Written by Pendell Meyers
A man in his 50s with prior history of anterior MI with LAD stent presented with acute chest pain similar but more intense than his last MI. He presented around midnight with pain that had started around 9pm the night before. He had taken NTG at home with no improvement, and immediately received morphine on arrival at the ED for severe chest pain (a very bad idea if your accuracy for finding OMI on ECG is low, since ongoing pain will be your last chance to identify those with ongoing untreated OMI).
Here is his triage ECG at 0012:
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| What do you think? What is the differential of this ECG? |
There is sinus rhythm. The QRS is narrow but has poor R wave progression and QS waves in V1-V3, followed by STE and upright potentially large T waves. There is some movement in the limb leads portion, but there is the question of subtle STE in aVL, and subtle reciprocal STD in some inferior leads.
The differential could include:
In the first rule, if there is any single T/QRS ratio in V1-V4 that is greater than 0.36, it is likely STEMI: for the ECG from 3 years prior, that would be lead V2.
Derivation (Smith): T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction
Here are my calculated T/QRS ratios in the ECG above:
8/26.5 in V3 = 0.30
4.5/14 in V4 = 0.32
1.5/4 in V5 (first QRS complex) = 0.375
2.5/4.5 in V5 (second QRS complex) = 0.55
So there are multiple leads with concerning ratios, and lead V5 is probably diagnostic according to the literature above.
But more importantly for visual learning, let us simply compare to baseline!
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| What do you think now? Did you need ratios? |
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| Ongoing OMI. |
The ECG was read again as no acute ischemia.
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| T waves are still hyperacute, but have deflated just slightly since last ECG, and there is the tiny beginning of TWI in V4, V5. These findings are typical of the evolution of completed infarction, plus or minus some reperfusion. |
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| Further evolution of terminal T wave inversions seen in both reperfusion and completed OMI. |
Formal echo was done before cath, which showed EF 20-25%, with global hypokinesis and focal anterior and apical WMA.
Angiography was performed around 12 hours after arrival and showed:
Basically all vessels had CAD with at least 70% stenosis or more. Among these, there was a 95% mid LAD stenosis that has no TIMI flow listed, and no indication of trying to figure out whether it was the culprit (no indication of whether there was thrombus, haziness, etc.). The cath report states there was no acute culprit found. No intervention was done.
His troponin elevation was attributed to NSTEMI, and the notes state there is uncertainty whether this was type 1 MI or type 2 MI due to "systolic heart failure with acute volume overload."
Cardiac MRI was then performed several days later which showed:
"27% EF with akinesis of the mid anterior, anteroseptal, and entire apical LV segments, indicating large transmural infarct along the mid anterior/anterior septal and entire apical LV segments (LAD territory), which is nonviable except for the first diagonal distribution which is entirely viable, RCA/circumflex/OM territories are entirely viable."
Medical management was chosen. He survived the index visit was discharged.
Learning Points:
After a patient already has LVA morphology in a particular area of the myocardium, recurrent OMI in that area is more difficult to appreciate, but can be done by understanding hyperacute T waves and using the formulas above. As always, the most viable and at risk tissue during OMI registers in the T wave as hyperacute T waves. This is still true even in the context of LVA.
Ongoing ischemic pain, rising troponins, despite maximal medical management is a class 1A indication for emergent catheterization in the current ACC/AHA guidelines. This patient is one of the roughly 90+% whose management violates these guidelines.
Learning the OMI progression helps free your mind from the prison of the STEMI criteria and allows you to start understanding OMIs.
Remember, STEMI(-) OMIs with delayed management have double the mortality and long term morbidity than their RCT counterparts who did not have OMI.
Get more practice with LVA and OMI here:
A woman in her 40s with acute chest pain
Subtle Anterior STEMI Superimposed on Anterior LV Aneurysm Morphology
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MY Comment, by KEN GRAUER, MD (4/13/2022):
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- This man in his 50s has documented CAD (ie, prior anterior MI with LAD stenting). He presents to the ED at midnight with a 3-hour history of new-onset chest pain that was worse than the chest pain that occurred with his previous MI. NTG provided no relief.
- Even without seeing the initial ECG — this clinical scenario (especially with any elevation at all in troponin) — should be viewed as clear indication for prompt cath.
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| Figure-1: I've labeled the initial tracing in today's case (See text). |
- There is significant baseline artifact in multiple leads on this tracing. Not being at the scene — I have no idea why there is so much artifact — but in this patient with such high likelihood of needing prompt cath — I would have immediately repeated this ECG (or repeated it within no more than 10-15 minutes) in the hope of obtaining a more interpretable tracing.
- That said — there is a regular sinus rhythm at ~80/minute in ECG #1. All intervals (PR, QRS, QTc) are normal.
