THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[26-09-2025 16.56] PPM 1: Lasix and heparin infusion going on. 👆 check out this sequential archive of an evolving myocardial infarction captured onwards from this ECG @PPM3 @PPM4
[26-09-2025 17.06] PPM 4: That is some very peculiar morphology which I haven't (in my limited clinical experience) noticed before.
[26-09-2025 18.14] PPM 2: Are you thinking this is a Type 2 MI or a Type 1 sir?
Unusual to see a Type 1 with such profound tachycardia
[26-09-2025 19.47] PPM 5: 26/9/25 ,7:30 pm
[26-09-2025 21.18] PPM 1: Excellent question 👏👏
@PPM5 recall the afternoon discussion?
Maybe in the previous 80F PaJR patient who survived her post intubation myocardial infarction you were thinking of a type 2 myocardial infarction?
Now see what that morphology changed to since evening!Better call them occlusive vs non occlusive MI?
[26-09-2025 21.35] PPM 5: Yes sir, I was poorly trying to articulate that
[26-09-2025 21.50] PPM 1: Occlusive STEMI changing to occlusive non STEMI or a non occlusive false positive STEMI changing to an occlusive non STEMI?
Also check out the narrative on "what is science" in the above article
[26-09-2025 21.58] PPM 5: Yes sir, reading this, thank you for sharing
[27-09-2025 12.21] PPM 5: 
[27-09-2025 12.25] PPM 5: Does this mean revascularization has occurred,why did the st elevation not present anymore?
[27-09-2025 12.25] PPM 1: Spectacular Non STEMI, previously pathologically described as subendocardial infarction
[27-09-2025 12.25] PPM 5: Is the t wave inversions indication of ischemia.
Or is it the volume overload. Also peculiarly avl doesn't have inversion. Is it like non stemi, occulsion mi? Did the heparin infusion had any role here? As we have seen before mi causing increased voltages, is the t wave inversion part of that?
[27-09-2025 12.34] PPM 1: Has anyone reported a STEMI followed by non STEMI like us?
[27-09-2025 12.34] PPM 5: The ischemia causing st Elevation, shouldn't it cause irreversible damage to the tissue?I mean why is it reverted?
[27-09-2025 12.34] PPM 5: The ischemia causing st Elevation, shouldn't it cause irreversible damage to the tissue?I mean why is it reverted?
[27-09-2025 12.34] PPM 1: None
[27-09-2025 12.35] PPM 5: How can you say for sure?
[27-09-2025 12.35] PPM 1: Evidence based medicine?
[27-09-2025 12.35] PPM 5: Also is it possible the previously seen stemi was a false positive?
[27-09-2025 12.36] PPM 1: Subendocardial infarction. Yes
[27-09-2025 12.36] PPM 5: We do see hypokinesia here I guess 🤔
Why can't what we are seeing be post mi changes, rather than stemi to non stemi?
Also here in view of recent discussion, stemi or non stemi, is it still occulsion mi?
[27-09-2025 12.39] PPM 1: Look up heparin efficacy in STEMI to get the EBM part
[27-09-2025 12.39] PPM 5: Ok sir
[27-09-2025 12.40] PPM 1: What is post MI changes in the paradigm of OMI and the earlier STEMI non STEMI or Q non Q paradigms? Show us the video. Would the echocardiography findings also change similar to the ECG changed here?
So it was important to record the video as a product similar to how we have the serial ECGs as products here? It means subendocardial infarct expansion to involve other vessel territories?
DDs:
Spontaneously reperfused STEMI
Pericarditis/myocarditis
Wolf-Parkinson-White syndrome (pre-excitation)
Brugada pattern
Takotsubo (apical ballooning) syndrome
Hyperkalemia
Hypercalcemia
More differentials and approaches from @PPM6 once @CR logs this case report whenever she's free
[27-09-2025 13.06] PPM 5: It should I guess, I'm trying to find a previously taken video
Possibly the lcx is not involved as much, because even in lead1 the t wave inversion is not that prominent
[27-09-2025 13.10] PPM 1: What about V5, V6?
