** **ACUTE MI/STEMI** **: Activate the cath lab if the patient has chest pain?

Written by Willy Frick

I was reviewing our institutional PMcardio account which we are using to improve early identification of patients with electrocardiographically subtle OMI. 

I came across this ECG:

What do you think?

Even before we have clinical context, this ECG simply does not appear concerning for OMI, notwithstanding the machine's interpretation ** ** ACUTE MI / STEMI ** **. 

I sent this ECG to Dr. Smith with no clinical context, and he immediately replied "Fake." 

I suspect most blog readers did not struggle with this one. But in the world of STEMI, this is a challenging ECG to most.

Furthermore, how many clinicians are truly comfortable setting aside the machine interpretation and sticking with their gut that this ECG does not look ischemic. Fortunately, the physicians seeing the patient were using the Queen of Hearts PM Cardio AI ECG OMI Model, and she had absolutely no concerns.

When the Queen has some suspicion of OMI, she asks if the patient has ACS Symptoms.  She did not even need to ask in this case, because even if the patient presented with chest pain, she would call it NEGATIVE.

When I reviewed the chart, I learned that the patient had presented with syncope. The emergency physician does cautiously (correctly) note that the ECG meets STEMI criteria in V3 and V4, but goes on to document absence of ACS symptoms. The patient ruled out for MI with serial troponin testing.

Most impressively, cardiology was never consulted! This reassuring assistance from AI improved the patient's care by preventing unneeded additional testing and involvement of specialists.

The Queen of Hearts not only is extremely sensitive for subtle OMI, but is also great at recognizing false positive ECGs.

The Queen decreases false positive cath lab activations.

We published this study, showing that false positive prehospital cath lab activations would be decreased by 58% if they used the Queen:

https://www.tandfonline.com/doi/abs/10.1080/10903127.2024.2399218

Artificial Intelligence Driven Prehospital ECG Interpretation for the Reduction of False Positive Emergent Cardiac Catheterization Lab Activations: A Retrospective Cohort Study

Peter O. Baker

,

Shifa R. Karim

,

Stephen W. Smith

,

H. Pendell Meyers

,

Aaron E. Robinson

,

Ishmam Ibtida

,

Rehan M. Karim

,

Gabriel A. Keller

,

Kristie A. Royce

 &

Michael A. Puskarich

Abstract

Objectives

Data suggest patients suffering acute coronary occlusion myocardial infarction (OMI) benefit from prompt primary percutaneous intervention (PPCI). Many emergency medical services (EMS) activate catheterization labs to reduce time to PPCI, but suffer a high burden of inappropriate activations. Artificial intelligence (AI) algorithms show promise to improve electrocardiogram (ECG) interpretation. The primary objective was to evaluate the potential of AI to reduce false positive activations without missing OMI.

Methods

Electrocardiograms were categorized by (1) STEMI criteria, (2) ECG integrated device software and (3) a proprietary AI algorithm (Queen of Hearts (QOH), Powerful Medical). If multiple ECGs were obtained and any one tracing was positive for a given method, that diagnostic method was considered positive. The primary outcome was OMI defined as an angiographic culprit lesion with either TIMI 0–2 flow; or TIMI 3 flow with either peak high sensitivity troponin-I > 5000 ng/L or new wall motion abnormality. The primary analysis was per-patient proportion of false positives.

Results

A total of 140 patients were screened and 117 met criteria. Of these, 48 met the primary outcome criteria of OMI. There were 80 positives by STEMI criteria, 88 by device algorithm, and 77 by AI software. All approaches reduced false positives, 27% for STEMI, 22% for device software, and 34% for AI (p < 0.01 for all). The reduction in false positives did not significantly differ between STEMI criteria and AI software (p = 0.19) but STEMI criteria missed 6 (5%) OMIs, while AI missed none (p = 0.01).

