ECG Blog #316 — What & When was the "Culprit"?

The ECG in Figure-1 — was obtained from an older man who presented to the ED (Emergency Department) with new-onset symptoms that began within the past 1-2 hours. The patient had a long history of smoking — but no prior history of heart disease.

• How would YOU interpret the ECG in Figure-1?
• Can you identify the “culprit”?
• Extra Credit: Why is there no ST elevation in lead aVL?

Figure-1: The initial ECG in today's case.

MY Thoughts on ECG #1:

The rhythm is sinus tachycardia at ~110/minute. The QRS complex is wide with morphology consistent with complete RBBB (ie, QR pattern in lead V1; wide terminal S waves in leads I and aVL).

• There are wide and deep Q waves in each of the inferior leads — and in leads V1-thru-V6. In fact — the QRS complex is tiny with complete loss of R wave in the most lateral chest lead ( = lead V6).
• There is marked ST elevation in no less than 9/12 leads in this tracing!

IMPRESSION:

The ECG is diagnostic of a huge ongoing STEMI — that by history, most probably began ~1-2 hours earlier.

• ST elevation is most marked in leads V2-thru-V6 — though it is also present in the inferior leads. This suggests either acute proximal LAD (Left Anterior Descending) coronary artery occlusion — or — LMain (Left Main) occlusion.

QUESTION: 

• With diffuse ST elevation in no less than 9/12 leads — Why is there no ST elevation in lead aVL?

ANSWER:

I suspect that the reason there is no ST elevation in lead aVL — is that there is a "cancellation" effect.

• Although lead aVL is often thought of as a "high lateral" lead — MRI studies suggest that its perspective actually views the anterior-medial wall of the left ventricle (Bayes de Luna — Circulation 114:1755-1760, 2006). As a result, most of the time with a proximal LAD occlusion — there will be ST elevation in lead aVL. There will also usually be reciprocal ST depression in the inferior leads.
• On the other hand — there may be anatomic "wraparound" of the LAD (such that the LAD is a longer vessel that extends beyond the anterior wall to also supply the inferior wall of the left ventricle). If there is acute occlusion of a "wraparound" LAD — then in addition to anterior lead ST elevation, there may also be ST elevation in the inferior leads (with reciprocal ST depression in lead aVL).
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• When there is both proximal LAD occlusion + anatomic "wraparound" — there may be extensive anterior and also inferior infarction, with resultant cancellation of some forces (consistent with the picture seen in Figure-1, in which there is ST elevation in chest leads and in inferior leads — but with a flat ST-T wave in lead aVL).

CASE Follow-Up:

In today's case — the severity of the situation was immediately recognized — and the patient was promptly transferred to a treatment center. Troponin was markedly elevated. Unfortunately, despite treatment — the patient died within 1-2 hours of presentation. 

• Echo with Doppler documented blood flow across the interventricular septum — indicative of VSR (Ventricular Septal Rupture).

About VSR (Ventricular Septal Rupture):

I found the concise Review of VSR by Mubarik and Iqbal insightful in today's case (NIH StatPearls Publishing — April, 2022). Below some highlights:

• VSR is an uncommon presentation of acute MI. Whereas the incidence of this complication used to be ~2% — this has decreased to a fraction of 1% of acute MIs because of improved treatment and revascularization of acute MI.
• The prognosis of acute VSR depends on the site in the septum and the size of the rupture. If the acute infarct is smaller with prompt reperfusion and stable hemodynamics — then stabilization of the patient may be possible, with the goal of enabling successful surgical closure.
• In contrast — the condition is likely to rapidly prove fatal when septal rupture results from a very large infarction that quickly leads to cardiogenic shock. This is presumably what occurred in today’s case. Development of bifascicular block with large Q waves in 9/12 leads (covering the inferior and antero-lateral walls) — document the extensive myocardial damage in today’s case. Acute biventricular volume overload from the septal rupture, added to an already compromised cardiac output from the huge infarction is unlikely to be treatable.
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• NOTE: Whereas surgical repair of VSR offers the only realistic chance for survival — immediate surgery is far more challenging than when surgery is delayed several days. This is because of the difficulty trying to distinguish between healthy and newly infarcted tissue — with inability of newly infarcted myocardium to hold sutures.

QUESTION:

Take another LOOK at the initial ECG in today's case (Figure-2). Considering the History — namely, that this older man presented to the ED within 2 hours after symptom onset — and then died 1-2 hours later after arrival in the hospital (with Echo Doppler confirming acute VSR) — Do YOU think it more likely that the "culprit" artery was:

• An acute proximal LAD occlusion? 
• Acute LMain occlusion? 
• Something else?

Figure-2: Another LOOK at the initial ECG in today's case.

The “Culprit” Artery in Today’s Case?

I do not know a definitive answer to the above question. The patient died before cardiac catheterization could be done — and no post-mortem examination was performed. That said — my thoughts are the following:

• Emergency providers rarely encounter patients with acute LMain occlusion. The reason for this is simple — Most such patients die quickly, usually before they reach the hospital.
• At the time the initial ECG in Figure-2 was recorded (which according to the information available, was 1-2 hours after symptom onset) — there are already extremely large Q waves in 9/12 leads (as well as RBBB and marked ST elevation in 9/12 leads). Yet despite this — the patient survived another 1-2 hours after arrival in the hospital. IF the "culprit" was the LMain coronary artery — I would not expect the patient to survive this long with the extensive damage suggested by his initial ECG.
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• MY Thought: Instead of LMain occlusion — I feel ( = my opinion) that a much more logical sequence of events in today's case is that there was acute proximal LAD occlusion — which because of the extensive damage that this already caused (evidenced by the RBBB and extremely large Q waves in inferior and anterolateral leads) — resulted in the uncommon complication of acute VSR (Ventricular Septal Rupture), after which the patient promptly decompensated.

WHAT then are the ECG Findings of Acute LMain Occlusion?

The final question raised by today's case, is what the ECG signs of acute LMain occlusion are?

• In a word — You can see almost anything!
• Dr. Stephen Smith reviewed his data and experience regarding this issue in the August 9, 2019 post in Dr. Smith's ECG Blog. 
• In my attempt to simplify the answer to this question — I summarize Dr. Smith's findings in Figure-3.

Figure-3: Reasons for the varied ECG presentation of acute LMain occlusion — excerpted from Dr. Smith’s 8/9/2019 post (See text).

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Acknowledgment: My appreciation to Kianseng Ng and Yap Wan Teng (from Malaysia) for the case and this tracing.

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Relevant ECG Blog Posts

• ECG Blog #193 — Reviews a case with a dominant LCx as the "culprit" artery (with ECG AUDIO Pearl on the concept of "OMI" and on Predicting the "Culprit" Artery).
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• ECG Blog #184 — That magical inverse relationship between leads III and aVL.
• ECG Blog #167 — More on that "magical" lead III-aVL relationship.
• ECG Blog #183 — deWinter-like T waves.
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• ECG Blog #56 — Posterior MI; Mirror Test.
• ECG Blog #80 — What’s the Culprit Artery? + the Mirror Test
• ECG Blog #82 — What’s the Culprit Artery?
• ECG Blog #162 — What’s the Culprit Artery?
• ECG Blog #193 — What's the Culprit Artery?
• ECG Blog #222 — What's the Culprit Artery?

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