Written by Pendell Meyers, with edits by Steve Smith
A man in his early 40s with history of MI s/p PCI presented with bilateral anterior chest pain described as burning and belching with no radiation since last night starting around 11pm (roughly 11 hours ago). He also described a syncopal episode just prior to onset of symptoms. He had used cocaine approximately 20 minutes prior to onset of symptoms.
He still had active pain on arrival to the ED.
Here is his triage ECG:
Progression of anterior OMI to full Q-wave MI with large pathologic Q-waves in V2-V4 with persistent STE which now meets STEMI criteria (after full thickness infarction/stunning).
The cath lab was now activated.
He was found to have 100% mid LAD occlusion. Thrombectomy performed, then stent placed with improvement of TIMI 0 to TIMI 3 flow.
Pre-PCI:
Post-PCI:
In this view you can see the extent of the "wraparound" distal LAD:
Peak troponin T was 35.70 (massive MI, rarely survivors at this level in my 3 years here).
Echo showed EF 30% with anterior, septal, apical, and inferior wall motion abnormalities.
ECG after cath:
Continued STE with anterior wall Q waves (LV aneurysm morphology), combined with extremely high troponin are likely indicative of full thickness irreversible MI (rather than stunning), and are high risk features for resulting LV aneursym. The extremely high troponin and ECG evidence of LVA morphology are very worrisome long term features for resultant morbidity and mortality.
Amazingly, he did not suffer any serious complication in hospital. He recovered and was discharged several days later. Long term follow up is unknown at this point.
Learning Points:
Even if NSTEMI Occlusions (STEMI- OMIs), overall prove to have slightly lower morbidity and mortality than STEMI Occlusions (STEMI+ OMI), there are many cases like this one showing that some of the worst, largest OMIs may not manifest STEMI criteria until far too late, if ever. Again, it is possible that this patient would have had obvious STE earlier in the time course of this MI, but we do not know. What we can say is that his initial ECG was certainly diagnostic and the delay of many hours could have been improved.
Wraparound type 3 LAD Occlusion causes STE in many leads including anterior, lateral, and inferior distributions. This is the most important exception to the classic teaching of "diffuse STE without reciprocal depression is less likely ACS, more likely pericarditis". Always keep in mind the possibility of diffuse STE (and other OMI findings) as being due to a type 3 LAD.
A man in his early 40s with history of MI s/p PCI presented with bilateral anterior chest pain described as burning and belching with no radiation since last night starting around 11pm (roughly 11 hours ago). He also described a syncopal episode just prior to onset of symptoms. He had used cocaine approximately 20 minutes prior to onset of symptoms.
He still had active pain on arrival to the ED.
Here is his triage ECG:
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| What do you think? |
His baseline ECG was on file:
--Sinus rhythm
--Subtle STE in V1-V5, II, III, and aVF
--Q-waves in V1-V5, as well as II, III, and aVF which must be assumed new until proven otherwise
--Possibly large area under the T-wave (concern for hyperacute T-waves) in V4, II, III, and aVF, with reciprocal negative T-wave in aVL
--These Q-waves are so fully developed that it appears to be a nearly completed MI, at a stage when it is likely that all ST elevation is resolved. STE occurs primarily in viable ischemic myocardium; persistent STE after completed infarction is ominous and portends development of an aneurysm.
--There is also an interesting Brugada-like morphology in V1 (also similar to hyperkalemia, which sometimes mimics brugada). This morphology can be cause by or associated with cocaine:
A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of ***STEMI***
This is OMI of the anterior, lateral, and inferior walls until proven otherwise. This distribution is classic for a type III "wraparound" LAD Occlusion.
But it does not meet STEMI criteria and it was not initially recognized. Whereas most STEMI(-) OMI is acute, this one might have had STE at its onset, or earlier in its course. We'll simply never know without ECGs from that time period.
The first troponin T was delayed for several hours for an unknown reason in the lab, and returned at 1.50 ng/mL (very elevated).
This prompted a repeat ECG (we do not have documentation from that time to tell us whether he had persistent, recurrent, or absent pain):
Progression of anterior OMI to full Q-wave MI with large pathologic Q-waves in V2-V4 with persistent STE which now meets STEMI criteria (after full thickness infarction/stunning).
The cath lab was now activated.
He was found to have 100% mid LAD occlusion. Thrombectomy performed, then stent placed with improvement of TIMI 0 to TIMI 3 flow.
Pre-PCI:
Post-PCI:
In this view you can see the extent of the "wraparound" distal LAD:
Peak troponin T was 35.70 (massive MI, rarely survivors at this level in my 3 years here).
Echo showed EF 30% with anterior, septal, apical, and inferior wall motion abnormalities.