Conclusions

In this single-center retrospective study, an AI-driven algorithm reduced false positive diagnoses of OMI compared to EMS clinician gestalt. Compared to AI (which missed no OMI), STEMI criteria also reduced false positives but missed 6 true OMI. External validation of these findings in prospective cohorts is indicated.

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MY Comment, by KEN GRAUER, MD (2/12/2025):  

===================================

As per Dr. Frick — the ST elevation and T wave inversion in today's ECG is not the result of an acute OMI. Instead — it is almost certain to be a longstanding finding in this patient with marked LVH.

• As I emphasized in My Comment at the bottom of the page in the December 14, 2022 post — We have reviewed many cases that illustrate the challenge posed by distinguishing between marked LVH — vs LVH + superimposed acute OMI.
• PEARL #1: In general, it is rare to see both marked LVH and acute OMI in the same tracing. It is for this reason — that we can get a "head start" in our interpretation of a patient with symptoms in which there is obvious LVH. This is because statistically (supported by our experience) — in the vast majority of cases, such tracings may mimic acute OMI, but acute coronary occlusion will rarely be seen.
• PEARL #2: The above said — Remember the rule of "N = 1". By this I mean that even though it is rare to see an acute anterior OMI in a patient with marked LVH — this can occur — so that we want to be prudent and avoid overlooking the rare OMI in a patient with marked LVH (See the above mentioned December 14, 2022 post for a case in which marked LVH and acute OMI coexist).
• BOTTOM Line: Awareness of the criteria for ECG diagnosis of LVH goes a long way toward facilitating interpretation. Toward this end — we've conveniently added a LINK for "LVH Criteria" in the Menu at the top of every page in Dr. Smith's ECG Blog. This link takes you to My Comment in the June 20, 2020 post — in which I review a user-friendly approach to ECG recognition of LVH and "Strain".

Figure-1: I've labeled today's ECG.

Regarding Today's CASE:

For clarity in Figure-1 — I've labeled today's tracing. 

• The diagnosis of marked LVH should be obvious in Figure-1. That said — overlap of R waves with S waves in multiple leads (especially with the long lead rhythm strips at the bottom of the tracing) — complicates accurate determination of QRS amplitudes (See my color-coding in Figure-1 for my best effort at calculating R wave and S wave amplitudes in the various leads).
• PEARL #3: The easiest way to avoid confusing lead overlap — is simply to repeat the ECG at half standardization. This was not done in today's tracing.
• The most difficult beats to assess QRS amplitude on are beats #7,8,9 — because there is overlap with each of the 3 simultaneously-recorded long lead rhythm strips (of leads V1,II,V5). For example — true amplitude of the S wave in lead V3 is almost entirely concealed by overlap of both the lead V1 and lead II rhythm strips below it. In such cases of multiple lead overlap — I look elsewhere for leads with less overlap (ie, in leads II and V1, which are outlined in YELLOW and PINK) to determine the true amplitude of the S and R waves in these leads. This allowed me to determine that the S wave in lead V3 (in light BLUE) measures 36 mm deep!
• PEARL #4: The KEY for determining that rather than "fulfilling STEMI millimeter-based criteria" for the amount of ST elevation in lead V3 — given the 36 mm deep S wave in this lead — this is in no way an "abnormal" amount of ST elevation (ie, the principle of "proportionality" reigns supreme for qualitative assessment of ST-T wave changes in a patient with marked LVH).
• As to the straightened shape of the ST segment takeoff in lead V3 — this shape is completely consistent with the appearance of LV "strain" in an anterior lead in a patient with extremely deep anterior S waves (See My Comment in the February 6, 2020 post).

What About ST-T Wave Changes in Other Leads in Figure-1?

