Monday, July 4, 2022

The ECG must be recorded at the right time, or the Occlusion (OMI) will be missed.

This was sent by one of our faculty, Steven Souchtchenko, who trained under me and works at another hospital most of the time, and with us at Hennepin some of the time.


53yoF with stuttering CP for 2 days, suddenly acutely worse tonight, now 10/10 pressing radiating to L arm.  

What do you think?

Steven wrote: 

"I called it "OMI" based on hyperacute T-waves."  (Dr. Souchtchenko understands that a hyperacute T-wave is not at all defined by its height, nor even by its size and bulk (though these are "bulky," but by its size in proportion to the QRS).

"Cardiology didn’t believe me.  I recorded a right sided ECG 16 minutes later." Here is the right sided ECG he recorded:

Remember that in a right sided ECG, V1R = V2 on the left sided ECG, and V2 = V1.  
So here V1 is reflecting V2

Look at the first ECG again, and use the 4 variable formula to distinguish normal ST Elevation in V2-V4 from STE in V2-V4 that is due to LAD occlusion:

There is a free app for Android called "Smith ECG"
18.2 is the most accurate cutpoint, with a value higher than 18.2 having about 87% specificity for LAD occlusion.  As with all dichotomous rules, the closer it gets to the cutpoint, the less reliable the value is.

The formula is FAR more accurate (more sensitive and just as specific) than ST Elevation "criteria."
Note there are many exclusions; the exclusions are features that are so specific for LAD occlusion that it would be dangerous to include such cases:

The reasons that the formula is so much better than ST elevation for the diagnosis of LAD occlusion:
1. It takes into account the prolongation of the QT in ischemia
2. It takes proportion into account (ST elevation is significant only in proportion to the QRS size, as measured by the R-wave in V4 and the QRS in V2).
3.  ST Elevation at 60 ms after the J-point measures not only ST Elevation, but also measures the upslope of the ST segment which predicts the size of the T-wave

Again, for many examples of use of the formula, go to this blog post: 

12 Example Cases of Use of 3- and 4-variable formulas, plus Simplified Formula, to differentiate normal STE from subtle LAD occlusion

Case continued

The initial troponin I returned at 0.146 ng/mL

The patient was taken for an angiogram:

95% LAD stenosis with TIMI-3 flow.  It was stented.

The post cath (but not necessarily peak), troponin I was 0.846 ng/mL.  This is not very high for OMI, but can be seen if the artery is only briefly occluded (whether due to very fast intervention or spontaneous reperfusion).

In our studies (see this one), we define OMI as: 

1) TIMI 0-2 flow, or 

2) Culprit + TIMI-3 flow +  peak troponin of at least 10.0 ng/mL for troponin I, 1.0 ng/mL for trop T, or 1000 ng/L for hs trop T.

So this case would qualify as a "false positive" using these research methods.  But it clearly is not a false positive!!   In other words, these research methods result in false false positives.  This is a necessary limitation of the research originating from the fact that we don't record the ECG at the same time as the angiogram, and thrombosis is dynamic, with thrombus alternately spontaneously lysing and propagating.  

Nevertheless, we must report them as false positives in our papers, even though they are actually true positives for OMI (false false = true).

The timing of ECG recording:

Had this ECG been recorded at some time point when there was TIMI-3 flow for an extended period, the OMI would not have been apparent.  The patient would have had an unrecorded transient STEMI and perhaps re-occluded in the middle of the night.  This is why it is so important to try to record an ECG during pain, not only AFTER pain or during gradual resolution of pain.

Comment by KEN GRAUER, MD (7/4/2022):
I liked this case by Drs. Souchtchenko and Smith — because it provides yet another example of when activation of the cath lab is indicated. In view of the very worrisome history of chest pain in today's case — the interventionist should not have doubted the need for prompt cath on the basis of the initial ECG, which for clarity I've reproduced in Figure-1.
  • In addition to satisfying Dr. Smith's 4-variable formula that supports LAD occlusion — I thought there were ST-T wave abnormalities consistent with at-the-least possible (if not probable) acute LAD OMI in at least 9/12 leads (Figure-1).

