — and the July 11, 2018 posts — among many others).
- In the context of the above ECG changes in 5/6 of the limb leads — there is also suspicious (albeit non-diagnostic) ST segment straightening in lead V6 of ECG #1 (RED line in this lead).
- BOTTOM Line: To emphasize that the above ECG changes in ECG #1 are non-diagnostic of an OMI — but in the context of a patient with known coronary disease who presents with persistent, severe CP — I interpreted these ECG changes as highly suspicious of possible OMI. As per Dr. Frick — even without any ECG changes, persistent ischemic-sounding CP is indication for prompt cardiac cath.
- As a result, after noting the above described abnormalities in the limb leads of ECG #1 — my "eyes" immediately focused on lead V2 — looking for any indication of "tell-tale" ST flattening or depression that might indicate posterior OMI, thereby confirming my suspicion of high-lateral OMI (by finding evidence of associated posterior OMI).
- Instead — lead V2 manifests an rSr' configuration with slight "saddleback" ST elevation. Rather than the South African Flag Sign — I thought the "extra" r' deflection that is not seen in the "old" ECG more likely suggested too-high placement of the lead V2 electrode. The shape of the ST elevation in lead V2 most commonly associated with a true S. African Flag Sign (due to acute OMI of D1 or D2) — is usually different than the gradual upsloping ST segment seen in the saddleback morphology of ECG #1. (See examples of OMIs with the S. African Flag Sign provided by Dr. McLaren — with additional detailed discussion of this entity in My Comment at the bottom of the page in the May 11, 2022 post in Dr. Smith's ECG Blog).
- In support of my suspicion that the "extra" r' in lead V2 of ECG #1 is the result of faulty placement of the lead V2 electrode — is the lack of any r' in the "old" ECG.
- NOTE: Although an rSr' deflect is seen in both leads V1 and V2 of the 3rd ECG done in today's case — the fairly deep negative component to the P wave in lead V1 of that tracing suggests too-high electrode placement of V1 and V2 in this final tracing done the next morning. (See My Comment in the April 17, 2022 post of Dr. Smith's ECG Blog for review of the 3 Clues to Too-High Placement of leads V1 and V2).
- BOTTOM Line: I thought the ST-T wave appearance in lead V2 of ECG #1 likely represented a "technical misadventure" (due to too-high placement of the V2 electrode on the chest). Given the diagnostic importance of lead V2 (in assessing for postero-lateral OMI from LCx occlusion) — and — my suspected inability to accurately assess leaad V2 — I would have immediately repeated ECG #1 after verifying correct electrode lead placement.
- We are not told when, or under what circumstances ECG #2 was recorded. We know that today's patient has had prior inferior OMI with stenting of his proximal RCA ~3 years earlier. The relatively wide Q wave (qRS complex) in lead aVF of ECG #2, in association with deep (with respect to QRS amplitude) symmetric T wave inversion in leads III and aVF suggest that this "old" ECG may have represented reperfusion if it was obtained soon after the prior inferior OMI. Doubtless that more than a single ECG would have been obtained during that admission — without us knowing what the ultimate "stable" ECG pattern of this patient's "baseline" really is.
- The shape and relative size of ST-T wave changes in the inferior leads is quite different between ECG #1 and ECG #2 (I thought depth of the T wave inversion in lead III to be clearly disproportionate given its equal amplitude to the S wave in this lead).
- BOTTOM Line: For prior tracings to be a valid source for comparison with a current tracing — we need to indicate clinical circumstances at the time the prior ECG was recorded (and ideally indicate if we know what the patient's true "baseline" ECG looks like).
- P.S.: Given the concerns I raise above about the initial ECG in today's case — I would have expected at least several serial ECGs to be done — which had this been accomplished, could have prompted diagnostic (and therapeutic) cardiac cath much sooner than actually occurred.
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