At 1st glance — the ST segment coving with seemingly "deep", symmetric T wave inversion in lead V5 might be of concern. That said — there are several reasons why I felt this ST-T wave appearance in lead V5 was not of concern:

• Again, by the principle of "proportionality" — the 38mm tall R wave in lead V5 suggests the relative size of the inverted T wave in this lead is not as deep as one might initially think.
• The slow downsloping, more rapid upsloping ST depression seen in lead V6 is absolutely typical for LV "strain" in this left-sided lead in which R wave amplitude is significantly increased (measuring 22 mm).
• Patients with marked LVH (especially those with longstanding hypertension) often manifest not only ST-T wave changes that are typical for LV "strain" — but also symmetric T wave inversion as seen here in lead V5.
• Finally — I interpreted the ST-T wave appearance in lead V5 as a "transition" lead that lies in between the ST coving and elevation seen in lead V4 — and the "strain"-like ST depression seen in lead V6. This ST-T wave pattern in lead V5 is not seen in other leads, as would be expected if this was truly a change of acute ischemia.

What about the R = S Phenomenon in the Inferior Leads?

I found the surprisingly tall R = S Waves in each of the inferior leads an interesting and unusual feature (R waves and S waves each ≥15 mm in leads II,III and aVF). I cannot remember the last time I saw this pattern in each of the 3 inferior leads.

• This R=S pattern of tall RS complexes brings to mind the Katz-Wachtel phenomenon described in pediatric patients — in which the finding of biphasic RS complexes of ≥50 mm in mid-chest leads V2, V3 or V4 suggests biventricular hypertrophy, especially in children with VSD (Ventricular Septal Defect).
• Clearly, the R=S waves in today's tracing are not as deep as occurs with the Katz-Wachtel phenomenon. That said, given the association of these inferior lead R=S waves with marked increase in chest lead amplitude — I would love to see an Echo on this patient, so as to correlate Echo findings with today's interesting ECG.

Conclusion:

The ECG in today's case is notable for marked LVH. As per Dr. Frick — this ECG is not suggestive of acute OMI. I attributed the diffuse ST-T wave changes to LV "strain" and not ischemia.

 

A 30-something with acute chest pain

This was sent to me from Sam Ghali (@EM_Resus) with no other information.  I assumed it was a patient with acute chest pain.

"What do you think, Steve?  Real or just fake?"

What do YOU think?

It has some inferior ST elevation with some reciprocal ST depression and inverted T in aVL.  This usually indicates inferior OMI.

My answer: "Fake: pretty certain, but not 100% certain."

Sam: "why do you say fake?"

Smith: "Gestalt, but if I must explain: well formed J-waves and high voltage R waves."

Sam: "Yeah I think too the negative QRS in aVL takes away from changes that may be interpreted as “reciprocal”"

Smith: "did the cath lab get activated?"

Sam: "Yes, this case was sent to me.  It was a man in his 30s with chest pain.  Coronaries were clean.  Troponins were all negative -- the patient ruled out for acute MI."

Finally, Sam: "Honestly in addition to expert ECG interpretation I think skilled bedside echo can prevent a lot of these activations."

I agree, however: 

1) I don't think you can get a good enough echo without bubble contrast.  

2) You need to be just as expert at echo as I am at the ECG.

3) Echo is another step that takes time.  Time is myocardium.

So the best course of action:

 Use the PMCardio Queen of Hearts AI in ECG interpretation.

Not OMI with High Confidence

Click here to sign up for Queen of Hearts Access

We showed that the Queen of Hearts decreases false positive cath lab activations:

1) Published recently in Prehospital Emergency Care

Baker PO et al. Artificial Intelligence Driven Prehospital ECG Interpretation for the Reduction of False Positive Emergent Cardiac Catheterization Lab Activations: A Retrospective Cohort Study

This showed a decrease of false positive cath lab activations from 69 by medics to 29 by use of the Queen of Hearts, while still identifying all 48 true positive OMI.   I had only 9 false positives but I missed 2 OMI.  The integrated device algorithm had 42 false positives and one missed OMI.

Full text!

