ECG Blog #374 — Do You Know the "Culprit"?

The ECG in Figure-1 was obtained from a 90-year old woman — who presented with a 2-to-3 day history of chest pain, that became worse on the day of admission.

• How would YOU interpret the ECG in Figure-1?
• Is there acute coronary occlusion? If so — What is the "culprit" artery?

Figure-1: The ECG in today’s case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

There is significant baseline artifact in a number of leads in ECG #1. That said — the rhythm is sinus, at a rate just under 100/minute. The PR interval is normal — but the QRS is wide:

• The reason for QRS widening is bifascicular block: i) The all upright and notched R wave in lead V1 — in association with wide terminal S waves in lateral leads I and V6 is consistent with RBBB (Right Bundle Branch Block); and, ii) Predominant negativity in each of the inferior leads is consistent with LAHB (Left Anterior HemiBlock).
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• A small q wave is seen in lead aVL. A tiny initial negative deflection (q wave) is also seen in lead V2. I suspect these small q waves are not clinically significant.
• What is clinically significant, especially in view of new chest pain over the past 2-3 days that this patient reports — are the significant ST-T wave deviations in multiple leads (Figure-2).

Figure-2: I've labeled today's ECG to highlight ischemic findings. The vertical RED lines mark the end of the QRS complex in each of the 12 leads — and the "Ts" highlight hyperacute T waves. (See text).

Looking Closer at Today's ECG:

The most challenging part of assessing ST-T wave deviations in today's tracing — is distinguishing between the end of the QRS complex — and — the beginning of the ST-T wave. To facilitate this distinction — I've added vertical RED lines to mark the end of QRS complex in each of the 12 leads.

• NOTE: Although the end of the QRS is not well seen in many of the leads in today's tracing — it is clearly delineated in leads II and aVR in the limb leads — and especially in lead V1 in the chest leads.
• To facilitate assessment of ST depression and/or elevation — I focused my attention on the relative position of the J-point (located just to the right of the vertical RED line) in each of the 12 leads — with respect to the short dotted RED lines that mark the ST segment baseline in each lead.

ST-T Wave Abnormalities in Figure-2:

• ST depression is most marked in the chest leads (clearly beginning in Lead V2 — and extending through to lead V6).
• The J-point also appears to be depressed in lead V1 — though this J-point depression with T wave inversion that we see in lead V1 is not necessarily abnormal given the RBBB.
• ST depression is also marked in lead I — and seen (albeit to a lesser extent) in limb leads II, aVL and aVF.
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• ST elevation is marked in lead aVR. It is not seen in other leads.
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• Hyperacute T waves (ie, being taller, "fatter"-at-their-peak and wider-at-their-base than expected given QRS amplitude in each respective lead) — are seen in multiple leads (ie, in leads II,III,aVF; and in leads V3-thru-V6 — as suggested by the "Ts" in these leads).

Putting It All Together: 

In view of the 2-3 day history of chest pain, that became worse at the time the ECG in Figure-2 was recorded — My thoughts were the following:

• The relatively rapid sinus heart rate (just under 100/minute) is potentially worrisome — since sinus tachycardia is usually not seen with acute MI unless there is hemodynamic compromise.
• There is bifascicular block (ie, RBBB/LAHB) — with fragmentation of the QRS complex. These 2 findings strongly suggest significant underlying heart disease in this 90-year old patient — although without a prior tracing for comparison, we can not tell what is "new" vs "old".
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• There is marked and diffuse ST depression in multiple leads (with ST elevation in lead aVR). This ECG pattern suggests coronary disease that may be acute — but which does not localize to any particular anatomic lead area. The underlying pathophysiologic process responsible for this ECG pattern is "supply-demand mismatch". The terminology favored to describe these ECG findings is diffuse subendocardial ischemia (See ECG Blog #271 — for more on diffuse subendocardial ischemia).
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• In addition to diffuse ST depression — there are hyperacute-looking T waves in multiple leads (that I've labeled with a Ts in Figure-2). This pattern of J-point ST depression rising to hyperacute-looking T waves in multiple chest leads in a patient with new chest pain — suggests deWinter-like T waves as a result of ongoing LAD (Left Anterior Descending) occlusion (See ECG Blog #183 — for more on deWinter T Waves).
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• NOTE: As stated a moment ago — without a prior tracing, we don't know if the RBBB/LAHB is "new" or "old". That said — this combination of conduction defects is very commonly seen with acute proximal LAD OMI (Occlusion-based MI).
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• BOTTOM Line: Looking at this single tracing — I wasn't sure about what the acute lesion might be, or when it may have happened. The patient's symptoms had been ongoing for "2-3 days" — and at 90 years of age with significant QRS fragmentation of her bifascicular conduction defect — much of what we see may have happened in the past. Other than lead aVR — there is no ST elevation in Figure-2. That said — the important point is her ongoing (and increasing) chest pain. Pending more data (ie, repeat ECG; troponins, Echo, etc.) — an extensive acute ongoing event must be assumed until proven otherwise.

CASE Follow-Up:

The patient's chest pain was controlled. Initial troponin was only minimally elevated. Echo revealed a localized apical wall motion abnormality. 

• Cardiac Cath — revealed a 90-99% LMain (Left Main) — and — a 90-99% proximal LAD narrowing. There was no significant disease in the LCx or RCA. 
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• PCI was successful — and this 90-year old patient did surprisingly well!
• Subsequent troponin values rose markedly — with a peak value = 77000.

Acute LMain Disease:

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.

• There is no “single” ECG presentation for patients with acute LMain occlusion. Quite literally — You can see almost anything!
• As shown in Figure-3 — the reason for the highly variable ECG presentation with LMain occlusion — is that multiple territories may be involved to varying degrees — making it impossible to predict how much ST elevation you will see — and how much opposing (reciprocal) ST depression will attenuate (if not completely cancel out) these initial ST segment vector forces.
• The ST-T wave appearance in lead aVR can be anything when there is acute LMain occlusion.
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• To Emphasize: We don't know for certain whether the LMain or the proximal LAD was the "culprit" vessel in today's case — as the patient's symptoms were ongoing for several days, and neither vessel was 100% occluded at the time of cath. It's almost certain there was at least some spontaneous reperfusion of one or both vessels. What was certain in today's case — was the need for prompt cath and PCI, that fortunately was accomplished.

Figure-3: Reasons for the varied ECG presentation of acute LMain occlusion — with this summary synthesized from Dr. Smith’s 8/9/2019 post in his ECG Blog. I discussed the findings of acute LMain occlusion further in My Comment in the January 16, 2020 post of Dr. Smith's ECG Blog.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) 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 #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
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• ECG Blog #271 — Reviews the concept of diffuse subendocardial ischemia.
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• ECG Blog #316 — The patient died. Was the LMain coronary artery the "culprit"?

Additional 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?