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

WHY Prompt Cath was Indicated:
Dr. Souchtchenko was appropriately concerned about hyperacute T waves in this initial ECG.
  • When faced with subtle-but-definitely-present ECG findings (as occurred in today's case) — I favor focusing my assessment on those leads that I know are clearly abnormal. In Figure-1 — I've enclosed the 2 leads with the most obviously abnormal ST-T waves within RED-YELLOW rectangles. In a patient with new worrisome chest pain — the T wave in lead V2 is clearly disproportionate compared to the QRS complex in this lead (ie, the T wave in V2 towers over its respective R wave — with a T wave that is fatter-at-its-peak and wider-at-its-base than it should be).

  • NOTE: Although the T wave in lead V2 might not seem all that tall — what counts is proportion. The QRS complex in V2 is quite small — and relative to the small size of this QRS — there should be no doubt that the T wave in this lead is clearly too big.

  • Although slightly less disproportionate — the T wave in lead V3 is still "too tall" (it equals R wave amplitude in this lead) — with a wider-than-expected base.
  • By the principle "neighboring leads(ie, knowing that the ST-T waves in leads V2,V3 are hyperacute until proven otherwise) — I thought the T wave in lead V4 was probably also "hypervoluminous". By itself — lead V1 might not be taken as necessarily "abnormal" — but most of the time, a straight takeoff with a 1.5 mm tall positive T wave will not be seen in this lead (so given its proximity to lead V2 that is definitely abnormal — I thought it likely that the ST-T wave in lead V1 was probably also hyperacute).
  • Changes in the limb leads were even more subtle — but nevertheless clearly present. While fully acknowledging that the ST segment straightening (highlighted in Figure-1 by RED lines) by itself would be non-specific — in the context of a patient with a history of very worrisome chest pain + at least 2 (if not 4) chest leads showing hyperacute T waves — I interpreted these limb lead abnormalities as adding support to suspicion of acute OMI until proven otherwise.

The Repeat ECG:
16 minutes after ECG #1 was recorded — Dr. Souchtchenko obtained a right-sided ECG. As noted above — in a right-sided ECG, lead V2R is comparable to lead V1 in a left-sided ECG (and lead V1R is comparable to lead V2 in a left-sided ECG).
  • For clarity — I have enlarged these 2 leads from ECG #2 ( = the right-sided ECG) — so that we can assess the effect of the repeat ECG done 16 minutes later on leads V1 and V2 (See Figure-2).

Figure-2: Comparison of the effect on leads V1 and V2 from repeating ECG #1 after 16 minutes. To account for the fact that ECG #2 was a right-sided ECG — I switched positions of these first 2 chest leads (See text).

The Difference 16 Minutes Made:
It should be apparent from Figure-2 that our presumption regarding the T waves being hyperacute in leads V1 and V2 of ECG #1 — was indisputably confirmed by progression of ST-T wave changes in these 2 leads, that is clearly seen in ECG #2. (Other left-sided chest leads on repeat ECG weren't available). 

Learning Points:
Recognition of hyperacute T waves is essential for early identification of acute OMI when STEMI criteria are not yet evident. This identification can be facilitated by:
  • Always considering the clinical context (which in today's case was the very worrisome history for acute cardiac chest pain). Faced with this history — I lower my threshold for calling subtle ECG findings abnormal until proven otherwise.
  • Looking for ECG findings in those 1 or 2 leads in which you know that ST-T wave appearance is not-as-it-should-be.
  • Applying the concept of "neighboring leads" — in which more subtle ST-T wave findings are probably also abnormal, if seen in leads in close proximity to leads that you know are abnormal.
  • Looking to see how many of the 12 leads show ST-T wave abnormalities (even if some of these abnormalities are subtle). The more leads that are abnormal in a patient with new chest pain — the greater the likelihood that an acute process is ongoing.

Wednesday, June 29, 2022

When Normal is only Pseudo-Normal, it can deceive the caregivers.

An Aussie friend down under sent me this case. 

