56 year old male had 5/10 chest pain for several hours, then presented to the ED in the middle of the night with 1/10 pain.

A 56 year old male with PMHx significant for hypertension had chest pain for several hours, then presented to the ED in the middle of the night.

He reported chest pain that developed several hours prior to arrival and was 5/10 in intensity.  The pain was located in the mid to left chest and developed after riding his bike.   There was associated fatigue when symptoms developed and mild shortness of breath at onset of chest pain however that has since resolved.  

The patient states he experienced similar 7/10 chest pain 2 days prior when he had to hurry to catch the bus.  He states he experienced shortness of breath and chest pain with exertion and once he sat on the bus his symptoms slowly resolved. 

He presented on this day because it did not go away.

Here is his first ECG (1/10 pain):

Smith: sinus rhythm with RBBB and normal ST-T.  No ischemia.

An ECG from 4 years prior was the same.

The Queen of Hearts interpreted "OMI with Low confidence".  This surprises me, but the Queen often sees things that I cannot see.  On the other hand, I have also seen quite a few false positive Queen interpretations in the presence of RBBB.

The explainability map is here:

It seems that part of the diagnosis of OMI is due to T-wave inversion in V4 and V5.  In RBBB, the T-wave should be normally upright, so this is indeed abnormal.

Case Continued

The first hs troponin I returned at 139 ng/L.

Management: The clinical scenario with a troponin of 139 makes the diagnosis of acute MI.  However, I would not activate the cath lab immediately.  Rather, I would manage medically.  If that did not resolve the symptoms, then I would activate the cath lab.  In the absence of clear ECG signs of OMI, one should always start with aspirin and NTG, perhaps intravenous NTG, and see if the pain can be managed.  Do not give opiate analgesics!!  They only mask the underlying pathology.

Aspirin and heparin were given, but no NTG.

Case continued

Another ECG was recorded 3 hours later, still 1/10 pain:

There is sinus bradycardia with RBBB.  There is minimal STE in I and aVL, but this can be quite normal in RBBB.  There is some minimal reciprocal STD in inferior leads.   There is some STD in V1-V3, but this is normal discordant STD in RBBB.  There is minimal STD in V4-V6, but it does not have an ischemic appearance.  There is some non-specific new T-wave inversion in inferior leads; this could be due to inferior reperfusion.  But there are also new Q-waves, stronly suggesting new infarction.

Overall interpretation: this does not look like OMI to me.  

A bedside cardiac ultrasound performed by a true EM expert (Robert Reardon, who wrote the cardiac ultrasound chapter in Ma and Mateer) showed an inferior wall motion abnormality.

This is a conundrum, because it is clear that the patient is having an acute MI, the ECG is dynamic, but the pain is very mild and there is no ECG evidence of active transmural ischemia.  An inferior wall motion abnormality does NOT say that there is active ischemia because previous ischemia will result in persistent wall motion abnormality (stunning).  

We already know that the patient is suffering an acute MI.  We already know that the ischemia is ongoing, though mild (because of the persistent pain).

Only the ECG and presence or absence of pain can tell you what is happening right now.

Again, I would give NTG and re-assess.

Case continued:

A 2nd troponin I returned at 744 ng/L.  So we know there is myocardial infarction and the patient has persistent pain, but it is very mild.

A rising troponin does NOT mean that there is active ischemia.  Troponin tells you what was happening hours ago, not what is happening now.  Again, active presence of ischemia (or absence) and the ECG are the only evidence you have of the present ischemic condition of the myocardium.

Sublingual NTG was given and the pain completely resolved, from 1/10 to 0/10.

3rd ECG at 4 hours, pain free:

ECG is dynamic, since the ischemia is dynamic.  Q-waves are even more pronounced.

Troponin profile

See how the troponins rise even after 3 AM when the ischemia is apparently gone.

No further trops were measured, even after PCI

So we don't know how high they would have gone

Echo the next AM showed dense inferior WMA.