2) To be presented at AHA conference in Chicago in 2 weeks: 

Sharkey SW et al.  Performance of Artificial Intelligence Powered ECG Analysis in Suspected ST-Segment Elevation Myocardial Infarction.  This showed a decrease in false positive cath lab activations from 637 out of 2526 (25%) to 403 our of 2526 (16%), a 37% decrease in false positive activations.  Of those with MI and a culprit, 4% were missed (called "Not OMI"), but these were not necessarily occlusions (most MI with an open artery have a culprit), and many were LBBB.

Click here to sign up for Queen of Hearts Access

===================================

MY Comment, by KEN GRAUER, MD (10/3/2024):  

===================================

I looked at the ECG in today’s case knowing only that the patient was a younger male adult with CP (Chest Pain).

• While statistical likelihood of acute OMI is clearly lower in younger adults — nothing is ruled out by age alone (as per My Comment in the January 9, 2023 and December 5, 2023 posts in Dr. Smith's ECG Blog).
• Without knowing more about today’s case — I also thought (as did Dr. Smith) — that this ECG (that I’ve labeled in Figure-1) was likely to be a “fake”. 

ECG Features suggesting "Fake"

As per Dr. Sam Ghali (who sent us today's case) — serial Troponins were clearly indicated since the patient presented to the ED. These were all negative. I'd defer on the question of whether cardiac catheterization was needed by saying, "Ya gotta be there" — but there clearly are ECG features suggesting no OMI.

• The rhythm for the ECG in Figure-1 is sinus — with normal intervals and axis (mean QRS axis about +80 degrees). There is no chamber enlargement.
• One wonders about lead placement, given abrupt transition from the similar-looking predominantly negative QRS complexes in leads V1,V2 — to a nearly all-positive QRS by lead V3.

Regarding ST-T Waves:

• There clearly is ST elevation in each of the inferior leads. 
• I suspect the presence of T wave inversion in lead aVL increased concern about reciprocal ST-T wave changes — which must have been perceived as suggestive of acute inferior OMI, since cardiac catheterization was performed.

There is No Reciprocal ST-T Depression:
We have often referred to the almost "magical" mirror-image relationship for ST-T waves in leads III and aVL when there is acute inferior MI (See My Comment in the September 30, 2019 post in Dr. Smith's ECG Blog, as well as many others). That said — I would not interpret ST-T wave appearance in lead aVL of today's ECG as a "reciprocal" change.

• The T wave vector often follows closely behind the QRS vector. As a result — when the QRS is predominantly negative in lead aVL — then the T wave in this lead may also be negative as a normal finding. This is precisely what we see in ECG #1 — in which the frontal plane axis is +80 degrees (which is most probably the reason for the shallow T wave inversion highlighted by the BLUE arrow in this lead).
• Contrast this normal amount of T wave inversion seen within the BLUE rectangle in ECG #1 — with the disproportionately "bulky" T wave inversion seen within the RED insert of lead aVL that I've excerpted from the initial ECG of a different patient who was having an acute OMI (See My Comment in the September 27, 2024 post).
• Therefore — there is no reciprocal ST-T wave depression in today's case!

There is No Sign of Posterior OMI:
It is common to see indication of posterior OMI when (if) there is inferior OMI. Posterior OMI is typically diagnosed by the finding of chest lead ST depression that is maximal in leads V2, V3 and/or V4. We do not see this in ECG #1.

• As noted above — the similar-appearing QRST complex in leads V1,V2 — followed by abrupt transition to a predominantly positive QRS by lead V3 — suggests there may be an error with precordial electrode lead placement.
• That said — None of the chest leads show ST depression.
• While the absence of indication of posterior OMI does not rule out the possibility of acute inferior OMI — it does make this less likely.