A 70-something male presented with sharp stabbing central CP.  Here is the initial ECG with 7/10 CP:


The pain was resolving, and another ECG was recorded with 3/10 CP:

Normal, but compared to the first, the T-waves in V2 and V3 are not as tall.  Hmm.......

The pain completely resolved:

What do you think?

Now there is an all-but-diagnostic terminal T-wave inversion in V2.  This is very subtle Wellens'.

The patient then developed 8/10 stabbing CP again:

The T-wave in V2 is again upright, indicating re-occlusion of the LAD.  There is also less T-wave inversion in aVL, so it is likely a proximal LAD.  There are subtle ST-T abnormalities in III, V5, and V6 as well.  
This is "Pseudonormalization" because it looks normal but it is not!!

The patient again became pain free:

Now there are unequivocal Wellens' pattern A waves (terminal T-wave inversion, biphasic up-down) in V2 and V3.  The T-wave is again deeper in aVL

Here is the high sensitivity troponin I profile (99% URL = 20 ng/L):

0852    8

1215    10

1730     8

2030     12

0535     12

The patient had chest pain again at 24 hours after presentation:

On its own, this ECG appears almost completely normal (for those with sharp eyes, there is abnormal ischemic ST depression in inferior and lateral precordial leads.  However, compared with all previous ECG, the T-waves are now upright, and there is much more ST Elevation than on any previous ECG.
Thus: Pseudonormalization AGAIN!

There is again Reocclusion.  I don't believe this was recognized as Re-occlusion because another troponin was measured, which returned at 30 ng/L (now elevated).  

Then this was recorded at 26 hours, without any intervention:

The ST elevation is resolved.  The T-wave is now normal.  There are Wellen's inverted waves in aVL.

Fortunately, the LAD spontaneously reperfused.  Otherwise, there would have been a lot of myocardial loss.

Here is the angiogram:

The Proximal LAD has an ulcerated plaque with 90% stenosis and there is TIMI II-III flow.  
There was successful PCI.

Here is the entire progression again.  Be sure to click on the image to enlarge it!!

Learning Points

1. Wellens' is reperfusion of OMI

2. The artery is has "hot" thrombus which can propagate and/or lyse, over and over.

3. This is really a Transient STEMI (better: Transient OMI, as it never meets STEMI criteria!)

4. Wellens' implies some (sometime tiny) amount of myocardial loss (infarction) and therefore some change in troponin.  In this case, it did rise by 4 ng/L, which is a significant rise (i.e., not due to natural variation or laboratory imprecision), but it did NOT rise above the 99th percentile, so this was unstable angina, until the later re-occlusion at which point the troponin DID rise above the 99th percentile and it was a type I MI.

5.  The re-occlusion was missed because the ECG looks nearly normal during LAD Occlusion.  The best clue that it was occluded was to look carefully for the VERY SPECIFIC changes (some changes in ECGs are not specific, but this morphology is very specific!)

6.  Optimally, patients with Wellens' would go immediately to angiography, because that hot thrombus is a transient STEMI.  Transient STEMI frequently need to go to the cath lab in the middle of the night if they don't go immediately

See this post:

Timing of revascularization in patients with transient STEMI: a randomized clinical trial

7. If you don't take them right away, they should get continuous 12-lead ST segment monitoring.

See these posts:

Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome

Comment by KEN GRAUER, MD (6/29/2022):
Illustrative case presented by Dr. Smith that emphasizes once again the following important concepts:
  • That part of the definition of Wellens' Syndrome requires a history of the patient having had chest pain — that has now resolved!
  • That there is a spectrum of ECG changes that may be seen with Wellens' Syndrome — including extremely subtle findings (as evidenced by the terminal T wave inversion in lead V2 of the 3rd ECG shown above). This could have been all-too-easy to overlook had the clinician not integrated the history with new development of this terminal T wave inversion at the time that the patient's chest pain had totally resolved!