Angiogram:

Culprit for the patient's non-ST elevation myocardial infarction is a thrombotic occlusion of the proximal RCA

Incidentally noted mid LAD occlusion that is suspected to be chronic given heavy proximal calcification and relatively well-developed left to left collaterals.

The culprit was opened and stented.

Learning points:

You must remember that if someone has a brief episode of ischemia, or for a few hours, and then it goes away, that the wall motion abnormality will remain (the myocardium is “stunned”).  Of course if there is infarction, there will also be persistent wall motion abnormality.  Similarly, the troponin that was released during the ischemia will keep rising even though the ischemia is now gone.  

ONLY the ECG and presence or absence of pain tells you the ischemic state of the myocardium at any moment.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO 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

A 29 year old male with chest pain, ST Elevation, and very elevated troponin T

By Magnus Nossen

This ECG is from a young man with no risk factors for CAD, he presented with chest pain. How would you assess this ECG? How confident are you in your assessment? What is your next step? Note: lead format is Cabrera

I was sent this ECG in real time. The patient is a young adult male with chest pain. The chest pain was described as pressure like and radiation to both arms and the jaw. Symptoms were on and off. The pain was worse in the night and better when moving. The patient sought medical attention when the pain recurred for a second straight night accompanied by arm numbness as well as radiating pain. The above ECG was recorded. 

It is easy to say pericarditis in such a case. (young male no risk factors and ST-elevation in several leads) As Dr. Smith has emphasized many times you diagnose pericarditis at your patient's and your own peril. The ST segment depression in V1 had me worried, the (inappropriately) almost isoelectric ST segment in V2 worried me even more. In conjunction with the inferior and lateral minimal ST elevation I felt I had to rule out inferoposterolateral OMI as the consequences can be catastrophic. 

I sent this out to our "EKG Nerdz" group and in spite of his usual warning, Dr. Smith texted back: "I am going to go out on a limb and say it is a fake."  

Dr. Smith's top 2 most important features for differentiating OMI from Pericarditis are 1) absence of reciprocal ST depression in any lead except aVR and 2) "flat" ST segments, meaning without large T-waves, perhaps more specifically stated as a low T/ST ratio.

I accepted the patient for transfer to our PCI center. On arrival patient was slightly tachycardic. HR about 90-100/min. Other vital signs normal. No fever. Hand held echo showed overall ejection fraction being normal. With normal EF the tachycardia is not compensatory. ACS then becomes less likely. Before the lab values returned this patient had an emergent coronary CT angiogram done that ruled out CAD. Final diagnosis was myocarditis. Initial Troponin T  returned at 1233ng/L. Myocarditis can be very difficult if not impossible to differentiate from OMI based on ECG changes. The ECG can show ST-elevation with reciprocal changes and myocarditis can have regional WMA on echo, just as OMI. Invasive or non-invasive angiogram should strongly be considered for this group of patients. A false positive cath lab activation is also off course acceptable for this diagnosis if you cannot get an emergent coronary CT angiogram. 

Retrospectively one can say that the ST depression in V1 and relative ST depression in V2 is likely reciprocal to diffuse ST elevation. (The same reciprocal relationship is seen in severe subendocardial ischemia, just with opposite vector direction where V1 can show ST elevation) 

Below you can find the 3D model of the heart and coronary vessels. Each main coronary artery (LAD, RCA and LCx) are shown in separate images. There are no coronary stenoses.

Description CCTA: Image quality is very good. There are no coronary stenoses. Minimal amount of pericardial effusion. 

Smith: this is an excellent use of CT coronary angiography!

The Queen of Hearts AI model for ECG interpretation is still in its early days. Her interpretation of today’s tracing was OMI high confidence. Maybe eventually she will be able to separate myocarditis from OMI based solely on the ECG. 

Do you think you can outperform the toddler version of the AI model? Keep an eye on the blog as an OMI QUIZ soon will be published where you test yourself vs the Queen!

The QoH groups ECGs into OMI and NOT OMI. Each category is subdivided into three levels of confidence. Thus you can get a reading of NOT OMI (low, mid or high). Or you can get a reading of OMI (low, mid or high). In other words there are six outputs with NOT OMI high confidence on one end and OMI high confidence on the other end. 