There ARE Signs of a Repolarization Variant:

Among the many posts in which we've reviewed cases of repolarization variants — is the May 23, 2022 post. From this post:

• Among the most suggestive ECG features of a repolarization variant — is the presence of an end-QRS notch (J wave) — and/or — a "slur" on the downslope of a prominent R wave.
• Although subtle — J-point notching is seen in leads V4 and V5 of ECG #1 (within the dotted PURPLE circles in these leads).
• A "slur" is seen on the downslope of the R waves in leads II,III,aVF and V6 (GREEN arrows in these leads).
• 
  
• Finally — Not only are reciprocal changes absent in ECG #1 — but a similar shape to the ST segments is seen in multiple leads (ie, leads I,II,III; aVF; V3,4,5,6) — which is more characteristic of a repolarization variant (as opposed to the ST-T wave changes of acute OMI that more often localize).

BOTTOM Line in Today's CASE: While fully acknowledging that in a patient who presents to the ED with CP — "Ya gotta be there" to best determine how much evaluation is needed to rule an OMI in or out. That said — I thought the ECG in Figure-1 looked more like a "fake" than like an acute OMI.

• Negative serial Troponins were needed to rule out an acute event.
• Serial ECGs would be expected to show no evolution.
• A normal Echo obtained during CP would support this being a repolarization variant.
• If a final test was perceived as "needed" — perhaps a normal coronary CT angiogram could have helped to avoid cardiac catheterization.

Figure-1: I’ve labeled the initial ECG in today's case. The RED Insert for lead aVL is excerpted from My Comment in the September 27, 2024 post in Dr. Smith's ECG Blog (taken from the initial ECG in that Sept. 27 post).

 

What do you think of this ECG that was texted to me?

This ECG was texted to me by a colleague.  I assumed it was from a patient with symptoms compatible with ACS/OMI.

What do you think?

There is sinus rhythm with RBBB and ST Elevation in V2 which is concordant with the QRS.  The ST segment in RBBB should be ST depression, discordant to the positive R'-wave (i.e., opposite direction of the upright R'-wave) .  But we sometimes see this concordant STE even in non-ischemic ECGs:

PseudoSTEMI and True ST elevation in Right Bundle Branch Block (RBBB). Don't miss case 4 at the bottom.

This STE suggests OMI, but we have seen many cases like this that are false positives (OMI mimics).  I thought it did not look like OMI but was not willing to risk the patient's life by saying so.

I sent it to some EKG nerd friends (Pendell of course among them) and Pendell responded: 

"So difficult. I’ll say real until proven otherwise.  Baseline could invalidate that in 10 seconds."

Of course he is right.  So I requested an old one.

And, of course, pretest probability is crucial, so I asked for the history: A 60 year old presented with palpitations and chest tightness.

In this case, if the patient needs PCI, he needs to be transferred because this hospital does not have a cath lab.

So getting the right diagnosis here is crucial.

I ran it by the Queen of Hearts PM Cardio app:

And then I got the Queen's explainability:

I relayed all our thoughts to my colleague.

The first troponin returned at 113 ng/L (elevated, but not by a lot).  This is compatible with any kind of MI: type 1 (OMI or NOMI) or type 2.  Or even with non-ischemic myocardial injury.

If you are convinced by all the data, including the troponin, that the patient's pain is due to ACS, and he has persistent pain, then he should go to the cath lab.  But the clinician was not convinced and the ECG is not convincing.

That is to say, the troponin is not of definitive help.  

Even if it were normal, it would not help: in 25% of proven occlusion, the first troponin is below the URL.

Wereski R, Chapman AR, Lee KK, Smith SW, Lowe DJ, Gray A, et al. High-Sensitivity Cardiac Troponin Concentrations at Presentation in Patients With ST-Segment Elevation Myocardial Infarction. JAMA Cardiol. novembro de 2020;5(11):1302–4.  

Wanamaker BL, Seth MM, Sukul D, Dixon SR, Bhatt DL, Madder RD, et al. Relationship Between Troponin on Presentation and In-Hospital Mortality in Patients With ST-Segment-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. J Am Heart Assoc. outubro de 2019;8(19):e013551.