  • Subtle cases like the one presented today "tell a story" — that may only become clear through sequential clinical correlation of serial tracings — in which the timing of ECGs — the presence and relative severity of patient symptoms — of serial troponin values (and of bedside Echo if done) — are all integrated.
  • Understanding all parts of the story explains how concepts such as "pseudo-normalization" of the ECG — and reocclusion of the "culprit" vessel — can easily be overlooked.

We have emphasized the importance of serial ECG comparison on numerous occasions in Dr. Smith's ECG Blog. For reference — I'll just cite 3 posts in which I focused on the "art" of serial ECG comparison in My Comment ( = the November 15, 2018 post — the June 28, 2018 post, in which Dr. Smith worked through another Wellens' Syndrome evolution  — and the August 20, 2020 post).
  • For clarity — I wanted to focus on just 1 of the 7 tracings shown today — which is the 4th ECG that was done (Figure-1). As discussed above by Dr. Smith — this 4th tracing was obtained in associated with the recurrence of chest pain (described by the patient as "8/10 and stabbing"). Without careful serial ECG comparison with the 3 previous tracings — the clinical significance of the ECG findings on this 4th ECG could easily be overlooked!
  • The fact that the patient's chest pain symptoms returned (with even greater severity than they had been) — in association with an element of "pseudo-normalization" (ie, the "tell-tale" terminal T wave inversion in lead V2 had been replaced by an upright T wave) — was diagnostic in this context of proximal LAD reocclusion.

The other point to emphasize about the ECG in Figure-1 — is that it is not a normal tracing.
  • Although there is no more than the most minimal ST depression — there is definite ST segment flattening — with an abrupt angulation at the junction of the flattened ST segments with the T wave that follows (RED lines in leads I,II; V4,V5,V6 in Figure-1). These are not normal ST-T waves.
  • What this ST segment flattening and angulation at the T wave junction means — is another matter. It depends. I've seen similar ST-T waves countless times in the thousands of primary care ECGs I interpreted in years past. By itself — it is purely a nonspecific finding, which can at times represent a subtle sign of underlying coronary disease — but at other times may be devoid of clinical significance.
  • That said — in the context of today's serial tracings — this ST segment flattening and abrupt angulation was clearly increased in ECG #4 compared to the 3 prior ECGs in today's case. Together with loss of the terminal T wave inversion in lead V2 of ECG #3 — this made for that many more leads in ECG #4 indicative of "dynamic" ST-T wave changes despite seeming "pseudo-normalization".

Figure-1: This is the 4th ECG shown in today's case — obtained shortly after the patient's chest pain returned (described as "8/10" and "stabbing" ).

Saturday, June 25, 2022

Acute chest pain and a difficult ECG

Written by Pendell Meyers

A man in his late 40s with several CAD risk factors presented with acute chest pain. He had several episodes lasting several hours over the past few days, with a more intense episode starting 1 hour prior to arrival. He described the pain as substernal squeezing and nonradiating, and associated with diaphoresis. He had some recent cocaine use 3 days ago. 

Here is his triage ECG:

I sent this ECG with no clinical context to several colleagues, with their responses below:

Smith: "I'm going to say LVH, but it's a tough one." (Meaning: I think that's not OMI but rather a mimic caused by LVH)
McLaren: "Looks like LVH, are V2-3 switched? What's currently labelled V3 looks hyperacute T, but other leads ok."
Grauer: "Assuming the history is acute chest pain...clear LVH...lead V2 is malpositioned (the abrupt tall R makes no sense) - but I'm concerned about the amount of ST elevation and the straight ST segment take-off in V3 - with ST coving and T inversion in V4 - so if history is concerning, this could be OMI in progress."

Smith: Notice that the T-wave inversion in V4-V6 is classic Benign T-wave Inversion MorphologySee countless examples here.

His baseline ECG from 1 year ago was available:

Triage ECG interpretation:
Sinus rhythm with LVH that appears slightly more severe than baseline ECG from 1 year ago. Next, for ischemia interpretation, there are many questions that must be considered:

Does the STE and potentially plus size T waves in V1-3 mean anterior OMI?
Do the terminal T wave inversions in V4-6 indicate reperfusion of OMI? Wellens?
Is the slight STD and T wave inversions in aVL worrisome for subtle inferior inferior OMI with tiny STE and budding hyperacute T waves in inferior leads?