ECG after cath:
Continued STE with anterior wall Q waves (LV aneurysm morphology), combined with extremely high troponin are likely indicative of full thickness irreversible MI (rather than stunning), and are high risk features for resulting LV aneursym. The extremely high troponin and ECG evidence of LVA morphology are very worrisome long term features for resultant morbidity and mortality.
Amazingly, he did not suffer any serious complication in hospital. He recovered and was discharged several days later. Long term follow up is unknown at this point.
Learning Points:
Even if NSTEMI Occlusions (STEMI- OMIs), overall prove to have slightly lower morbidity and mortality than STEMI Occlusions (STEMI+ OMI), there are many cases like this one showing that some of the worst, largest OMIs may not manifest STEMI criteria until far too late, if ever. Again, it is possible that this patient would have had obvious STE earlier in the time course of this MI, but we do not know. What we can say is that his initial ECG was certainly diagnostic and the delay of many hours could have been improved.
Wraparound type 3 LAD Occlusion causes STE in many leads including anterior, lateral, and inferior distributions. This is the most important exception to the classic teaching of "diffuse STE without reciprocal depression is less likely ACS, more likely pericarditis". Always keep in mind the possibility of diffuse STE (and other OMI findings) as being due to a type 3 LAD.
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Comment by KEN GRAUER, MD (7/19/2019):
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I was intrigued by the challenge of clinical correlation posed by the ECGs in this case. The patient is a man in his 40s with a history of prior MI (s/p PCI) — who presented to the ED with new chest pain that had begun ~11 hours earlier. His initial ECG in the ED ( = ECG #1) is shown in Figure-1. The patient was still with ongoing chest pain at the time ECG #1 was done.
- A baseline tracing was found on this patient ( = ECG #2).
- Several hours later a follow-up ECG was obtained in the ED, because the 1st troponin came back significantly elevated ( = ECG #3).
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| Figure-1: The first 3 ECGs that were shown in this case (See text). |
CHALLENGE: How did YOU interpret ECG #1 before you looked at ECG #2?
- As we soon learned in this case — this patient has had a new STEMI. Cardiac cath (which was done soon after ECG #3) told us that this STEMI was the result of 100% mid-LAD occlusion (LAD with wraparound). But the BEST way to enhance one’s ECG interpretation skills is to always interpret the initial tracing in the context of the brief clinical history given (which in this case, was new chest pain that began 11 hours earlier).
- Strive to interpret this initial ECG before you look at additional information. THEN look for previous tracings in the patient’s chart, repeat ECGs, troponin and Echo results + the patient’s clinical course. This sequence of assessment will not slow you down — and it is the BEST way to optimally “grow” as an astute ECG interpreter.
My THOUGHTS on ECG #1 (determined BEFORE I looked at ECG #2):
Remember the History = a man in his 40s with known prior MI (s/p PCI) — who presented to the ED with new chest pain that had begun ~11 hours before ECG #1 was done.
Descriptive Analysis of ECG #1:
- The rhythm is sinus at a fairly regular rate of ~80-85/minute. The PR, QRS and QTc intervals are all normal. The frontal plane axis appears to be normal — though the axis is difficult to calculate because of nearly isoelectric complexes in 4 of the 6 limb leads (leads I, III, aVL and aVF). There is no chamber enlargement.
Regarding Q-R-S-T Changes:
- There are multiple Q wavesin ECG #1. Although small in size — the inferior Q waves are likely to be significant (ie, indicative of inferior MI at some point in time) — because relative to QRS dimensions, inferior Q waves are both large and relatively widened. There are large Q waves (relative to QRS complex size) in leads V1, V2 and V3. There is marked fragmentation of the QS complex in lead V3.
- PEARL: Although Q waves in leads V4, V5 and V6 become much smaller and narrower — the fact that the Q wave in lead V4 is decidedly larger than the Q waves in leads V5 and V6, tells us that the Q in V4 is significant (ie, part of the infarction process suggested by the Q waves in V1-V3). With normal “septal” q waves — the opposite progression occurs (ie, Septal q waves are uncommon in lead V4 — and when present, a septal Q in V4 should be smaller than the septal Q in V5 and V6).
- The area of Transition (ie, where the R wave becomes taller than the S wave is deep) is slightly delayed in ECG #1 (ie, it occurs between leads V4-to-V5).
Regarding — ST-T wave Changes:
- As noted by Drs. Meyers and Smith — there is an interesting Brugada-like morphology to the ST-T wave in leads V1 and V2 (convex down RED line in V1,V2 of ECG #1). There is not enough ST elevation to qualify this as a Brugada-1 pattern — but, the clinical significance of recognizing this pattern is that the slight ST elevation in these leads is more likely to reflect a Brugada “phenotype” rather than acute septal infarction.
(For more on assessment of Brugada ECG patterns — CLICK HERE for a link to my 29-minute video on the subject. If you click on SHOW MORE under the video on the YouTube page — you’ll see a linked Contents to all in the video).