The colleague looked harder for an old ECG and finally found one:

To me, this confirmed that the STE is a mimic, a false positive

Further investigation revealed that the patient has a history of PSVT and that he probably was having a type 2 MI from an episode of prehospital PSVT.

He did not have OMI.

False positive ECGs are a source of frustration, and their frequency makes it harder to persuade interventionalists to take patients to the cath lab who have a subtle true positive.  The old story of "Crying wolf" is a problem because when a wolf really is prowling, people won't believe you.

The Queen of Hearts PM Cardio AI app is amazing at differentiating ischemic ECGs from mimics.  We believe it will result in far fewer false positive cath lab activations.

We are in the process of studying the Midwest STEMI Consoritium 20,000 cases of cath lab activation to see how well the Queen identifies false positives.

Stay tuned.

YOU TOO CAN HAVE THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

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MY Comment, by KEN GRAUER, MD (11/1/2023): 

===================================

I thought today's case presented a rather unique variation that is good to be aware of. As per Dr. Smith — the tracing in Figure-1 was texted to him and to Dr. Meyers without the benefit of clinical information.

• I was intrigued by this case — because it raises 2 Clinical Questions: i) Is this an acute OMI? (and should the cath lab be activated?) — and, ii) If not an acute OMI — What is likely to be going on?

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

MY Thoughts on Today's Case:

The rhythm in ECG #1 is sinus at ~85/minute. The PR interval is normal — but the QRS is prolonged with typical morphology for complete RBBB (Right Bundle Branch Block = rSR' in lead V1 with wide terminal S waves in lateral leads I and V6).

• The QRS complex is fragmented in multiple leads.
• Although the R wave in lead II is relatively tall (ie, ~6 mm) — QRS depolarization activity is predominantly negative in each of the 3 inferior leads — consistent with LAHB (Left Anterior HemiBlock). Therefore — there is bifascicular block (RBBB/LAHB).
• 
  
• Small q waves are present in high-lateral leads I,aVL — and slightly larger q waves are seen in leads V3-thru-V6. While the lateral q waves look like benign septal q waves — it is much less common to see a q wave in lead V3, though the significance of this is uncertain.
• Fairly prominent R waves are seen in leads V4,5 — though not quite satisfying voltage criteria for LVH.

The most concerning finding in ECG #1 — are the ST-T waves.

• My attention was immediately drawn to lead V2 — since the 2 mm of ST elevation seen in this lead looks like it could be acute. What makes the ST elevation in this lead worrisome — is that there is complete RBBB, with appropriate ST-T wave depression in lead V1. 
• As noted by Dr. Smith — ST elevation should not normally be seen in lead V2 when there is complete RBBB and ST-T wave depression in lead V1. Instead — there is usually at least some ST-T wave depression in lead V2 (and usually also in lead V3) when there is complete RBBB.
• 
  
• NOTE: It is not uncommon in patients who do not have OMI, but who manifest complete RBBB — to see some ST elevation in selected limb leads (especially in leads I and aVL — or in lead III) — and/or in lateral chest leads. That said — I do not recall having seen as a "benign variant" the type of acute-looking ST-T wave elevation that we see here in lead V2, in a patient with complete RBBB.
• 
  
• NOTE: Other leads in Figure-1 also manifest some ST elevation (as highlighted by the dotted RED lines). That said — I would not have been concerned about the ST elevation in these other leads were it not for the ST-T wave appearance in lead V2.

BOTTOM Line Regarding Today's Initial ECG: 

My impression on seeing ECG #1 without the benefit of any additional information was virtually identical to that expressed by Dr. Meyers: "So difficult. I'll say real until proven otherwise. A baseline ECG could invalidate that in seconds".