Or are all these findings due to LVH?

LVH causes some of the most difficult OMI and STEMI mimics out there. In my opinion based on many ECGs I've seen in the past, all the questions above are answered by LVH alone, except potentially the concern for possible hyperacute T wave in V3. In other words, the terminal T wave inversion in V4-6 is a Wellens mimic caused by LVH, the TWI in I and aVL are appropriately discordant from the LVH. As for V3, I am slightly reassured when I look to its next-door neighbor, lead V4, and see no corroborating signs of hyperacute T waves. So I would be concerned and keep an eye on this area in subsequent repeat ECGs, but I would not yet consider it diagnostic for OMI.

Case continued:

Initial high sensitivity troponin I = 40 ng/L (99% upper reference limit for men is 20 ng/L for this assay)

He was given aspirin and nitroglycerin shortly after arrival, and approximately 20 minutes later, his pain completely resolved.

The case and the ECG were discussed with cardiology who basically said "there's no STEMI, so let us know what the troponin is."

After pain resolution, another ECG was recorded:

The patient was admitted for high risk chest pain and further evaluation.

Later that day:

Next day

Again, the benign T-wave inversion morphology shows itself in V4-V6

Repeat troponins:

39 ng/L

40 ng/L

40 ng/L

39 ng/L


Moderate concentric LV hypertrophy

EF 61%

No segmental wall motion abnormalities

No pericardial effusion

The medicine team consulted cardiology, who advised that no further workup was indicated at this time. They referred to a coronary CT angio performed about 1 year ago which showed several coronary arteries with nonobstructive CAD. Somehow this was used as part of the reasoning not to perform further workup.

No definitive cause of chest pain was found. The discharge note described possible musculoskeletal, esophageal, and cocaine-related causes as possibilities.

Learning Points:

Abnormal depolarization usually results in abnormal repolarization, and learning the expected repolarization patterns is critical for improving diagnostic performance in ECG interpretation.

LVH produces some of the most difficult STEMI and OMI mimics out there.

OMI is not just an ECG diagnosis.

We must focus on learning false positive ECG patterns in parallel with learning the false negative STEMI(-) OMI patterns.

Comment by KEN GRAUER, MD (6/25/2022):
Today's case by Dr. Meyers provides yet another example that illustrates the challenge of distinguishing between acute OMI vs LVH. I am not aware of any "magic formula" that instantly makes this distinction — and therein lies the difficulty!
  • Most of the time (as was true for today's case) — a single ECG will not suffice for telling you if the cath lab needs to be immediately activated. Instead — comparison with prior and/or serial tracings + troponins (and optimally stat Echo) — will be needed for optimal decision-making.

Dr. Meyers' discussion above makes the excellent point that LVH may account for all of the ECG findings in today's initial ECG tracing. While I completely agree with this assessment — I wanted to offer another perspective on how I would have proceeded in today's case.
  • For clarity — I've reproduced the initial ECG in Figure-1.

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

The Initial ECG:
The rhythm in ECG #1 is sinus at ~85/minute. Intervals (PR, QRS, QTc) are all normal. The frontal plane axis is slightly leftward (about -10 degrees) — but this is not enough to qualify for LAHB.
  • Small and narrow q waves are seen in leads I, aVL; V4 and V5 — but strangely enough, not in lead V6. That said — I still suspect these are normal septal q waves.
  • Criteria for LVH are easily satisfied in multiple leads (ie, very tall R in aVL ~14 mm; very tall R in V5 22 mm + S in V1 >35 mm). For "My Take" on a user-friendly approach to the ECG diagnosis of LVH — See My Comments in the June 20, 2020 and April 27, 2019 posts in Dr. Smith's ECG Blog.