How did the Queen do?

The queen was fooled by this one!!

Version 1 was not trained to detect myo- or pericarditis.

Version 2 will do that.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO 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

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

MY Comment, by KEN GRAUER, MD (4/11/2024):

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

One can never get too much practice in recognizing acute tracings that must be distinguished from OMI mimics. I'll add the following thoughts to the interesting presentation by Dr. Magnus Nossen.

• For clarity in Figure-1 — I've reproduced today's ECG. I highlighted in RED the 3rd lead on the left to remind readers that this is lead -aVR (which corresponds to a frontal axis angle = +30 degrees) — in this ECG that displays the Cabrera Format (See My Comment at the bottom of the page in the October 26, 2020 post of Dr. Smith's ECG Blog for review of the Cabrera format). 
• This case is challenging because of the young age of this patient, who presented with severe chest pain — and because of the fairly subtle abnormalities on ECG. In addition to the V1,V2 leads that concerned Dr. Nossen — I would add that there is straightening of the ST segment takeoff in sequential leads -aVR through to lead III, each of which are associated with subtle-but-real J-point ST elevation. (There is a Q wave in lead III of uncertain significance).
• Support that these ST-T wave findings in the limb leads are real, is forthcoming by the utterly flat ST segment in lead aVL. While not the "mirror-image opposite" picture featured by the "magical" reciprocal lead III-to-lead aVL relationship typically seen when there is acute inferior OMI — I interpreted this uncharacteristic ST-T wave flattening in lead aVL as a reciprocal ST-T wave change.  
• Similar straightening of the ST segment takeoff, with slight ST elevation is also seen in leads V5,V6.
• And the patient has sinus tachycardia ... (at ~100/minute).

BOTTOM Line: There clearly is enough on this initial ECG to support Dr. Nossen's concern that a definitive diagnosis needed to be made on this young man with new, persistent chest pain. The significantly elevated Troponin, Echo showing normal LV function without localized wall motion abnormality — and negative coronary CT angiogram all pointed to acute myocarditis.

• As emphasized many times in Dr. Smith's ECG Blog — it may sometimes not be possible to distinguish between acute myocarditis vs acute OMI on the basis of ECG findings and clinical history (See My Comments in the April 25, 2023 —  July 21, 2019 — December 10, 2019 — and January 10, 2020 posts).
• 
  
• P.S.: A diagnosis of acute myocarditis (rather than acute OMI ) — is a much better "fit" for this case because: i) The patient is younger than the usual OMI patient — and description of his chest pain is somewhat atypical; and, ii) The ECG is not quite as we'd expect for an acute infero-postero OMI (ie, there is abnormal ST flattening in lead aVL, but not the expected mirror-image opposite picture of ST-T wave changes as seen in lead III — there is no reciprocal ST-T wave change at all in lead I — and lead V1 rather than V2,V3,V4 shows the clearly abnormal ST segment straightening).

Figure-1: The initial ECG in today's case. The insert that I've added in the lower right shows the rationale for limb lead sequencing used in the Cabrera format. (NOTE: To improve visualization — I've digitized the original ECG using PMcardio).

 

A young woman with chest pain, cath lab activated

This case came from a friend whose sister was the patient. She knew I was interested in ECGs, so she took a photo of this one.

A young woman presented with acute chest pain.

This was her presenting ECG:

What do you think?

This is clearly Brugada phenotype.  There is downsloping ST Elevation in V1 and V2.  To an experienced interpreter, it is clearly not due to OMI.  And it is clearly Brugada phenotype.

The conventional algorithm did not interpret Brugada. 

In fact, it read: ** **ACUTE MI / STEMI ** **

The physicians caring for the patient activated the cath lab for "STEMI".

The interventionalist and cath team came to the hospital, and when the interventionalist saw the ECG, he inquired further and elicited a family history of Brugada syndrome.  He then cancelled the cath lab activation.