• As I stated at the beginning of My Comment — Today's case raises 2 clinical questions: i) Is this an acute OMI? — and, ii) If not — What is likely to be going on? In my opinion — both of these questions need to be answered by the emergency provider.
• 
  
• In today's case — We never learn the age, sex or history (beyond learning that the patient has had reentry SVT on one or more occasions in the past). Even if this patient does not have OMI — I would want to know this information to help figure out what might be going on.
• The presence of bifascicular block with fragmentation in multiple leads and the ECG findings described above — could indicate potentially significant underlying heart disease. At the least — I would want to know Echo findings regarding the presence (and potential severity) of any underlying heart disease.
• An initial troponin was elevated — albeit not be a lot.
• 
  
• The "good news" = a prior ECG was found, which strongly suggested that none of the ST-T wave findings described above were acute. As a result — OMI in need of acute catheterization was felt to be safely ruled out!
• 
  
• My Final Thoughts: I remain intellectually curious as to what may have been going on in today's patient. The potential is there for significant underlying heart disease (possibly with an entity such as recurrent myocarditis or something else that might need attention with additional measures for optimal management). That said — Today's 1st question as to whether or not to activate the cath lab can be answered with a NO.

Right Bundle Branch Block and Posterior OMI????

 This 39 year old patient presents with syncope.

What do you think?

There appears to be RBBB with excessively discordant ST depression (2-2.5 mm) in V2 and V3, suggestive of RBBB with posterior OMI

Whenever you see abnormal ST-T (ST elevation, ST depression, hyperacute T-waves), you MUST look at the entire ECG (rhythm, rate, P-waves, intervals, and QRS) to see if there is some abnormality among these which can explain the ST-T.  

One's first impression is that this is RBBB (tall R-wave in V1).  But that is ONLY if you don't look at it closely, and don't look at the intervals.

Differential of a Tall R-wave in V1: 

1. RVH

2. RBBB

3. WPW

4. Old "posterior" infarct

5. Lead placement

6. Septal hypertrophy (HOCM)

7. Normal Variant

There is a short PR interval. There are several Q-waves which have a slow downslope (Negative delta waves).  There are clear positive delta waves in many leads.

WPW has abnormal depolarization, with pre-excitation, through an accessory pathway.  And this abnormal depolarization (QRS) usually leads to abnormal repolarization (ST-T).

Diagnosis: 

WPW with repolarization abnormalities.  

Superimposed OMI cannot be ruled out, but the patient has syncope, not chest pain.

Here are many more examples of this:

See this recent post: 

Chest pain and anterior ST depression. What’s the cause(s)?

See this post: 

5 cases of WPW mimicking and/or obscuring acute OMI

==================================

My Comment by KEN GRAUER, MD (12/16/2022):

==================================

Fascinating case — for which we unfortunately have no follow-up. That said — I still thought it worthwhile to explore this case further.

My Initial THOUGHTS on Today’s Tracing:

Clearly, I noticed the short PR interval with initial slurring of the QRS in multiple leads — so, like Dr. Smith, my 1st impression was to wonder if this was all WPW. That said — I have never seen delta waves this large (ie, 7 mm deep — and ~0.09 second wide in lead I).

• If this was all WPW — then I wondered about the boundaries of the delta wave. The vertical RED time lines that I’ve dropped in Figure-1 — suggest that IF delta waves comprised everything to the left of these vertical RED time lines, then this would mean that there was a biphasic appearance to the delta waves in leads like I, II, aVL, and V6 (ie, an initial large negative component to the delta wave — with a much shorter terminal positive component as the delta wave returned to the baseline). This was also something that I was not used to seeing — since most (albeit not all) of the time, delta waves in most leads tend to blend in with the initial direction of the QRS complex

PEARL: In patients with WPW — preexcitation can be: 

• i) Total (ie, all impulses traveling first down the AP [Accesory Pathway]) — in which case the QRS will probably be very wide — the PR interval will be obviously short — and prominent delta waves will be present in multiple leads.
• ii) Occult (in which case there are no delta waves, the QRS is not wide, and the PR interval is not short — because all impulses travel down the normal AV nodal pathway) — OR — 
• iii) Partial (ie, a certain relative percentage of impulses simultaneously travel down the AP and the normal AV nodal pathway). Depending on the relative amount of impulses traveling down the AP (compared to down the normal AV nodal pathway) — the QRS may not be overly wide, and delta waves may be extremely subtle and only seen in a limited number of leads.