- There is marked left axis deviation (ie, at least -60 degrees) — which is consistent with LAHB (Left Anterior HemiBlock).
- Voltage criteria for LVH are satisfied in ECG #1, primarily because of the very deep (~25 mm) S wave in lead V3 (both Cornell and Peguero Criteria are satisfied — as discussed in My Comment of the June 20, 2020 post of Dr. Smith's Blog).
- Because the left anterior hemifascicle lies anatomically in front of (ie, "anterior") to the posterior hemifascicle — ventricular activation with LAHB is initially posteriorly-directed (toward the intact left posterior hemifascicle). As a result — LAHB may cause (or exacerbate) poor R wave progression.
- As we have shown on many ECG Blog posts in Dr. Smith's Blog — the presence of LVH can complicate assessment of anterior ST elevation — because the "reciprocal" of lateral lead LV "strain" in patients who manifest LVH with deep anterior S waves, is ST elevation in these anterior leads (See My Comments in the December 27, 2018 post — the February 6, 2020 post — and the June 20, 2020 post, to name a few).
- Today's case is further complicated — because the known history of prior anterior MI may itself result in deeper anterior S waves not due to LVH (ie, loss of anterior forces from the anterior infarction may result in unopposed posterior forces).
- That said — ECG #1 lacks the tall R waves so common with LVH in left-sided leads (ie, in leads I, aVL and V6) — and it lacks deep S waves in anterior leads V1,V2 — so despite satisfying textbook "voltage criteria" for LVH — I'm not convinced we can diagnose LVH on the basis of this tracing (ie, formal Echo would be needed to do so).
- BOTTOM LINE: Even though definitive conclusions can not be reached — It's important to be aware of potential interaction that LAHB, LVH and prior anterior infarction may all have when attempting to assess the initial ECG in today's case!
- Q Waves: QS complexes are seen in leads V1 and V2. A small-but-present initial positive deflection (r wave) is present in lead V3. This initial r wave gets a little bit larger in leads V3 and V4 — until transition to a predominant R wave finally occurs in lead V6.
- There is PRWP (Poor R Wave Progression) — given how small the initial r wave is until lead V6. This is consistent with the patient's prior anterior infarction.
- As I emphasized earlier — significant baseline artifact complicates assessment. Two of the most concerning leads to me in ECG #1 were leads aVL and aVF. But WHICH of the 3 beats in these 2 simultaenously-recorded leads are the "real" ones? In this patient with new-onset and persistent chest pain — there clearly is worrisome ST elevation in complex "B" in lead aVL (with corresponding reciprocal ST depression in lead aVF). There is still ST elevation in complex "A" in aVL, albeit to a lesser degree. But I don't think we can say there is any definite ST elevation in the artifact-laden ST segment of complex "C" in this aVL lead.
- Similar pitfalls in interpretation of ST-T wave changes are encountered in simultaneously-recorded leads V4 and V5. If complex "C" in leads V4 and V5 represents the "real" ST segment — then there is no doubt that this is a hyperacute T wave. But although the ST-T waves for "A" and "B" in leads V4, V5 are still abnormal — the abnormality is not nearly as decisive.
- Lead V3 at least shows consistency — in that ST-T wave morphology for each of the 3 complexes recorded in this lead looks the same. Let me emphasize that I completely agree with Dr. Meyers' assessment — namely, that despite the deep S wave in lead V3, the amount of J-point ST elevation and height of T wave peaking is highly suspicious. But given potential complicating factors I described above — I was not at this point 100% certain that ECG #1 represented an acute process.
- Given technical faults with the quality of ECG #1 — plus persistence of severe chest pain — plus a slightly elevated initial troponin — this delay between tracings was far too long.
- A prior tracing on this patient was found soon after. Although this prior tracing was apparently looked at by the health care team — lead-by-lead comparison could not have been done — otherwise there would be no way not to notice the difference between the prior tracing and the initial ECG (ECG #1) in today's case (See side-by-side comparison figure by Dr. Meyers above). The most accurate (and time-efficient) way to compare serial tracings, is that after you have interpreted one of the ECGs — to compare lead-by-lead the 2 tracings in front of you (I illustrate this approach in My Comment in the August 8, 2020 post — and in the August 21, 2020 post of Dr. Smith's Blog).
- Closing Thought: As detailed above by Dr. Meyers — Oversights in today's case continued for ~12 hours after ED arrival, until cardiac cath was finally performed. My belief has always been that the best way to learn from mistakes made — is to retrace events, and soul-search the decisions made. The decision to perform cardiac cath should have been made long before the 2nd ECG ( = the 2:00am tracing) was obtained.
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