ECG Interpretation: ECG Blog #326 — This Case Was Missed ...

The ECG in Figure-1 was obtained from a man in his 60s with known coronary disease — who called EMS for an episode of more severe CP (Chest Pain) that day. The patient describes increasing angina over the previous ~2 months. ECG #1 was recorded when EMS arrived — at which time the patient's CP had totally resolved.

In light of this history — HOW would you interpret ECG #1?
Would you activate the cath lab?

Figure-1: The initial ECG in today's case. The patient's chest pain had totally resolved at the time this tracing was recorded.

MY Thoughts on ECG #1:

The underlying rhythm in ECG #1 is sinus. Although it is difficult to be certain of the reason for the irregularity without a long lead rhythm strip — it appears that the early beats are the result of PACs (Premature Atrial Contractions).

There is significant baseline artifact in the limb leads. That said — we still can interpret this tracing.
In addition to sinus rhythm with PACs — intervals (PR, QRS, QTc) and the frontal plane axis (about +30 degrees) are normal.

Regarding Chamber Enlargement:

There is LAA (Left Atrial Abnormality) — suggested by the deep negative component to the P wave in lead V1 (See ECG Blog #75 — for ECG diagnosis of LAA/RAA). The reason I do not suspect too-high placement of leads V1,V2 — is that the QRS complex in these leads looks so very different than the QRS in lead aVR (See ECG Blog #274 — for detection of when Leads V1,V2 are placed too high on the chest).
Criteria for LVH are satisfied. That is, the S wave for the 2 sinus-conducted beats in lead V2 + the R wave in lead V5 ≥35 mm. Voltage criteria for LVH may also be satisfied in lead V3 — as what appears to be a very deep S wave in this lead is "cut off" by the limits of the ECG paper (See ECG Blog #245 — regarding ECG criteria for LVH).
The ST depression in leads V5,V6 may at least in part be the result of LV "strain".

Regarding Q-R-S-T Changes:

Large Q waves (relative to QRS amplitude in the same lead) are present in leads III and aVF. A small-but-definitely-present Q wave is also seen in the 3rd inferior lead ( = lead II).
R wave progression is normal — with Transition (where the R wave becomes larger than the S wave is deep) occurring appropriately between leads V3-to-V4.

The most concerning findings in ECG #1 relate to ST-T wave appearance in a number of leads:

The ST-T wave in lead III looks hyperacute! Specifically — there appears to be subtle-but-real ST elevation, with a straightened ST segment takeoff — that terminates in T wave negativity.
While lacking the suggestion of ST elevation — the ST segment in lead aVF also ends in T wave negativity.
Lead II (which is the 3rd inferior lead) — does not show these changes.
PEARL #1: In a patient with new chest pain — one KEY to interpretation of this tracing is the reciprocal change in lead aVL (ie, with respect to the hyperacute ST-T wave, with terminal T wave negativity in lead III). Specifically — the ST segment in lead aVL is straightened, angulates subtly downward — and ends with a surprisingly tall positive T wave (ie, resembling mirror-image opposite changes to what we see in lead III). This reciprocal appearance of lead aVL to lead III suggests recent (or acute) inferior OMI until proven otherwise! (See ECG Blog #184 re this "magical" reciprocal relationship with OMI between leads III and aVL).
To a lesser extent — reciprocal change is also seen in the other high-lateral lead ( = lead I), in the form of ST segment straightening, slight ST depression and terminal T wave positivity.
PEARL #2: The T waves are taller and more-peaked-than-expected in leads V2 and V3. This more-peaked-than-expected T wave appearance continues in leads V4 and V5. In a patient with suspected recent or acute inferior OMI — this is strongly suggestive of reperfusion T waves from associated posterior wall MI.
PEARL #3: There is ST depression in leads V4, V5 and V6. This may be multifactorial (ie, could be from LV "strain" — or — reflect reciprocal ST depression in a similar way as is seen in leads I and aVL — and/or — could reflect ischemia from multi-vessel disease).
NOTE: For more on concepts mentioned above — See ECG Blog #193 (regarding the concept of OMI = Occlusion-based MI) — and ECG Blog #258 (regarding how to "date" an MI — and appearance of peaked anterior T waves as indication of posterior wall reperfusion).

Putting It All Together:

The patient in today's case is a man in his 60s with known coronary disease. He reports recent anginal symptoms — with an episode of more severe chest pain on the day of admission. BUT — this chest pain has completely resolved by the time his initial ECG (shown in Figure-1) is obtained.