Can You EVER Diagnose Acute OMI with WPW?

Because significant preexcitation will alter both the QRS complex and the resulting ST-T wave in unpredictable fashion — it becomes much more difficult to recognize acute OMI in such patients. I suspect that most acute OMIs in patients with WPW are overlooked (See My Comment at the bottom of the page in the October 13, 2022 post in Dr. Smith's ECG Blog). That said — there are times when despite WPW, you can suspect acute OMI on ECG:

• CLICK HERE — for a case of a patient with WPW and new-onset chest pain. Would you have recognized the acute posterior OMI?
• CLICK HERE — for an example of acute OMI in a patient with intermittent preexcitation (occurring every-other-beat)!

What About Today's Tracing?

I admittedly was not sure about the reasons for the strange appearance of the ECG in Figure-1.

• IF everything to the left of the vertical RED time line is delta wave — and IF everything to the right of this RED line is the underlying QRS — then this would make for huge, biphasic delta waves in multiple leads with a surprisingly narrow QRS (looking to the right of the RED line in leads V1,V2,V3).

I asked David Richley (who is truly an expert in this area — as former Cardiac Physiologist at NHS — UK) — for his opinion as to whether the ECG in Figure-1 was all WPW? Dave completely agreed with Dr. Smith — and wrote me the following:

• Hi Ken. 100% WPW. It is the initial part of the QRS that is broadened — not the terminal part. Nice negative delta waves in the inferolateral leads, mimicking Q waves.
• The delta waves are certainly huge! This suggests to me that the ventricles are almost completely pre-excited. The T wave vector is almost opposite the delta wave vector — which might be expected given the probably large mass of muscle that’s pre-excited. I really do not know whether there is any evidence of a superimposed acute event.
• 
  
• I think everything to the left of the RED line is delta wave — and the narrow bit to the right is probably mainly due to normal ventricular activation (although there is bound to be some overlap!). Maybe the narrow bit is of low amplitude because most of the myocardium has already been depolarised. 
• In the limb leads the pre-excitation and normal conduction vectors are about 180 degrees from each other — hence the biphasic complexes. I suspect there is less of a difference in the horizontal plane, so most of the complexes in the chest leads are not biphasic — and the broad R waves in the anterior leads are probably a combination of pre-excitation and normal conduction. That said — of course, we can not prove the above ...

Is There Evidence of Acute OMI in Figure-1?

With full acceptance of expert commentary from Stephen Smith and David Richley — the ECG in Figure-1 almost certainly represents WPW with virtually complete preexcitation and pseudo-Q waves formed by the huge negative delta waves in no less than 5/12 leads. That said — given the clinical presentation of syncope, I still wondered if despite WPW — we might be seeing suggestion of acute OMI because:

• The T waves in leads I and aVL look like they may be hyperacute.
• There is ST segment coving, significant J-point depression — and surprisingly deep T wave inversion in leads V2-thru-V4 (with the amount of T wave inversion increasing in leads V2 and V3 compared to what it was in lead V1).
• The T wave in lead V6 looks similar to what we saw in leads I and aVL (ie, possibly hyperacute).
• 
  
• To EMPHASIZE: Because of WPW (especially given near total preexcitation in today's tracing) — there is no way to know if the above ST-T wave changes are simply part of this patient's WPW appearance — OR — if they might represent superimposed acute ischemia/OMI?

How I wish we had follow-up on this case ... 

Figure-1: I've added time lines to today's tracing — in order to better appreciate the likely boundaries of the delta waves (See text).