- Back to ECG #1: As per Drs. Meyers and Smith — there is subtle-but-real ST elevation in multiple leads. That said — the almost horizontal elevated ST segments in the inferior leads look less acute than one might have expected. These elevated ST segments are associated with prominent inferior T waves — and, reciprocal (albeit shallow) T wave inversion in lead aVL.
- Similarly the subtle-but-real ST elevation in leads V3, V4 and V5 has a shape that looks less acute than one might have expected (gently upward concave, as suggested by curved BLUE lines in V3 and V4 of ECG #1).
- NOTE: The different shape of the slightly elevated ST segments in leads V1,V2 of ECG #1 (curved-down RED lines) — vs the upward concavity ST segments in leads V3-thru-V6 (curved-UP BLUE lines) — in my opinion, adds further support that these are 2 different processes (ie, Brugada-like phenotype for the ST-T waves in leads V1,V2— vs recent acute injury for the elevated ST segments in leads V3-thru-V6).
Clinical IMPRESSION: Before finding this patient’s baseline tracing — I would have been hard pressed to know how much of what I was seeing in ECG #1 might have been due to the prior MI that this patient had — vs what might have developed since the onset of chest pain 11 hours earlier. This is the CHALLENGE I put forth to you earlier! Realizing there is NO way to be certain — these were my thoughts:
- What we see in ECG #1 probably did not just happen. Although possible to develop new Q waves in as little as 1-2 hours after acute infarction — I thought the size and number of Q waves seen here + the fragmentation in lead V3 suggested that at least some of these Q waves were the result of this patient’s prior MI. I would have guessed from the prominent T waves and subtle ST elevation that this patient manifests in ECG #1 — that he had suffered an acute event at the onset of symptoms (ie, ~11 hours earlier).
- That said — because there is still ST elevation in ECG #1, with inferior T waves that look like they may still be hyperacute + ongoing chest pain — cardiac cath sooner-rather-than-later seems indicated to clarify the clinical picture.
At this point in time — Finding a Baseline Tracing on this patient ( = ECG #2) proved invaluable! My thoughts on comparing ECG #2 with ECG #1:
- I was wrong about my hunch that at least some of the Q waves in ECG #1 were old. Other than lead V1 — there are no Q waves at all in ECG #2! Instead, R wave progression in this earlier baseline tracing was normal — with development of a fairly tall R wave already by lead V3. This means that the extensive Q waves in ECG #1 (including the fragmentation in lead V3) are new since the baseline ECG #2 was done. We have to presume (until proven otherwise) that these ECG findings are new since the onset of symptoms 11 hours earlier.
- There is virtually no ST elevation in ECG #2. Overall, I don’t see much difference in T wave appearance between ECG #1 and ECG #2. This left me with uncertainty regarding how acute the subtle-but-real ST elevation now present in ECG #1 might be. Did it develop days or weeks earlier? — or, sometime after the onset of symptoms within the 11-hour period prior to presentation in the ED? That said — persistence of chest pain + the ECG changes that developed between ECGs #1 and 2 would be indication for acute cath to clarify the clinical picture.
Apparently — the new ST elevation that developed in ECG #1 (compared to the baseline ECG) was not recognized. Several hours later, when the 1st troponin came back elevated — ECG #3 was obtained.
- I see no significant change in ST-T wave appearance in the limb leads between ECG #1 and ECG #3 done several hours later.
- However – there has been marked change in ST-T wave appearance in the chest leads in ECG #3! Even accounting for slight change in QRS morphology and amplitude in the mid-chest leads (suggesting some variation in precordial lead placement) — there clearly is now straightening of the ST segment takeoff (slanted BLUE lines in ECG #3) with more ST elevation in leads V3 and V4.
- Beyond-the-Core: The Brugada-like morphology in lead V1 of ECG #3 looks the same as it did in ECG #1 (curved-down RED line). It is interesting that the shape of the elevated ST segment in lead V2 of ECG #3 now manifests a flattened (BLUE-RED line) morphology that is intermediate between the curved RED line in lead V1 — and the upward slanting BLUE line in lead V3. I suspect the reason for this is a “fusion” between the Brugada-like ST segment effect being exerted on lead V2 — with what is now acute ST straightening and elevation in leads V2, V3 and V4 from the actively evolving anterior STEMI.
- Putting It All Together — Despite the history of a prior MI (with PCI) — the baseline tracing ( = ECG #2) shows no evidence of prior infarction. From the information available — it’s impossible to know if a 2nd event occurred sometime after ECG #2 was done — but before the onset of symptoms associated with this admission. What can be said — is that regardless of whether this marks a 2nd or 3rd cardiac event, that there is definite ECG and troponin evidence of an acute STEMI that is actively evolving between the time that ECGs #1 and #3 were done.
Our THANKS to Drs. Meyers and Smith for this challenging case!