  • ST-T wave changes in high-lateral leads I and aVL look completely typical for LV "strain" — because there is no more than minimal J-point depression with a slow downslope to the ST segment, followed by a more rapid upslope. The amount of ST-T wave depression in these leads is perfectly proportional to what I'd expect given the R wave amplitude in these same leads.
  • In contrast — the ST-T wave changes in lateral chest leads V5 and V6 look different. That is, the ST segment is flat — and the T waves are symmetrically inverted, consistent with either LV "strain" and/or ischemia. That said, the important point given this patient's presentation to the ED with new chest pain — is that nothing I've described thus far suggests acute OMI or the need for immediate cath.

As Dr. Meyers noted above — the one lead I was most concerned about was lead V3. This lead clearly shows significant J-point ST elevation, with straightening of the ST segment "takeoff" and a wide T wave base — which taken together could represent a hyperacute T wave in this patient with new-onset chest pain. 
  • Given modest depth of the S wave in lead V3 — the reason for my concern was that I thought the amount of J-point ST elevation in this lead V3 was more than I'd expect for the anterior ST elevation sometimes seen with LVH.
  • I suspected the ST-T wave appearance in lead V4 represented a transition between the positive ST-T wave of lead V3 — and the T wave inversion of lead V5. That said — the ST segment in lead V4 was clearly coved, so I thought it impossible to say that this was not acute.

My problem was with lead V2. The nearly isoelectric QRS complex in this lead made no physiologic sense given predominantly negative QRS complexes before it (in lead V1) — and after it (in lead V3).
  • To Summarize: The patient in today's case presented with new-onset chest pain. While I was not at all convinced that ECG #1 represented an ongoing acute process — I felt there was no denying that: i) Lead V3 could represent a hyperacute ST-T wave; ii) If lead V3 did represent a hyperacute ST-T wave — then the ST segment coving in lead V4 could be the tail end of this process; iii) While not necessarily abnormal taken by itself — the ST-T wave in lead V1 was clearly taller than is usually seen in this lead; andiv) I had no doubt that lead V2 was malpositioned
  • Given i), ii) and iii) in the above bullet Summary — I felt the "true" appearance of lead V2 was essential for accurate interpretation of this initial ECG. Therefore — I would have verified lead placement — and immediately repeated the initial ECG on this patient.

  • Of note — R wave progression was normal on the baseline ECG done 1 year earlier (ie, the 2nd ECG shown above in this case).
  • After pain resolution in the ED — the ECG was repeated. This is the 3rd ECG shown above in today's case — and it once again strongly suggests malposition of lead V2 (once again rendering this lead useless in our interpretation). Since this repeat ECG was recorded in the ED not long after the initial tracing — I suspect that the same technician (who was responsible for malposition of lead V2 in the initial tracing) — was probably also the one to record this repeat ECG after chest pain resolved.
  • Later that day — and again on the next day — a 4th and 5th ECG was obtained. Both of these last 2 tracings showed normal R wave progression. Since these tracings were done presumably hours (or moreafter the first 2 ECGs — presumably a different technician recorded these tracings (which is why I suspect that R wave progression is now normal).

  • In Conclusion: Whereas I did not feel we could rule out an OMI from the initial tracing shown in Figure-1 — none of the subsequent tracings in today's case were suggestive of an acute event. I suspect that IF the initial ECG would have been immediately repeated with accurate chest lead electrode placement — that there may not have been any need for concern about a possible acute event from the initial ECG.

  • Learning Point: When clinical decision-making hangs in the balance and you strongly suspect an error in lead placement — it is best to immediately repeat the ECG — after correct lead placement is verified. Sometimes, you may need to verify correct placement yourself. I know of no other way to ensure accurate interpretation of the ECG in question.

Thursday, June 23, 2022

Acute Chest pain with LBBB. What is going on?

This history and ECG were texted to me from a far away ED on a Friday night:

"Very elderly make with history of coronary disease on an angiogram 1 year prior presents with 2 hours of chest pain, sternal, pressure, and mild diaphoresis."

What do you think?