In view of this history — ECG #1 strongly suggests that infero-postero OMI (Occlusion-based MI) occurred at the time of this patient's episode of severe chest pain.
The terminal T wave negativity in leads III and aVF — as well as the more-peaked-than-expected anterior lead T waves both suggest that spontaneous reperfusion has occurred in these infero-postero leads.
The fact that this patient's chest pain is totally relieved in association with ECG #1 — strongly suggests that at this time, the "culprit" artery (almost certainly the RCA or LCx) is open!
PEARL #4: This sequence of events, in association with a pain-free state at the time reperfusion T waves are seen is consistent with Wellens' Syndrome. While the ST-T wave changes of Wellens' Syndrome are almost always associated with LAD (Left Anterior Descending) coronary artery occlusion — Wellens' Syndrome can also be seen in the inferior leads — and that appears to be what today's case represents!
PEARL #5: Recognition of Wellens' Syndrome tells us there has been recent coronary occlusion with at least momentary spontaneous reperfusion. BUT — What has spontaneously reopened — may just as easily spontaneously close again. BOTTOM Line: Timely cardiac cath is indicated — with the goal of preventing reocclusion of the "culprit" artery. KEY: The history in today's case — in association with the ECG findings in Figure-1 — indicate the need for prompt cath!

A Bit More on Wellens' Syndrome:

As emphasized above in Pearls #4 and #5 — the vast majority of Wellens' Syndrome cases are seen in the anterior leads, and are indicative of a high-grade proximal LAD stenosis. Lessons learned about this syndrome since its initial description by de Zwaan, Bär and Wellens in 1982 include the following:

There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
There should be no more than minimal (if any) troponin elevation.
There are no new infarction Q waves.
There may be slight (but not marked) ST elevation in one or more of the chest leads.
There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4).

What Wellens' Syndrome is NOT:

Greatest misunderstanding relates to what Wellens' Syndrome is not! Avoidance of this misunderstanding is best accomplished by appreciating the pathophysiology of this syndrome. In essence — the characteristic biphasic T wave appearance with terminal negativity reflects a reperfusion T wave! The patient has recently had total coronary occlusion for a brief period of time — but has now spontaneously reperfused.

The chest pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. But the reason the definition of Wellens' Syndrome requires the patient to be pain-free at the time the defining ECG is done — is that the "culprit" lesion is now open. IF the "culprit" lesion was still occluded — then rather than a warning of an impending large infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
There is no more than minimal (if any) troponin elevation — because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. IF there is greater troponin elevation — this implies that significant myocardial damage has already occurred (which by definition means that you are dealing with a completed infarction — and not with Wellens' Syndrome).
For this same reason — there should ideally not be new infarction Q (or QS) waves. That said — I take this criterion as "relative" — because it has been shown that Q waves can sometimes form in as little as 1-2 hours — and that Q waves can resolve when reperfusion of the "culprit" artery occurs quickly.
NOTE: There is no more than slight ST elevation — because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).
Instead — the characteristic biphasic T wave with rapid T wave descent into terminal negativity is an indication that there was brief total occlusion — but that the "culprit" artery has now reperfused. This ECG finding is a reperfusion T wave. It may look identical to the ST-T wave appearance after a STEMI with marked troponin elevation that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).
To Emphasize: The risk posed clinically by Wellens' Syndrome — is that it is proof there has already been acute thrombotic occlusion of the "culprit" artery (albeit brief in duration and followed by spontaneous reopening of the vessel). But what spontaneously occluded and then reopened — is at high-risk of spontaneously occluding again (with no guarantee that there will again be spontaneous reopening the next time the vessel occludes).

The CASE Continues:

The EMS team correctly interpreted the initial tracing in today's case as highly suggestive of a recent acute event. Twenty minutes later — the patient's chest pain returned, and ECG #2 was obtained.

QUESTION:

In view of the above clinical scenario — HOW would you interpret the repeat ECG shown in Figure-2?

Figure-2: Comparion of the initial ECG — with the repeat ECG done ~20 minutes later when the patient's chest pain returned.