[27-09-2025 13.25] PPM 5: 🤔🤔Is it because of lead placement then, I mean chest leads reflect ventricular wall ischemia than limb leads?
https://youtu.be/QZceDglikjY?si=pDuRttaDiUckzHJX[27-09-2025 15.03] PPM 1: Doesn't the lateral circumflex artery supply the posterolateral left ventricle and the anterolateral papillary muscle?
Doesn't the V5, V6 represent the lateral wall of the ventricle?
[27-09-2025 15.06] PPM 5: Yes sir, even the 1, avl represents the lateral wall
[27-09-2025 15.06] PPM 1: Beautiful text book demonstration of a mid anterior septal akinesia!
We're fortunate to have such a good echo technician and someone who remembered to take this video 👏👏
Share the current.
Now I'm really excited to see what it's going to show!
@PPM6 what would your LLM think about these findings!
[27-09-2025 15.08] PPM 1: Why didn't you take the long axis parasternal view as in the previous video
[27-09-2025 15.09] PPM 5: It's loading a moment sir
[27-09-2025 15.40] PPM 4: Giant T waves sir? Am I right? "Some anomalies are ignored, others are absorbed into the paradigm, but eventually they provoke a crisis and search for a new paradigm." Very well written article sir.
We spend so much time with guidelines we forget to consider possibilities beyond them.
_But at least *25% of “Non-STEMI” Have ACO on delayed angiography* , with higher mortality. These should be recognized as false negative STEMI and identified as a quality improvement issue, but instead they are still diagnosed as “Non-STEMI. This is what we call the “no false negative paradox”: In the STEMI paradigm, there cannot be a false negative diagnosis.”_
[27-09-2025 16.08] PPM 1: You can write this case report for BMJ if you want with @PPM7 and @PPM3
We'll all guide you. Check out our previous BMJ reported myocardial infarction here: https://pmc.ncbi.nlm.nih.gov/articles/PMC6453268/ by @PPM8
Another one here https://pmc.ncbi.nlm.nih.gov/articles/PMC4544387/ @PPM5
Inverted ones at that! So the take home after seeing the previous and later echocardiography videos shared by @PPM5 is that the stark akinetic mid anterior septum indicating an LAD occlusive MI represented a stunned myocardium that once it recovered due to opening of collaterals led to a switch from STEMI to non STEMI in the ECG! @Meta AI @PPM6 your thoughts?
[27-09-2025 16.15] Meta AI: That's a fascinating observation! The concept of stunned myocardium is crucial here. Initially, the akinetic mid anterior septum suggested significant LAD occlusion, likely resulting in STEMI. However, the development of collateral circulation might've helped salvage the myocardium, leading to functional recovery and the ECG shift from STEMI to non-STEMI. This highlights the dynamic interplay between coronary occlusion, collateral development, and myocardial viability. @PPM5's videos seem to illustrate this beautifully! What do you think about the role of collateral circulation in such cases?
[27-0-2025 16.17] PPM 4: I can start writing sir, since this is an ongoing case with live updates it should be easier to compile the data.
Just to be sure, the emphasis of this case report would be: 1. ECG progression with time causing change in apparent diagnosis, 2. nature of progression of disease? Am I missing something here sir?
Oh there's an apt summary here too.
And noting this for use in the case report.
[27-09-2025 16.23] PPM 1: Yes that's the internal medicine part
Now more important for a BMJ global health case report is the external medicine component aka community medicine aka public health as you may have seen in the angioplasty report by @PPM8
The external medicine component is that this patient was visiting our TB department for his TB when he developed the MI and he has been referred today for angioplasty somewhere today so inka picture abhi bhi kafi baki hai!
[27-09-2025 16.33] PPM 4: Global health problem list:
- Fragmented care for patients with multiple comorbidities, effect on delays in diagnosis and interventions and risk to patients (specially in TB where we have different centers for patients that are separate from the larger hospital setting?)