There is sinus tachycardia with LBBB.  There is concordant ST depression (STD) in lead V2, and excessively proportionally discordant STD in all of leads V3-V6.  Thus, there is one lead (V2) that meets the Sgarbossa criteria and the Smith modified criteria, and 4 other leads (V3-V6) that meet the alternative Smith modified criteria (proportionally excessively discordant ST depression at an ST/R ratio >0.30). 

Additionally, there is ST Elevation in aVR.  The ECG is low resolution and so it is difficult to determine the exact measurements, but I believe it measures at 1.5 mm.  The S-wave is 3.0 mm, and so this lead ALSO meets the Smith Modified Sgargossa criteria.  So the criteria are met in 6 leads, when only one is necessary!! In both of our studies of the Modified Sgarbossa criteria, not only was the presence of the criteria in just one lead much better than the original Sgarbossa criteria, but the proportionally excessively discordant findings were present in far more leads than in the Original criteria, and so it was more visually obvious and stunning.

In the case, the maximal ST depression is in lead V4, both in an absolute millimeter measurement and as a proportion to the preceding R-wave amplitude.  Whether normal conduction or LBBB, STD maximal in V1-V4 is very specific for posterior OMI, whereas V5-V6 is typical of non-occlusive but obstructive ischemia.     

In either case, cath lab activation is indicated!!

The physician who sent this tried to transfer the patient to an interventional center, but initially failed.

He wrote: "I'm going to try interventional cardiologist at XXXXXX as the cardiologist at the first hospital was not impressed."

So he called the interventional cardiologist at the other receiving center, and this was the response: "Interventional cardiologist at YYYYYY said that is is not a real STEMI."

I told him: "Send the patient!!  Do not take "no" for an answer!!"

And so he did.   And forced their hand.

Subsequent events

When the patient arrived, the troponin (not high sensitivity) was 29.4 ng/mL (very high, typical of large STEMI).  On arrival, the symptoms were improved, but we do not have another ECG to see if it, too, is improved.

At angiogram, they found this:

Here is the critical info:

The Ramus Intermedius had a 99% stenosis with TIMI-2 flow and they did NOT intervene because the "Ramus is unlikely to cause the ST changes and chest symptoms!"  

But these ECG findings are EXACTLY what you would expect from severe ACS of the Ramus.  (The Ramus Intermedius is a large coronary artery not present in all individuals that originates at the angle between the circumflex and the LAD; it supplies roughly the same territory as the first diagonal (D1) off the LAD.)

Furthermore, whenever there is a lesion with flow less than TIMI-3 (TIMI 0-2), it is an acute lesion; if it is resulting in ischemia and can be stented, my understanding is that it generally should be stented.

I don't understand this.

Left Main and 3-vessel disease in LBBB

In our validation study of the Smith Modified Sgarbossa criteria, we identified 4 patients who did not meet our definition of ACO yet did have notable catheterization findings and outcomes warranting immediate diagnosis and intervention.  These 4 patients were found to have AMI and new 3-vessel or left main coronary artery disease with either 1) an acute but non-occlusive culprit lesion, or 2) very high troponin. Peak 24-hour troponin T levels were 0.25, 0.75, 1.04, and 6.61 ng/mL. Two of these 4 required urgent or emergent coronary artery bypass graft. We categorized these patients as having acute 3-vessel/left main disease myocardial infarction(3V/LMD). Three of these 4 patients had discordant ST elevation (STE/S ratio > 20% in lead aVR), but only 1 of these 3 was positive by the 25% modified criteria. Two of the four 3 V/LMD patients also met the ST depression criteria (ST Depression to R-wave > 30%) due to widespread ST depression in various other leads, including III, aVF, V5, and V6.  None of the 4 met the weighted or unweighted original Sgarbossa criteria. If new 3V/LMD(without a specific culprit lesion identified) had been classified as equivalent to a culprit lesion in our definition of ACO, the sensitivity of each rule would be reduced by 1% to 3%, and specificity would remain unchanged, but more patients with potential need for urgent revascularization would have been identified.

Learning Points:

1. Formerly, it was thought that myocardial infarction (MI) could not be diagnosed in LBBB.  "MI" formerly meant "Old MI" as represented by Q waves.  "Acute transmural ischemia" is different from "MI".  In fact, infarction is the end result of completed transmural ischemia.