MY Thoughts on the Repeat ECG:

It looks like the rhythm in ECG #2 has changed from sinus — to a low atrial rhythm, because the P wave in lead II is now smaller than the P wave in lead I, and the P wave is entirely negative in lead III. Otherwise — the frontal plane axis and QRS morphology are very similar to ECG #1. The most remarkable change between these 2 tracings relates to subtle-but-real differences in the limb leads:

PEARL #6: Awareness that the initial ECG in today's case was obtained at the time the patient was pain-free and was highly suggestive of an inferior lead Wellens' Syndrome — greatly facilitates our interpretation of ECG #2, because we know what to look for!
The T wave in each of the inferior leads of ECG #2 all now look hyperacute! The terminal T wave negativity that was seen in leads III and aVF of ECG #1 is gone, and replaced by taller, more upright T waves. There is more ST elevation in lead III. The T wave in lead II has clearly become more positive than it was in ECG #1.
Confirmation that these inferior lead ST-T wave changes are real — is forthcoming from scrutiny of high-lateral leads I and aVL. Both of these leads clearly show more J-point ST depression — with decrease in the amplitude of the terminal T wave positivity that had been present in ECG #1. Increased angulation of ST segment descent in lead aVL makes for a perfect reciprocal pattern to the increased hyperacuity and ST elevation now seen in lead III.
PEARL #7: ECG #2 was obtained at the time this patient's chest pain returned. The above-described ST-T wave changes in association with this return of chest pain tell us that the "culprit" vessel (most probably the RCA) has once again occluded!

Unfortunately — the above ECG changes were not recognized by clinicians at the PCI receiving center. The patient was not accepted as a candidate for acute intervention.

The CASE Continues:

Five minutes later — the patient's chest pain suddenly resolved. Another ECG was obtained at this time (Figure-3).

QUESTION:

Is the fact that ECG #3 was obtained at the time this patient's chest pain suddenly resolved — consistent with the interpretation of this case thus far?

Figure-3: Comparison of the 3 ECGs in today's case.

MY Thoughts on ECG #3:

It looks like sinus rhythm has returned in ECG #3, albeit with PACs (ie, the P wave for the 1st and 3rd beats in lead II are sinus-conducted — and once again show a larger P wave than is seen in lead I).

The "culprit" artery (most probably the RCA) — has once again reopened! We know this — because the patient's chest pain suddenly resolved corresponding to ECG #3, that shows resolution of inferior lead hyperacute T waves (that now show symmetric T wave inversion in leads III and aVF = reperfusion T waves!).
Lateral leads I and aVL now show resolution of ST depression, with return of marked terminal T wave positivity.
There is also less ST depression in lateral chest leads V4,5,6 than was present in ECG #2.
BOTTOM Line: Within the space of 25 minutes — the sequential ECGs in Figure-3 confirm that today's patient manifested an inferior lead version of Wellens' Syndrome, with "dynamic" ST-T wave changes indicative of repetitive reopening and reclosing of the "culprit" artery.

Lessons To Be Learned:

The importance of obtaining serial ECGs in patient with new symptoms can not be overstated.
Correlation of serial ECG findings with the coming and going (and with the relative severity) of patient symptoms can tell a "story" that may let you know when the "culprit" artery has reopened and/or is reoccluding.
Awareness that this course of changing symptoms, in association with "dynamic" ST-T wave changes is indication for prompt cath (because spontaneous reopening of the "culprit" vessel may be temporary — and the next time the vessel occludes it might not spontaneously reopen again).
The receiving provider team in today's case did not recognize the significance of ECG evolution correlated to changing symptom severity. As a result — acute intervention did not occur. The limited follow-up that I have of this case indicates that recognition of an acute event only occurred later when serum troponin returned elevated. There is much to be learned.

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Acknowledgment: My appreciation to Sam Collis (from England) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery.
ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.
ECG Blog #254 — What Wellens' Syndrome is and is not.
ECG Blog #320 — Wellens' Syndrome with acute 1st Diagonal OMI.
For Review on the "History" of Wellens' Syndrome (from the original 1982 article) — Please SEE My Comment at the bottom of the page in the August 12, 2022 post in Dr. Smith's ECG Blog.
ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T waves).
ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

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ADDENDUM (August 15, 2022):

Included below are a series of links and other material relevant to detection of the “culprit” artery — and my thoughts for making the case to replace the term “STEMI” with “OMI” (in the hope of substantially increasing detection of acute coronary occlusion).

Free PDF Downloads from relevant Sections in my ECG-2014-ePub:

PDF File: Overview on the Cardiac Circulation and the “Culprit” Artery in Acute MI —
PDF File: Posterior MI and the “Mirror Test” —

Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.

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Today’s ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.

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Today’s ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.

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