Further history revealed that she had had many episodes of syncope.  

She was subsequently diagnosed with Brugada syndrome and received an ICD.

I sent this ECG to the Queen of Hearts:

Also note: how the digitization takes a sideways ECG and makes it perfect!

You may think this is ECG is so obvious that it needs no AI to diagnose. But the conventional algorithm diagnosed STEMI, and an emergency physician activated the cath team based on this ECG.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO 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

Ventricular Fibrillation, ICD, LBBB, QRS of 210 ms, Positive Smith Modified Sgarbossa Criteria, and Pacemaker-Mediated Tachycardia

An elderly man collapsed. There was no bystander CPR.  Medics found him in ventricular fibrillation.  He was defibrillated, but they also noticed that he was being internally defibrillated and then found that he had an implantable ICD.

He was unidentified and there were no records available

After 7 shocks, he was successfully defibrillated and brought to the ED.

Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines.

Here is the initial ED ECG.  

What do you think?

Rhythm:  Residents asked me why it is not VT.  If you use calipers (or equvalent), it is clear that the rhythm is irregularly irregular.  So it must be atrial fibrillation.  Then I always look to see if the initial deflection of the QRS has a lot of voltage change per change in time (seen in tachycardias that are initiated from above the ventricle because the propagate through fast conducting purkinje fiber.  In other words, is the initial deflection "steep" [fast depolarization (supraventricular)] or is it not very steep [slow (VT)]?

Answer: it is irregularly irregular and the initial part of the QRS is fast, so this is atrial fibrillation with Left Bundle Branch Block (LBBB).

QRS: very wide (213 ms)

ST-T: The ST-T has a lot of proportionally discordant ST Elevation.  In lead III, the ST/S ratio is 25% (ST measured at the J-point, relative to the PQ junction, is 4.5 mm; the S-wave is 18 mm.  This meets the Smith Modified Sgarbossa criteria for acute OMI in LBBB and Paced Rhythm.

So we should activate the cath lab, right?

I was there and said, "No, I think this is all due to severe chronic cardiomyopathy and cardiac arrest due to primary ventricular fibrillation, not due to ACS."

_____________

Why did I say that?

1. Patient has an ICD, which is primarily placed in patients with cardiomyopathy.

2. The QRS is extremely wide.  (Other thought this was due to hyperkalemia, but the ECG does not have the appearance of hyperkalemia but does have the appearance of severe cardiomyopathy -- LBBB with very wide QRS)

3. The bedside echo showed dilated cardiomyopathy with relatively thin walls.

4. Tachycardia exaggerates ST Elevation in LBBB and Paced rhythm

5. Post cardiac arrest with low flow states can also distort ST and T-wave

See these 3 posts:

--Massive Excessively Discordant Anterior ST Elevation in a Paced Rhythm due to cardiomyopathy

--Wide Complex Tachycardia with Huge ST Elevation. ST segments distorted by tachycardia

--Patient with Paced Rhythm in Severe Cardiomyopathy Presents with SOB due to Acute Decompensated Heart Failure

My suspicion was that the Queen of Hearts would say this was OMI, and I am glad that she did because it is too nuanced to say Not:

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO 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

__________________________

Case continued

He was intubated.  There was hypotension, initially controlled with an epinephrine infusion.  We considered attempting electrical cardioversion to improve blood pressure, but I suspected that he is in chronic atrial fibrillation that would be resistant to cardioversion, either electrical or chemical.

Strangely, the monitor began to show a ventricular paced rhythm at tachycardic rates up to 130.  Why?   Pacemaker mediated tachycardia!  Atrial sensing lead senses, which leads to firing of the ventricle, which creates an impulse going back to atrium and around and around in an endless loop.

Pacemaker mediated tachycardia, also called "Endless Loop Tachycardia," cannot happen during atrial fibrillation, so the A fib must have converted.  The way to terminate PMT is with a magnet, which eliminates sensing so that the infinite loop is terminated.

At this point, the patient was hemodynamically stable.  Moreover, it was not until later that I recognized we were dealing with PMT, so we did not apply a magnet.

