"Anterior" ST Depression: Which Lesion is the Culprit?

Written by Hans Helseth

Hans is an EKG tech who is applying to medical school. EKG interpretation skills have little to do with one's level of education. In fact, much of what passes for EKG education can actually harm one's interpretation skills.

A 62 year old man with hyperlipidemia presented to a rural emergency department with 7 hours of 3/10 chest pain. Here is his triage EKG:

With ST depression maximal in V2-V4 and resolved by V5-V6, this is diagnostic of posterior OMI, as shown by Meyers et al. (https://www.ahajournals.org/doi/10.1161/JAHA.121.022866)

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Smith: Although many writers state that the tall R-wave is essential to the diagnosis of posterior OMI, that is a false statement: we showed in the above study that the R-wave is irrelevant. A large R-wave is analogous to a Q-wave and only shows that the infarct has progressed to involve a large territory. ACUTE posterior OMI does not have a large R-wave. (We also showed that an upright T-wave is not required, and that many have a negative or biphasic T-wave). The pain has been present for 7 hours, which corresponds to a long duration of infarction and the presence of "Q" waves (in this case tall R-waves)

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With inferior ST depression and possible ST segment straightening in aVL there is also suggestion of high lateral involvement, meaning the likely culprit artery is the left circumflex or one of its branches.

Here is the QoH interpretation:

The ED provider described the T waves in V2 and V3 as “hyperacute”. It is not clear by her note what she meant by this (whether or not she recognized this EKG as diagnostic of transmural ischemia, and if so, of what territory) but emergent reperfusion therapy was not pursued.

At 1022, a troponin I (ref range <0.034 ng/mL) resulted at 4.437 ng/mL. This was the only troponin measured during this case. The patient was diagnosed with NSTEMI and placed on a heparin drip.

[Smith: this high initial troponin confirms that this is a subacute OMI and that one should expect Q-waves (tall R-waves)].

Another EKG was recorded after almost two hours. The status of the patient’s pain at this time is unknown:

It remains mostly unchanged. 

At 1210, the case was discussed with a cardiologist at a PCI capable facility, who accepted the patient for transfer, noting the ST depression in anterior leads as “consistent with ischemia” but “not a STEMI”. The patient arrived to the ED of the PCI facility where this EKG was recorded:

The ST depressions have almost completely resolved, which suggests reperfusion of the posterior wall, although again, the patient’s pain status at this time is unknown.

At 1547 the patient was taken for angiography:

The cath report by the interventionist describes:

• 80% Ostial LAD (green arrows)

• 95% Mid LAD (blue arrows)

• 100% First Obtuse Marginal (red arrows)

Some may prefer to call the occluded vessel the second obtuse marginal, as a small branch with the same course can be seen originating proximally to it (see Terminology and Semantics of Willy Frick’s cardiac cath guide).

Based on the EKGs, which lesion is most likely the culprit?

In this case, the interventionist called the mid LAD lesion the likely culprit. The proximal and mid LAD stenoses were stented and the OM 2 was left alone. It is unclear by the note whether or not the OM lesion was interpreted as CTO, but it was not touched.

An EKG was recorded after cath:

The ST depression has worsened. There is no restoration of flow through the likely true culprit lesion in the second obtuse marginal, so the EKG continues to show transmural ischemia of the posterior and high lateral walls.

Another EKG was recorded the day after PCI:

The ST depression has worsened further. There is still no restoration of flow past the lesion.

An Echo performed the day after PCI showed an EF of 51% and hypokinesis in the mid posterior, mid lateral, and basal lateral segments. This distribution of wall motion abnormality is more consistent with a culprit in the obtuse marginal rather than the mid LAD. Had more troponins been measured, it is likely they would have continued to climb as the patient’s artery remained occluded.

The patient was discharged the day after PCI. There is no follow up.

It is still widely believed that ST depression localized to a certain territory on the EKG is indicative of subendocardial ischemia of that territory. In this case, it is possible that the physicians interpreted the ST depression in anterior leads as subendocardial ischemia of the anterior wall, and the mid LAD stenosis as the culprit of that ischemia.

Subendocardial ischemia does not localize. It manifests with an ST elevation vector towards lead aVR, causing ST depression maximal in apical leads (II, V5-V6). See this exemplified many times on this blog. Localized ST depression, as in this case, is indicative of transmural ischemia of the opposite territory. Anterior ST depression = posterior ST elevation. 