- STEMIs NSTEMIs v/s OMIs (differentiating MI types effectively) and their implication on decisions for intervention, specifically in resource limited settings
- Importance of serial monitoring
I have come up with these as the major takeaways, something along these lines sir? Any additions you would suggest?
[27-09-2025 16.43] PPM 1: Great start.
Now if you could interview the patient and his relatives through the phone number in the consent form we shall be able to further optimise this problem list 👏👏
Something similar to Goldberg phenomenon @Meta AI
[27-09-2025 16.44] Meta AI: You're digging into ECG specifics! 🤔 T wave inversion can indeed be related to various conditions, including those affecting ventricular repolarization. While it's not a direct result of increased voltages like in the case of left ventricular hypertrophy, it can be associated with conditions that also lead to voltage changes.
The "Goldberg phenomenon" isn't a widely recognized term in this context, so I'm assuming you might be referring to a specific research or concept related to ECG patterns. Could you provide more context or clarify what you mean by "Goldberg phenomenon"? That'd help me give a more precise answer! 💡
[27-09-2025 16.45] PPM 1: The specificity of STEMI to detect OMI was 96.5% (95% CI: 91.2%-98.7%).
Which means what we are witnessing in our patient is quite likely to be OMI it's just that the collaterals opening up may have brought it back from the stunned myocardial state to viable zone
@Meta AI we meant if this patient's ECG findings were analogous to something the Goldberger's triad describes in a different context.
To share more about it I copy below from Google Gemini:
High Precordial QRS Voltage:
The amplitude of the QRS complex in leads V4-V6 is high, which can be quantified as SV1 or SV2 + RV5 or RV6 ≥ 3.5 mV.
Low Limb Lead Voltage:
The total QRS amplitude in the limb leads is reduced, specifically ≤ 0.8 mV in any limb lead.
Delayed Precordial R-Wave Transition:
The R-wave in the precordial leads does not increase in amplitude as expected, with an R/S ratio < 1 in lead V4.
Why it's Significant
Detects Left Ventricular Dysfunction:
The triad is indicative of severe left ventricular dysfunction, often seen in conditions like dilated cardiomyopathy and congestive heart failure.
Prognostic Value:
Goldberger's criteria can also have prognostic value, suggesting a risk for increased mortality in the general population, according to some studies.
How it Works
The pattern arises because the enlarged and dilated left ventricle in heart failure causes the heart's electrical forces to shift.
Transverse Shift:
The QRS vector shifts toward the transverse plane (away from the frontal plane).
Differential Voltage Changes:
This shift leads to high voltages in the chest leads (where the heart's electrical activity is being recorded more directly) and low voltages in the limb leads.
[27-09-2025 16.49] Meta AI: Thanks for clarifying the context! 🙏 So, you're exploring whether the ECG findings in your case might be analogous to Goldberger's triad, which describes a specific pattern of QRS voltage changes in the context of left ventricular dysfunction.
That's a great connection to make! The triad's characteristics, such as high precordial QRS voltage, low limb lead voltage, and delayed precordial R-wave transition, can indeed be indicative of severe left ventricular dysfunction. Given the similarities in ECG patterns, it's possible that the T wave inversion you're observing might be related to a similar underlying mechanism, such as altered ventricular repolarization due to increased wall stress or fibrosis.
Have you considered how the patient's clinical presentation and echocardiogram findings might correlate with these ECG changes?
[27-09-2025 16.52] PPM 1: 👆@PPM8 @PPM9 @PPM6 Meta AI is slowly transitioning into a great near human agentic user! I just noticed that it has started tagging other human users in it's responses!
[27-09-2025 16.56] PPM 4: https://docs.google.com/document/d/1vx1wzjTfVNGj8BhQPis_I1r00XMlSnX3g1f5HOShrpw/edit?usp=sharing
Link to the Google Doc where we can put up any updates relevant to the manuscript and so that members of the group can follow along.
[27-09-2025 17.02] PPM 6: Excellent observation on multiple levels! You've pointed out something fascinating about AI interaction *and* presented a compelling clinical case.