Calcium was given for possible hyperkalemia, but K returned at 3.4 mEq/L.

Another ECG was recorded 12 minutes later:

Paced rhythm, probable Pacemaker-Mediated Tachycardia?

Now there is increased ST Elevation and increased ST/T ratio.

This gave me pause, but I still thought this was a false positive due to severe cardiomyopathy.

At 51 minutes, another was recorded:

Still higher ST/S ratio

Ken Grauer notes possible P-waves preceding the 2nd complex, and in 2 of the last 3 complexes in the long lead rhythm strip.

First high sensitivity troponin I returned at 200 ng/L.

Then the patient's electronic record from an outside hospital appeared.

It stated that he had a non-ischemic cardiomyopathy, with EF of 15% and atrial fibrillation, and a normal angiogram 3 years prior.

I wrote the following note in the chart:

"V Fib arrest, has ICD.  Bedside US shows extremely poor EF with dilated cardiomyopathy.  In A fib with RVR, sometimes being paced.

"ECG with LBBB and QRS of > 210 ms.  The ECG meets Smith modified sgarbossa criteria but this often is the case with severe cardiomyopathy.  Presence of ICD and dilation on bedside US is c/w chronic severe cardiomyopathy, with large end diastolic diameter and thin walls.

"For this reason we did not believe this was an acute coronary event and did not activate the cath lab.

"Cardiology agreed.

"Subsequent ECGs showed even more ST elevation, but I still thought this was chronic.

"Old records still had not appeared.

"Around 1015 we were able to access Care everywhere and this showed that he has a non-ischemic cardiomyopathy with EF of 15%.  Angiogram in 2021 was normal.  Could not obtain a previous 12-lead ECG even by calling the U. They stated there were none in the record (hard to believe).  Initial trop ~200.  

"This confirmed my suspicions.

"The patient was admitted without angiogram."

Here is the troponin profile overnight:

This is consistent with cardiac arrest without acute coronary occlusion.

An ECG was recorded the next AM:

Pacemaker-mediated tachycardia is resolved

Ken Grauer noted that there appear to be P-waves preceding pacer spikes (I don't think this changes anything significantly).

Now with a lower heart rate and less proximity to cardiac arrest, the ST segments are proportional.

A few hours later, a formal echo was recorded:

The estimated left ventricular ejection fraction is 11 %.

The estimated pulmonary artery systolic pressure is 23 mmHg + RA pressure.

No wall motion abnormality

Decreased left ventricular systolic performance, severe

Left ventricular enlargement, marked

Dilated cardiomyopathy severe

Est. stroke volume 52 cc at HR 70 = 3.64 l/min cardiac output.

Est. Cardiac index: 1.39 l/min/m2

 

Decreased right ventricular systolic performance .

Asynchronous interventricular septal motion IVCD

Asynchronous interventricular septal motion left bundle branch block.

Device lead(s) visualized in right heart chambers.

Asynchronous interventricular septal motion right ventricular pacing. 

Follow Up:

Later history: a witness who was present with the patient when it all started stated that he became short of breath before collapsing.  

ICD Interrogation:  ICD interrogation the next day showed that the patient had developed an irregular supraventricular tachyarrhythmia (probably atrial fibrillation with RVR, which was the probable etiology of shortness of breath) that incited internal defibrillation into ventricular fibrillation (whereupon he collapsed). Patient received 11 shocks by ICD and was in V-fib when EMS arrived. 

Finally, the pacer is a biventricular pacer for "CRT = cardiac resynchronization therapy."  Most patients with heart failure with reduced ejection fraction and left bundle branch block with a QRS over 130 ms should get one.  Briefly, LBBB causes "dyssynchrony" between the ventricles.  In other words, the RV contracts before the LV and this results in diminished LV EF.  So a dual chamber pacer is placed with one lead through the coronary sinus to the LV.  Then, during placement, the electrophysiologist varies the interval between the stimuli of the 2 ventricles until EF is optimal.

The patient awoke and had a good outcome!