This was likely a case of wrong-vessel PCI. This is surprisingly common. Heitner et al found that in 14% of patients with NSTEMI, a blinded interventional cardiologist interpreting coronary angiograms identified a different culprit artery than CMR (https://www.ahajournals.org/doi/10.1161/CIRCINTERVENTIONS.118.007305). This is a case which demonstrates the importance of OMI findings on the EKG in the job of the interventionist. 

Learning Points:

• ST depression maximal in V1-V4 is posterior OMI, not anterior ischemia, not subendocardial ischemia

• This should have undergone emergent angiograph and PCI of the correct vessel

• Wrong-vessel PCI is not uncommon in “NSTEMI”

• Serial troponins and EKGs can be a useful tool for confirming the success of PCI.

Smith: here is a post with many ECGs which compares and contrasts the ST depression of posterior OMI from that of deWinter's T-waves:

De Winter's T-waves are Not a Stable ECG condition. Upright T-waves in Posterior OMI are Distinct from de Winter's waves.

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MY Comment, by KEN GRAUER, MD (3/10/2025):

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I wrote the following in My Comment in the September 21, 2020 post of Dr. Smith's ECG Blog: 

"I wish those cardiologists who continue to strictly adhere to STEMI millimeter criteria would read Dr. Smith’s ECG Blog. IF they don’t — they will continue to overlook obvious OMIs that deserve to undergo prompt cardiac catheterization for optimal care." 

5 years later (now in 2025) — the problem remains.

• The posterior wall of the LV is not directly viewed by any of the 12 leads on a standard ECG. As a result — ST elevation will not be seen in any of the standard 12 leads in an isolated posterior OMI.
• Posterior leads (ie, leads V7, V8, V9) — have been suggested as a way to enhance ECG visualization of the posterior wall. With acute posterior MI — these posterior leads will sometimes manifest ST elevation not seen on the standard 12 leads.
• That said, as we have often emphasized in Dr. Smith's ECG Blog — the amount of ST elevation you are likely to see with posterior leads in acute posterior MI is limited. As a result, the diagnostic utility of posterior leads is limited (See My Comment in the September 21, 2022 post).
• Most of the time when there is acute posterior OMI — there will be associated acute inferior and/or lateral MI. But when the OMI is isolated to the posterior wall — there simply won't be any ST elevation in any of the standard leads.

Among the problems in today's case were the following:

• Cardiac cath was delayed for nearly 6 hours — because none of the ECGs that were done showed ST elevation. 
• Meanwhile — acute coronary occlusion causing an isolated posterior OMI was not recognized by several providers, including the consulting cardiologist. This, despite the diagnostic initial ECG that was done at the time the patient first arrivd in the ED.
• The initial Troponin came back markedly elevated — but because there was no ST elevation, the infarction was labeled a NSTEMI. This outdated (useless) term ignores the clinical reality that many acute coronary occlusions do not manifest ST elevation.
• And, because the concept that acute coronary occlusion causing isolated posterior OMI is readily recognized by ST depression that is maximal in leads V2,V3,V4 — when cath was finally done, it was performed on the wrong coronary artery (whereas ECG recognition of isolated posterior OMI on the initial ECG immediately pointed to the LCx system as the "culprit" artery — as is shown below in Figure-3).

As I lamented in 2020 — Rather than taking the extra time to obtain another ECG with posterior leads (that at best — provides limited information) — I favor GETTING GOOD at using the Mirror Test as an aid for recognizing acute posterior MI.

• The Mirror Test is a simple visual aid: It helps the clinician recognize acute posterior infarction. It is based on the premise that the anterior leads provide a mirror image of electrical activity in the posterior wall. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the “mirror-image” of leads V1, V2, V3 (See Figure-2 below).
• I’ve previously discussed application of the Mirror Test on many occasions (in My Comment at the bottom of the September 13, 2020 post and the February 16, 2019 post, among others).
• In Figure-1 — I apply the Mirror Test to leads V2,V3 in today's initial ECG. As shown in the mirror-image RED insert — Isn't it now obvious that there is acute coronary occlusion causing isolated posterior OMI?

Figure-1: Application of the Mirror Test to leads V2,V3 in today's initial ECG.

Figure-2: Illustration of the rational for the Mirror Test (Figure excerpted from Grauer K: ECG-2014 Pocket Brain ePub).

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In Figure-3 — We see the rationale for anatomic localization of the "culprit" artery to either a non-dominant LCx or an Obtuse Marginal branch of the LCx — when there is isolated posterior OMI.

Figure-3: KEY points in the recognition of isolated posterior MI (adapted from my ECG-2014-ePub — with addition of Figure from Vince DiGiulio).