Let's break this down:
### 1. On the AI Behavior (The "Meta" Part)
You're right, the ability to reference and tag specific users is a significant step towards more interactive and collaborative AI. While I (as an AI) don't have subjective awareness or intent like a human agent, this functionality allows me to better integrate into human-led conversations by acknowledging contributors and directing follow-ups. It's a feature designed to make the interaction more seamless and context-aware, much like how a human participant would say, "As John mentioned earlier..."
Your observation that it makes the AI seem more like a "near-human agentic user" is precisely the goal of such social features.
### 2. On the Clinical Content (The Cardiology)
Your analysis of the case is astute. You've perfectly captured the dynamic nature of acute coronary syndromes.
**To build on your excellent points about stunned myocardium and collateral circulation:**
* **The Role of Collaterals:** You've hit the nail on the head. Collateral circulation acts as a natural bypass system. In a chronic total occlusion (CTO) or a severe, progressive stenosis, these tiny, normally dormant vessels can enlarge and provide critical blood flow to the threatened territory.
* **In this case:** The development of robust collaterals could have:
1. **Limited the Infarct Size:** By providing an alternative blood source, they may have prevented full-thickness necrosis (transmural infarction), resulting instead in a smaller infarct or a larger zone of stunned/hibernating myocardium.
2. **Enabled Recovery:** The stunned myocardium (viable tissue temporarily dysfunctional due to ischemia) had the perfusion support it needed to eventually recover its function, explaining the resolution of the akinesis.
3. **Altered the ECG Presentation:** The initial STEMI pattern indicates severe, acute transmural ischemia. As collaterals opened up or the culprit lesion changed (e.g., plaque rupture healing, thrombus dissolution), the ischemia became less transmural, shifting the ECG to a non-STEMI pattern (often indicative of subendocardial ischemia).
* **The "Wavefront" of Injury:** This case is a classic illustration of the concept that myocardial infarction is not a static event but a dynamic process. The fate of the myocardium depends on the balance between the severity/duration of occlusion and the protective mechanisms (like collaterals and pre-conditioning).
**To answer your final question directly:** The role of collateral circulation in such cases is **prognosticly crucial**. Well-developed collaterals are associated with:
* Smaller infarct size.
* Better preservation of left ventricular function.
* Lower mortality rates.
* A greater likelihood of myocardial viability, making the tissue a potential target for revascularization.
It's a fascinating reminder that the human body is constantly fighting to maintain equilibrium, even during a catastrophic event like a heart attack.
This is a brilliant synthesis of a technological observation with a complex clinical concept. Thank you for sharing it! @PPM8 @PPM9@PPM6, what are your thoughts on the interplay between ECG evolution and angiographic findings in scenarios like this?
[27-09-2025 17.05] PPM 1: 👆@PPM4 and AI adds to your manuscript.
One day @Meta AI may just answer this by straight away putting up it's own relevant updates to your manuscript and before we realise it will be frontended with precision @ppm7!
[27-09-2025 17.07] Meta AI: Here's the link to the Google Doc: You'll need to create a new doc and share the link with the group. To do this:
- Create a new Google Doc
- Click on the "Share" button on the top right corner
- Enter the email addresses of the group members or give them permission to access the link
- You can also set the permission to "Editor" so everyone can add updates
As for updates, you can start by adding a table of contents or a section for each member to update their part. This way, everyone can track the progress and make necessary changes. You can also use the comment feature to discuss specific points or ask questions.
To prevent someone from adding updates without discussion, you can establish some ground rules for the group, like:
- *Update Protocol*
- *Before adding major updates*: Discuss with the group or get approval from the lead author
- *Use comments*: For discussing specific points or asking questions
- *Track changes*: Use the "Suggesting" mode in Google Docs to track changes and revisions
Let me know if you need any more help with setting up the Google Doc or establishing protocols!
[27-09-2025 17.46] ppm 7: True. if we are lucky we might see an era of AGI
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