2. The STEMI criteria used in normal conduction (absence of BBB) are NOT very sensitive for Acute Transmural Ischemia (OMI) because they do not use proportionality or any other features of acute ischemia other than a fixed millimeter amount of ST Elevation.  

In fact, the Smith Modified Sgarbossa criteria in LBBB are far more sensitive for OMI than are the STEMI criteria in normal conduction!!!  This is because they use proportionality and because, contrary to conventional wisdom, LBBB does NOT hide transmural ischemia if you use proportions.

Comment by KEN GRAUER, MD (6/23/2022):
In the past, it was thought that one could not diagnose an acute STEMI (ST Elevation Myocardial Infarction) in the presence of LBBB. This notion has been completely refuted — and we have posted numerous illustrative cases demonstrating this in Dr. Smith's ECG Blog. Although it may be more difficult to diagnose acute ischemia or infarction in a patient with chest pain who presents in complete LBBB — in a surprising number of such patients, there will be at least strong suggestion on the initial ECG of acute STEMI despite the presence of underlying LBBB.
  • When acute ECG changes in a patient with LBBB are subtle — diagnostic aids such as Smith-modified-Sgarbossa criteria may be helpful. At other times (such as for the ECG in Figure-1) — the diagnosis of an acute cardiac event is obvious, even without the need to invoke modified Smith-Sgarbossa criteria.

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

MThoughts on the ECG in Figure-1:
The rhythm is sinus at ~90-95/minute. The PR interval is at the upper limit of normal — but the QRS is obviously wide, and consistent with complete LBBB. As per Dr. Smith's discussion above — Smith-modified-Sgarbossa Criteria are easily satisfied in no less than 6 leads — when only 1 lead is necessary!
  • In addition to use of Smith-modified-Sgarbossa criteria — I routinely favor a qualitative approach. Realizing that conduction defects (LBBB, RBBB, IVCD) and ventricular pacing may each alter expected ST-T wave appearance — I look for those leads that clearly show ST-wave findings that should not bthere

  • Among the flagrant ST-T wave changes in Figure-1 that should be immediately apparent — the ST segment coving and huge amount of J-point ST depression (that exceeds 5 mm in lead V4!) — in this elderly patient with new-onset chest pain — should prompt the need for immediate cath without having to delay for additional data.

Additional Observations:
Although I completely agree that today's tracing is best classified as "LBBB" — it is worthwhile pointing out that QRS morphology is not completely typical for this conduction defect.
  • For typical LBBB — there should be predominant negativity (ie, no more than a tiny initial r wave) in right-sided lead V1 — as well as in other anterior leads. The fact that a significant R wave is already present in lead V3 is not expected with a "typical" LBBB.
  • Looking closer at QRS morphology in lead V3 — there is alternation for the 4 beats seen in this lead between a qRS pattern (for the 1st and 3rd beats in this lead) — with a "fat" initial R-slur-R'-S for the 2nd and 4th beats in this lead. This is bizarre. It doesn't seem to be artifact. If "true" QRS morphology in lead V3 is the qRS pattern — then this initial q wave is abnormal and suggestive of infarction. If instead the R-slur-R'-S pattern is the "true" morphology — then this is marked fragmentation, consistent with "scar" from underlying heart disease.

  • In left-sided leads with typical LBBB morphology — there should be a monophasic (all upright) R wave. We see this in leads I and aVL — but there is a fairly deep S wave (of 5 mm) in lead V6. While true that many patients with LBBB and LVH only develop a monophasic R wave in more laterally placed leads (such as lead V7 or V8) — awareness that QRS morphology is indeed somewhat atypical for LBBB is relevant for helping us to interpret the significance of ST-T wave changes. There is simply no way that the ST segment coving in leads V3-thru-V6 could be "normal" (not to mention the huge inappropriate amount of ST depression).

  • BOTTOM Line: As per Dr. Smith — this elderly man with new-onset chest pain should have been accepted for immediate cath on the basis of his initial ECG.

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